Journal articles on the topic 'HFHC'
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Hammoud, Rola, Emanuela Pannia, Chih-Sheng Liao, Ruslan Kubant, Erland Arning, Teodoro Bottiglieri, Zdenka Pausova, and G. Harvey Anderson. "Choline Supplementation Mitigates the Adverse Effects of a High Folic Acid Maternal Diet on Food Intake Regulation in the Offspring." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 1806. http://dx.doi.org/10.1093/cdn/nzaa067_033.
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Abstract Objectives Folic acid (FA) intake by many women in North America is exceeding recommendations. We have shown that high maternal FA induces methylation-dependent programming of energy regulation associated with an obesogenic phenotype in adult rat offspring. However, it is unclear if this is a direct effect of high FA or due to an imbalance between FA and other methyl-nutrients (i.e., choline) in the 1-carbon cycle. Unlike FA, choline intake by women is below recommendations and is absent from most prenatal supplements, potentially affecting fetal development. The objective of this study was to examine the mechanisms and effects of choline content in high FA maternal diets on in-utero programming of energy regulation and later-life offspring phenotype. Methods Pregnant Wistar rats were fed an AIN-93 G diet with recommended FA and choline (1X, RFRC, control), or 5X-FA diet with choline at 0.5X-(HFLC), 1X-(HFRC), or 2.5X- (HFHC). In pups at birth, brain and liver 1-carbon metabolites, hypothalamic DNA methyltransferase (DNMT) activity and global DNA methylation (5-mC%) were measured. At weaning, one male pup/dam was fed the control diet and weekly weight-gain and food intake were recorded for 20 weeks. Results Offspring born to dams on the HFLC and HFRC, but not HFHC diet, had higher food intake (P < 0.05) and weight-gain (P < 0.01) than controls. In liver at birth, free choline was lower in HFHC than in HFLC pups, but betaine was unaffected. In contrast, in brains, betaine but not free choline concentrations, directly reflected the maternal choline diets. These results suggest that choline may modulate central food intake pathways via the methyl-donor betaine, warranting further investigation. Hypothalamic DNMT activity was highest (P < 0.05) in HFLC pups but global methylation was not affected. Thus, gene expression by RNA sequencing and gene-specific methylation in the hypothalamus is in progress to elucidate the mechanisms underlying the observed phenotype. Conclusions Increased maternal choline mitigates the high FA diet induced increase in body weight and food intake in the adult offspring and results in tissue-specific changes in 1-carbon metabolism at birth. These findings have potential application to human health, providing support to optimize choline and FA intakes by women of childbearing age. Funding Sources CIHR-INMD.
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Valdes, J., A. Armas, J. Gagné Sansfaçon, V. Reyes-Nicolas, N. Rivard, G. Marrero, N. Perreault, and A. Menendez. "A259 HIGH-FAT/HIGH-CHOLESTEROL DIETS PREDISPOSE THE HOST TO EXACERBATED ENTERIC INFECTIONS." Journal of the Canadian Association of Gastroenterology 3, Supplement_1 (February 2020): 136–37. http://dx.doi.org/10.1093/jcag/gwz047.258.
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Abstract Background High-fat/high-cholesterol diets are a well established risk factor for cardiovascular and metabolic diseases, given their propensity to trigger perturbations ranging from altering whole body lipid profile to the induction of intestinal dysbiosis. However much less is known about their effects on the host’s susceptibility to enteric infections. Aims To determine the effects of high-fat/high-cholesterol diets over the host’s susceptibility to enteric bacterial infections and identify the underlying molecular mechanisms. Methods C57BL/6 mice were given two different high-fat/high-cholesterol diets; HFHC (40% kcal fat, 1.25% cholesterol) or HFHCC (40% kcal fat, 1.25% cholesterol, 0.5% sodium cholate) and a control, normal diet (ND, 10% kcal fat, 0% cholesterol, 0% sodium cholate). After four weeks of administration, animals were euthanized and colonic tissue samples taken for histology, immunofluorescence, gene expression analyses, total protein lysates and microbiome sequencing (16S). A separated group of animals was gavaged with FITC-dextran to measure intestinal permeability. Mice fed with the diets for three weeks were infected with ~5x108 cfu of Citrobacter rodentium DBS100/StrpR by oral gavage, and kept on the corresponding diets after the infections. Bacterial shedding in the feces was followed for up to 30 days after infection. Results Administration of the HFHC and HFHCC diets caused an increase in intestinal permeability. Colonic sections stained with H&E and alcian blue evidenced a decreased in the number of mucin-filled goblet cells and a thinner mucus layer, suggesting a defect in the assembly and/or stability of the mucus layer. Expression analyses revealed a drop in the mRNA levels of Muc1 and Muc2, suggesting reduced mucin production. The concentration of IgA was slightly reduced in colon lysates and the transcript levels of the antimicrobial peptide genes Ang4, Leap2 and Cramp were also significantly reduced. Immunofluorescent microscopy showed that goblet cell granules of HFHC- and HFHCC-fed mice were devoid of Relmβ and Tff3, indicating defective production of those two factors critical for intestinal epithelial defense and homeostasis. Collectively, our results suggest that HFHC and HFHCC diets induce differentiation and functional defects in goblet cells. Fecal shedding of C. rodentium showed an increased bacterial burden in HFHC- and HFHCC-fed animals, indicating a more aggressive bacterial infection, accompanied by increased epithelial damage. Conclusions Consumption of high-fat/high cholesterol diets perturb the colonic homeostasis and alter intestinal defenses and the integrity of the intestinal barrier, predisposing the host to a higher susceptibility to enteric infections. Funding Agencies CIHRNSERC
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Kamada, Yoshihiro, Shinichi Kiso, Yuichi Yoshida, Norihiro Chatani, Takashi Kizu, Mina Hamano, Mayumi Tsubakio, et al. "Estrogen deficiency worsens steatohepatitis in mice fed high-fat and high-cholesterol diet." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 6 (December 2011): G1031—G1043. http://dx.doi.org/10.1152/ajpgi.00211.2011.
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Recent studies indicate an accelerated progression of nonalcoholic steatohepatitis (NASH) in postmenopausal women. Hypercholesterolemia, an important risk factor for NASH progression, is often observed after menopause. This study examined the effects of estrogen on NASH in ovariectomized (OVX) mice fed a high-fat and high-cholesterol (HFHC) diet. To investigate the effects of estrogen deficiency, OVX mice and sham-operated (SO) mice were fed normal chow or HFHC diet for 6 wk. Next, to investigate the effects of exogenous estrogen replenishment, OVX mice fed with HFHC diet were treated with implanted hormone release pellets (containing 17β-estradiol or placebo vehicle) for 6 wk. OVX mice on the HFHC diet showed enhanced liver injury with increased liver macrophage infiltration and elevated serum cholesterol levels compared with SO-HFHC mice. Hepatocyte monocyte chemoattractant protein-1 (MCP1) protein expression in OVX-HFHC mice was also enhanced compared with SO-HFHC mice. In addition, hepatic inflammatory gene expressions, including monocytes chemokine (C-C motif) receptor 2 (CCR2), were significantly elevated in OVX-HFHC mice. Estrogen treatment improved serum cholesterol levels, liver injury, macrophage infiltration, and inflammatory gene expressions in OVX-HFHC mice. Moreover, the elevated expression of liver CCR2 and MCP1 were decreased by estrogen treatment in OVX-HFHC mice, whereas low-density lipoprotein dose dependently enhanced CCR2 expression in THP1 monocytes. Our study demonstrated that estrogen deficiency accelerated NASH progression in OVX mice fed HFHC diet and that this effect was improved by estrogen therapy. Hypercholesterolemia in postmenopausal women would be a potential risk factor for NASH progression.
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Zhuang, Zhen-Jie, Chao-Wen Shan, Bo Li, Min-Xia Pang, Han Wang, Yan Luo, Yin-lan Liu, et al. "Linarin Enriched Extract Attenuates Liver Injury and Inflammation Induced by High-Fat High-Cholesterol Diet in Rats." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/4701570.
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The aim of this study was to explore the potential beneficial effects of linarin enriched Flos Chrysanthemi extract (Lin-extract) on nonalcoholic steatohepatitis (NASH) induced by high-fat high-cholesterol (HFHC) diet in rats. SD rats received normal diet, HFHC diet, or HFHC diet plus different doses of Lin-extract. The liver content of triglyceride and total cholesterol markedly increased in HFHC diet-fed model rats while middle and high dose of Lin-extract lowered liver cholesterol significantly. The expression of stearoyl-CoA desaturase (SCD1) was upregulated by HFHC diet and further elevated by high dose Lin-extract. High dose of Lin-extract also markedly lowered the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and inhibited the activation of c-Jun N-terminal kinase (JNK) induced by HFHC in livers. The HFHC-increased mRNA levels of hepatic inflammation cytokines, including monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-α(TNF-α), and chemokine (C-X-C motif) ligand 1 (CXCL1), were suppressed by Lin-extract dose-dependently. Furthermore, pathology evaluation showed that high dose Lin-extract greatly improved lobular inflammation. Our results suggest that Lin-extract could attenuate liver injury and inflammation induced by HFHC diet in rats. Its modulatory effect on lipid metabolism may partially contribute to this protective effect.
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Kim, Hye-Lin, You Mee Ahn, So Min Lee, Chang-Seob Seo, Seong-Hwan Park, Ok-Sun Bang, and Jeeyoun Jung. "Anti-Obesity Effects of Aqueous Extracts of Sunbanghwalmyung-Eum in High-Fat- and High-Cholesterol-Diet-Induced Obese C57BL/6J Mice." Nutrients 14, no. 14 (July 17, 2022): 2929. http://dx.doi.org/10.3390/nu14142929.
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Sunbanghwalmyung-eum (SBH) is a traditional herbal medicine that exhibits various pharmacological properties, such as antioxidant, anti-inflammatory, and anticancer activities. In this study, we investigated the systemic anti-obesity effects of an aqueous extract of SBH in the liver, adipose, and muscle tissue from high-fat and high-cholesterol diet (HFHCD)-induced obese C57BL/6J mice. After 6 weeks of an HFHCD, the mice were continuously fed HFHC with oral administration of SBH (100 mg/kg/day), Sim (simvastatin, 5 mg/kg/day, positive control), or water (HFHC only) for another 6 weeks. Our results showed that SBH attenuated the HFHCD-induced body weight gain and fat accumulation in the liver, and improved plasma lipid levels, such as those of triglycerides (TGs), blood total cholesterol (TC), and low-density lipoprotein (LDL-c). SBH and Sim inhibited the inflammation accompanied by obesity via decreasing inflammatory cytokine interleukin (IL)-1β, tumor necrosis factor α (TNFα), and monocyte chemoattractant protein 1 (MCP1). Moreover, SBH downregulated the expression of protein levels of adipogenic-related factors, including peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα), in the liver, adipose, and muscle tissue. The SBH and Sim treatment also significantly upregulated the phosphorylation of AMP-activated protein kinase α (AMPKα) in the liver and hormone-sensitive lipase (HSL) in the adipose tissue. Overall, the effects of SBH on HFHCD-induced obesity were similar to or more potent than those of simvastatin. These results indicated that SBH has great potential as a therapeutic herbal medicine for obesity.
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Morin, Caroline, Eric Rousseau, Pierre U. Blier, and Samuel Fortin. "Effect of docosahexaenoic acid monoacylglyceride on systemic hypertension and cardiovascular dysfunction." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 1 (July 1, 2015): H93—H102. http://dx.doi.org/10.1152/ajpheart.00823.2014.
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ω-3 Fatty acid supplementation has been associated with lower blood pressure. Cardiovascular diseases are also known to be linked directly to an increase in ω-6 and a reduction in ω-3 fatty acid levels in blood circulation and tissues. To determine the effect of docosahexaenoic acid monoglycerides (MAG-DHA) on blood pressure, lipid profiles, and vascular remodeling in rats fed a high-fat/high-carbohydrate (HFHC) diet. Studies were performed in male rats subjected to 8 wk of HFHC diet supplemented or not with 3 g/day MAG-DHA. After 8 wk of daily MAG-DHA treatment, rats in the HFHC + MAG-DHA group had lower arterial blood pressure and heart rate compared with the HFHC group. Moreover, MAG-DHA prevented the increase aortic wall thickness, whereas lipid analysis of aortic tissues revealed an increase in DHA/AA ratio correlated with the production of resolvin D2 and D3 metabolites. Histological analysis revealed that MAG-DHA prevented the development of LVH in the HFHC group. Serum lipid profile analysis further showed a decrease in total cholesterol (TC) and LDL, including very low-density lipoprotein (VLDL) and triglyceride (TG) levels, together with an increase in HDL levels after 8 wk of MAG-DHA treatment compared with the HFHC group. Furthermore, daily MAG-DHA treatment resulted in reduced proinflammatory marker levels such as CRP, IL-6, TNFα, and IL-1β. Altogether, these findings revealed that per os administration of MAG-DHA prevents HFHC-diet induced hypertension and LVH in rats.
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Alake, Sanmi, Winyoo Chowanadisai, John Ice, Dingbo Lin, Edralin Lucas, Brenda Smith, and Karen Wozniak. "Wheatgerm Supplementation Reduces Gut Inflammation and Epithelial Barrier Dysfunction in IL-10 KO Mice Fed Atherogenic Diet." Current Developments in Nutrition 6, Supplement_1 (June 2022): 972. http://dx.doi.org/10.1093/cdn/nzac068.001.
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Abstract Objectives Wheat germ (WG) contains many bioactive compounds with the potential to maintain an anti-inflammatory gut environment. This study investigated the effects of WG supplementation on gut inflammation and integrity in high-fat fed interleukin (IL)-10 KO mice. Methods Eight-wk-old female B6.129P2-Il10tm1Cgn/J (IL-10KO) and C57BL/6 (WT) mice (n = 10/group) were randomly assigned to diets: WT fed a control diet (WTCO; AIN93-M) and IL-10 KO mice fed control (KOCO), high-fat with high-cholesterol (HFHC; 45% fat kcal, 1% cholesterol), or HFHC + 10% WG (HFWG) for 3 m. Disease activity indices (fecal blood, ruffled fur, stool softness, and rectal prolapse) were monitored twice a week. Fecal indole and short chain fatty acids (SCFAs) concentration were assessed at the beginning and end of study. Proinflammatory cytokines were assessed in the serum and ileum. Ileal and colonic protein expression of transcription factors (STAT3, p-STAT3, PPARg, FoxP3, and AhR), tight junction proteins (ZO-1, occludin), and tryptophan catabolizing enzyme (IDO-1) were assessed by immunoblotting. Relative ileal and colonic gene expression of IL-22 and antimicrobial peptides (Reg3b and Reg3g) were assessed using qRT-PCR. P < 0.05 was considered statistically significant. Results WG increased (P = 0.003) colon length compared to the HFHC group. Weight loss (12.2% in HFHC vs WTCO) was not prevented by WG, but disease activity indices were significantly reduced in the WG vs HFHC group. WG also increased fecal indole, total SCFAs and acetate accompanied by an increase in colonic protein expression of PPARg (P < 0.0001) and FoxP3 (P = 0.001). Ileal STAT3 phosphorylation was reduced (P = 0.0076) due to WG supplementation. An increased colon and ileal protein expression of IDO-1 in the HFHS group was reduced by WG, while also increasing the expression of AhR, ZO-1, and occludin. The relative gene expression of the antimicrobial peptides (Reg3b and Reg3g) was increased (P < 0.05) while serum and ileal tissue concentration of the proinflammatory cytokine, IL-17 was reduced (P = 0.0165 and p = 0.0248 respectively) by WG. Conclusions WG modulated changes that are associated with HF-feeding in IL-10 KO mice, and might be a promising regimen for ameliorating the effects of gut inflammation. Funding Sources Oklahoma Agriculture Experiment Station, Jim and Lynn Williams Professorship, and Barbara K. Pass Grant.
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Lim, Sangbin, Hyeran Won, Yeonghwan Kim, Miran Jang, K. R. Jyothi, Youngseol Kim, Paresh Dandona, Joohun Ha, and Sung Soo Kim. "Antioxidant enzymes induced by repeated intake of excess energy in the form of high-fat, high-carbohydrate meals are not sufficient to block oxidative stress in healthy lean individuals." British Journal of Nutrition 106, no. 10 (June 8, 2011): 1544–51. http://dx.doi.org/10.1017/s0007114511002091.
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It has been reported that high-fat, high-carbohydrate (HFHC) meals increase oxidative stress and inflammation. We examined whether repeated intake of excess energy in the form of HFHC meals alters reactive oxygen species (ROS) generation and the expression levels of antioxidant enzymes and mitochondrial proteins in mononuclear cells, and to determine whether this is associated with insulin resistance. We recruited healthy lean individuals (n 10). The individuals were divided into two groups: one group (n 5) ingested 10878·4 kJ/d (2600 kcal/d; 55–70 % carbohydrate, 9·5–16 % fat, 7–20 % protein) recommended by the Dietary Reference Intake for Koreans for 4 d and the other group (n 5) ingested a HFHC meal containing 14 644 kJ/d (3500 kcal/d). Then, measurements of blood insulin and glucose levels, together with suppressor of cytokine signalling-3 (SOCS-3) expression levels, were performed in both groups. Also, cellular and mitochondrial ROS levels as well as malondialdehyde (MDA) levels were measured. Expression levels of cytosolic and mitochondrial antioxidant enzymes, and mitochondrial complex proteins were analysed. Repeated intake of HFHC meals induced an increase in homeostasis model of assessment-insulin resistance (HOMA-IR), together with an increase in SOCS-3 expression levels. While a single intake of the HFHC meal increased cytosolic and mitochondrial ROS, repeated intake of HFHC meals reduced them and increased the levels of MDA, cytosolic and mitochondrial antioxidant enzymes, and several mitochondrial complex proteins. Repeated intake of HFHC meals induced cellular antioxidant mechanisms, which in turn increased lipid peroxidation (MDA) and SOCS-3 expression levels, induced hyperinsulinaemia and increased HOMA-IR, an index of insulin resistance. In conclusion, excess energy added to a diet can generate detrimental effects in a short period.
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Parra-Vargas, Marcela, Ana Sandoval-Rodriguez, Roberto Rodriguez-Echevarria, Jose Dominguez-Rosales, Arturo Santos-Garcia, and Juan Armendariz-Borunda. "Delphinidin Ameliorates Hepatic Triglyceride Accumulation in Human HepG2 Cells, but Not in Diet-Induced Obese Mice." Nutrients 10, no. 8 (August 10, 2018): 1060. http://dx.doi.org/10.3390/nu10081060.
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Anthocyanin consumption is linked to benefits in obesity-related metabolic alterations and non-alcoholic fatty liver disease (NAFLD), though the functional role of delphinidin (Dp) is yet to be established. Therefore, this study examined the effects of Dp on metabolic alterations associated with NAFLD, and molecular mechanisms in HepG2 cells and diet-induced obese mice. Cells incubated with palmitate to induce lipid accumulation, concomitantly treated with Dp, reduced triglyceride accumulation by ~53%, and downregulated gene expression of CPT1A, SREBF1, and FASN without modifying AMP-activated protein kinase (AMPK) levels. C57BL/6Nhsd mice were fed a standard diet (control) or a high-fat/high-carbohydrate diet (HFHC) for 16 weeks. Mice in the HFHC group were subdivided and treated with Dp (HFHC-Dp, 15 mg/kg body weight/day) or a vehicle for four weeks. Dp did not affect body weight, energy intake, hyperglycemia, insulin resistance, or histological abnormalities elicited by the HFHC diet. Furthermore, the messenger RNA (mRNA) expressions of Acaca, and Fasn in hepatic or epididymal adipose tissue, and the hepatic sirtuin 1 (SIRT1)/liver kinase B1 (LKB1)/AMPK and proliferator-activated receptor alpha (PPARα) signaling axis did not significantly change due to the HFHC diet or Dp. In summary, Dp effectively reduced triglyceride accumulation in vitro through the modulation of lipid metabolic gene expression. However, a dose of Dp administrated in mice simulating the total daily anthocyanin intake in humans had no effect on either metabolic alterations or histological abnormalities associated with HFHC diets.
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Dandona, Paresh, Husam Ghanim, Sanaa Abuaysheh, Kelly Green, Manav Batra, Sandeep Dhindsa, Antoine Makdissi, Reema Patel, and Ajay Chaudhuri. "Decreased insulin secretion and incretin concentrations and increased glucagon concentrations after a high-fat meal when compared with a high-fruit and -fiber meal." American Journal of Physiology-Endocrinology and Metabolism 308, no. 3 (February 1, 2015): E185—E191. http://dx.doi.org/10.1152/ajpendo.00275.2014.
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This study was conducted to investigate whether a high-fat/high-carbohydrate (HFHC) meal induces an increase in plasma concentrations of glucagon, dipeptidyl peptidase-IV (DPP-IV), and CD26 expression in mononuclear cells (MNC) while reducing insulin, C-peptide, proinsulin, GIP, and GLP-1 concentrations. Ten healthy normal subjects were given either a 910-calorie HFHC meal or an American Heart Association (AHA) meal rich in fruit and fiber during the first visit and the other meal during the second visit in crossover design. Blood samples were collected at baseline and at 15, 30, 45, 60, 75, 90, 120, 180, and 300 min following the meal. There was a significantly greater increase in glucose concentrations and lower increase in postprandial insulin, C-peptide, and proinsulin concentrations and lower insulin/glucose ratios following the HFHC meal. HFHC meal intake induced marked increases in plasma glucagon and DPP-IV concentrations and an increase in CD26 mRNA expression in MNC compared with the AHA meal. In addition, the HFHC meal induced a reduction in GIP and peak GLP-1 secretion compared with the AHA meal. This was associated with a significantly greater increase in oxidative stress and proinflammatory mediators including, ROS generation, TNFα, and IL-1β mRNA expression and plasma concentrations of TBARS, FFA, and LPS. We conclude that the proinflammatory HFHC meals result in lower insulin, C-peptide, proinsulin, and GIP secretion in association with higher plasma glucagon and DPP-IV concentrations and CD26 expression in MNC compared with the AHA meal.
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Kulhanek, Debra, Rachel Weigel, and Megan E. Paulsen. "Maternal High-Fat–High-Carbohydrate Diet-Induced Obesity Is Associated with Increased Appetite in Peripubertal Male but Not Female C57Bl/6J Mice." Nutrients 12, no. 10 (September 24, 2020): 2919. http://dx.doi.org/10.3390/nu12102919.
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Diet-induced maternal obesity might play a critical role in altering hypothalamic development, predisposing the offspring to obesity and metabolic disease later in life. The objective of this study was to describe both phenotypic and molecular sex differences in peripubertal offspring energy homeostasis, using a mouse model of maternal obesity induced by a high-fat–high-carbohydrate (HFHC) diet. We report that males, not females, exposed to a maternal HFHC diet had increased energy intake. Males exposed to a maternal HFHC diet had a 15% increased meal size and a 46% increased frequency, compared to the control (CON) males, without a change in energy expenditure. CON and HFHC offspring did not differ in body weight, composition, or plasma metabolic profile. HFHC diet caused decreased hypothalamic glucocorticoid expression, which was further decreased in males compared to females. Maternal weight, maternal caloric intake, and male offspring meal frequency were inversely correlated with offspring hypothalamic insulin receptor (IR) expression. There was a significant interaction between maternal-diet exposure and sex in hypothalamic IR. Based on our preclinical data, we suggest that interventions focusing on normalizing maternal nutrition might be considered to attenuate nutritional influences on obesity programming and curb the continuing rise in obesity rates.
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Ghanim, Husam, Manav Batra, Sanaa Abuaysheh, Kelly Green, Antoine Makdissi, Nitesh D. Kuhadiya, Ajay Chaudhuri, and Paresh Dandona. "Antiinflammatory and ROS Suppressive Effects of the Addition of Fiber to a High-Fat High-Calorie Meal." Journal of Clinical Endocrinology & Metabolism 102, no. 3 (December 1, 2016): 858–69. http://dx.doi.org/10.1210/jc.2016-2669.
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Abstract Background: Fiber intake is associated with a reduction in the occurrence of cardiovascular events and diabetes. Objective: To investigate whether the addition of fiber to a high-fat, high-calorie (HFHC) meal prevents proinflammatory changes induced by the HFHC meal. Design: Ten normal fasting subjects consumed an HFHC meal with or without an additional 30 g of insoluble dietary fiber on 2 separate visits. Blood samples were collected over 5 hours, and mononuclear cells (MNCs) were isolated. Results: Fiber addition to the HFHC meal significantly lowered glucose excursion in the first 90 minutes and increased insulin and C-peptide secretion throughout the 5-hour follow-up period compared with the meal alone. The HFHC meal induced increases in lipopolysaccharide (LPS) concentrations, MNC reactive oxygen species generation, and the expression of interleukin (IL)-1β, tumor necrosis factor α (TNF-α), Toll-like receptor (TLR)-4, and CD14. The addition of fiber prevented an increase in LPS and significantly reduced the increases in ROS generation and the expression of IL-1β, TNF-α, TLR-4, and CD14. In addition, the meal increased Suppressor of cytokine signaling (SOCS)-3 and protein tyrosine phosphatase 1B (PTP-1B) messenger RNA and protein levels, which were inhibited when fiber was added. Conclusions: The addition of fiber to a proinflammatory HFHC meal had beneficial anti-inflammatory and metabolic effects. Thus, the fiber content of the American Heart Association meal may contribute to its noninflammatory nature. If these actions of dietary fiber are sustained following long-term intake, they may contribute to fiber’s known benefits in the prevention of insulin resistance, type 2 diabetes, and atherosclerosis.
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Elmes, M. J., D. S.-Y. Tan, Z. Cheng, D. C. Wathes, and S. McMullen. "The effects of a high-fat, high-cholesterol diet on markers of uterine contractility during parturition in the rat." REPRODUCTION 141, no. 2 (February 2011): 283–90. http://dx.doi.org/10.1530/rep-10-0378.
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Increasing levels of obesity within women of reproductive age is a major concern in the UK. Approximately, 13% of women aged <30 and 22% of 31- to 40-year-old women are obese. Obesity increases complications during pregnancy and the risk of caesarean section due to prolonged labour and poor uterine activity. The aim was to investigate whether a high-fat, high-cholesterol (HFHC) diet decreases markers of uterine contractility during parturition in the rat. Female Wistar rats were fed control (CON,n=10) or HFHC (n=10) diets for 6 weeks. Animals were mated and, once pregnant, maintained on their diet throughout gestation. On gestational day 19, rats were monitored continuously and killed at the onset of parturition. Body and fat depot weights were recorded. Myometrial tissue was analysed for cholesterol (CHOL), triglycerides (TAG), and expression of the contractile associated proteins gap junction protein alpha 1 (GJA1; also known as connexin-43, CX-43), prostaglandin-endoperoxide synthase 2 (PTGS2; also known as cyclo-oxygenase-2, COX-2) and caveolin-1 (CAV1) and maternal plasma for prostaglandin F2α(PGF2α) and progesterone. HFHC fed rats gained greater weight than CON (P<0.003) with significant increases in peri-renal fat (P<0.01). The HFHC diet increased plasma CHOL, TAG and progesterone, but decreased PGF2αversus CON (P<0.01,P<0.01,P=0.05 andP<0.02 respectively). Total CHOL and TAG levels of uterine tissue were similar. However, HFHC fed rats showed significant increases in PTGS2 (P<0.037), but decreases in GJA1 and CAV1 (P=0.059). In conclusion, a HFHC diet significantly increases body weight and alters lipid profiles that correlate with decreases in key markers of uterine contractility. Further work is required to ascertain whether these changes have adverse effects on uterine activity.
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Liu, Yun-Ta, Haw-Wen Chen, Chong-Kuei Lii, Jia-Hua Jhuang, Chin-Shiu Huang, Mei-Ling Li, and Hsien-Tsung Yao. "A Diterpenoid, 14-Deoxy-11, 12-Didehydroandrographolide, in Andrographis paniculata Reduces Steatohepatitis and Liver Injury in Mice Fed a High-Fat and High-Cholesterol Diet." Nutrients 12, no. 2 (February 18, 2020): 523. http://dx.doi.org/10.3390/nu12020523.
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14-Deoxy-11,12-didehydroandrographolide (deAND), a diterpenoid in Andrographis paniculata (Burm. f.) Nees, acts as a bioactive phytonutrient that can treat many diseases. To investigate the protective effects of deAND on reducing fatty liver disease, male mice were fed a high-fat and high-cholesterol (HFHC) diet without or with 0.05% and 0.1% deAND supplementation. Cholesterol accumulation, antioxidant, and anti-inflammatory activities in liver and liver injury were evaluated after deAND treatment. The results show that deAND treatment for seven weeks reduced plasma alanine aminotransferase activity and lowered hepatic cholesterol accumulation, tumor nuclear factor-α, and histological lesions. The 0.1% deAND treatment reduced HFHC diet-induced apoptosis by lowering the caspase 3/pro-caspase 3 ratio. After 11 weeks of deAND treatment, increased NOD-like receptor protein 3 (NLRP3), capase-1, and interleukin-1β protein levels in liver were suppressed by deAND treatment. In addition, nuclear factor erythroid 2-related factor 2 (Nrf2) mRNA expression, heme oxygenase-1 protein expression, and the activities of glutathione peroxidase and glutathione reductase were increased in mice fed the HFHC diet. However, those activities of antioxidant enzymes or proteins were also upregulated by 0.1% deAND treatment. Furthermore, deAND treatment tended to lower hepatic lipid peroxides. Finally, deAND treatment reversed the depletion of hepatic glutamate level induced by the HFHC diet. These results indicate that deAND may ameliorate HFHC diet-induced steatohepatitis and liver injury by increasing antioxidant and anti-inflammatory activities.
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Freeman, Linnea R., and Ann-Charlotte E. Granholm. "Vascular Changes in Rat Hippocampus following a High Saturated Fat and Cholesterol Diet." Journal of Cerebral Blood Flow & Metabolism 32, no. 4 (November 23, 2011): 643–53. http://dx.doi.org/10.1038/jcbfm.2011.168.
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The long-term effects of a diet rich in saturated fat and cholesterol on the hippocampus were evaluated in this study. It has previously been shown that this type of diet is detrimental to health, particularly affecting peripheral organs such as the heart and liver. However, effects on the brain have not been fully evaluated. This study focused on the hippocampus, a brain region instrumental for learning and memory and vulnerable to ischemic damage. Reduced blood—brain barrier (BBB) integrity and increased microgliosis were observed in the hippocampus of rats fed a high-saturated-fat and cholesterol (HFHC) diet for 6 months. Interestingly, an increase in hippocampal protein levels of occludin, a tight junction protein, was found in HFHC-treated rats as well. Further investigation revealed decreased expression of the occludin protein in blood vessels and increased expression in the dentate gyrus hilar neurons and mossy fibers of the hippocampal cornus ammonis 3 in HFHC-treated rats. Our results show alterations in BBB integrity and expression of tight junction proteins after long-term exposure to HFHC diet in rats. These findings may suggest a biologic mechanism for previously observed behavioral deficits occurring in rats fed this diet.
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Asai, Akihiro, Pauline M. Chou, Heng-Fu Bu, Xiao Wang, M. Sambasiva Rao, Anthony Jiang, Christine J. DiDonato, and Xiao-Di Tan. "Dissociation of hepatic insulin resistance from susceptibility of nonalcoholic fatty liver disease induced by a high-fat and high-carbohydrate diet in mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 306, no. 6 (March 15, 2014): G496—G504. http://dx.doi.org/10.1152/ajpgi.00291.2013.
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Liver steatosis in nonalcoholic fatty liver disease is affected by genetics and diet. It is associated with insulin resistance (IR) in hepatic and peripheral tissues. Here, we aimed to characterize the severity of diet-induced steatosis, obesity, and IR in two phylogenetically distant mouse strains, C57BL/6J and DBA/2J. To this end, mice (male, 8 wk old) were fed a high-fat and high-carbohydrate (HFHC) or control diet for 16 wk followed by the application of a combination of classic physiological, biochemical, and pathological studies to determine obesity and hepatic steatosis. Peripheral IR was characterized by measuring blood glucose level, serum insulin level, homeostasis model assessment of IR, glucose intolerance, insulin intolerance, and AKT phosphorylation in adipose tissues, whereas the level of hepatic IR was determined by measuring insulin-triggered hepatic AKT phosphorylation. We discovered that both C57BL/6J and DBA/2J mice developed obesity to a similar degree without the feature of liver inflammation after being fed an HFHC diet for 16 wk. C57BL/6J mice in the HFHC diet group exhibited severe pan-lobular steatosis, a marked increase in hepatic triglyceride levels, and profound peripheral IR. In contrast, DBA/2J mice in the HFHC diet group developed only a mild degree of pericentrilobular hepatic steatosis that was associated with moderate changes in peripheral IR. Interestingly, both C57BL/6J and DBA/2J developed severe hepatic IR after HFHC diet treatment. Collectively, these data suggest that the severity of diet-induced hepatic steatosis is correlated to the level of peripheral IR, not with the severity of obesity and hepatic IR. Peripheral rather than hepatic IR is a dominant factor of pathophysiology in nonalcoholic fatty liver disease.
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Wu, Yue, Ming-Jiang Xu, Zhiyou Cao, Chun Yang, Jinjie Wang, Bijue Wang, Jian Liu, et al. "Heterozygous Ldlr-Deficient Hamster as a Model to Evaluate the Efficacy of PCSK9 Antibody in Hyperlipidemia and Atherosclerosis." International Journal of Molecular Sciences 20, no. 23 (November 26, 2019): 5936. http://dx.doi.org/10.3390/ijms20235936.
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Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a key role in cholesterol homeostasis and atherogenesis. However, there are only limited rodent models, with a functional low-density lipoprotein receptor (LDLR) pathway and cholesteryl ester transfer protein (CETP) to evaluate the drug candidates targeting the PCSK9/LDLR pathway, that are translatable to humans. Here, by using our recently generated LDLR heterozygote (Ldlr+/−) hamster model with functional LDLR pathway and CETP function, we seek to evaluate the effect of a PCSK9 antibody, evolocumab, on dyslipidemia and atherosclerosis compared with ezetimibe, an effective inhibitor of cholesterol absorption, as a positive therapeutic control. We show that the plasma levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglyceride (TG) were significantly increased in Ldlr+/− hamsters fed a high-fat high-cholesterol (HFHC) diet; therefore, areas of atherosclerotic lesion in the aorta were obviously increased and positively correlated with plasma LDL-C and TC. Circulating free PCSK9 was downregulated by the HFHC diet and was undetectable in the evolocumab treated group, as expected. Most importantly, either evolocumab or ezetimibe treatment prevented HFHC diet-induced hyperlipidemia and subsequent atherosclerotic plaque formation. The results indicate that Ldlr+/− hamsters fed an HFHC diet represent an ideal rodent model to evaluate drug candidates that affect LDLR pathways.
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McPhee, Natalie, Aimee Dordevic, Margaret Murray, Ralf Schittenhelm, and Gary Williamson. "Proteomic Analysis of Peripheral Blood Mononuclear Cells Following a Single High Fat High Carbohydrate Meal Challenge." Current Developments in Nutrition 5, Supplement_2 (June 2021): 944. http://dx.doi.org/10.1093/cdn/nzab050_011.
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Abstract Objectives An individual's ability to adapt to a dynamic environment is termed ‘phenotypic flexibility’ and can be weakened by chronic stress, leading to dysregulation of normal homeostatic processes. A long-term high energy and high fat high carbohydrate (HFHC) diet increases risk of metabolic diseases, however, the acute effect of a single HFHC meal on disturbances in metabolic homeostasis is less understood. In this study, we aimed to characterise the effect of a single HFHC meal on the postprandial proteome of peripheral blood mononuclear cells (PBMCs). Methods Twelve healthy men (22.7 ± 3.4 years, BMI of 22.2 ± 1.5 kg/m2) were recruited. Participants consumed a HFHC milkshake after fasting overnight. The meal contained 16 g of carbohydrate and 15 g of fat per 100 g and had a total energy content of 64 kJ/kg body weight. PBMCs were collected at fasting, 3 and 6 hours following the meal. The proteome was measured via LC-MS/MS using untargeted label-free quantification. Differentially expressed proteins were identified with a modified paired t test (limma, R v.4.0.3). Gene ontology analysis was performed with ClueGO v2.5.7 in Cytoscape v3.8.2. Results After filtering to include only high confident proteins consistently detected in each condition, 6007 proteins were identified and included in analysis. Changes in protein expression relative to fasting were observed at 3 hours (143 proteins) and 6 hours (210 proteins) post meal (fold change > ±1.2, p < 0.05). The most highly altered biological processes observed at each timepoint were ‘zymogen activation’ (GO:0,031,638, 31.25% of groups at 3 hours) and ‘ribosome biogenesis’ (GO:0,042,254, 19.15% of groups at 6 hours). Conclusions These results reveal adaptations that occur in the PBMC proteome in response to a single HFHC meal. Changes to proenzyme activation shows a general response in PBMCs to meal-induced changes in the cellular environment, whilst regulation of ribosome synthesis pathways may reflect changes in energy regulation pathways caused by increased nutrient availability. This study characterises the PBMC response in healthy men, and provides a useful reference for future studies that investigate how PBMCs lose the ability to maintain homeostasis following a HFHC meal. Funding Sources Monash University, Melbourne, Australia
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Abu-Elheiga, Lutfi, Hongmei Wu, Ziwei Gu, Rubin Bressler, and Salih J. Wakil. "Acetyl-CoA Carboxylase 2−/− Mutant Mice are Protected against Fatty Liver under High-fat, High-carbohydrate Dietary and de Novo Lipogenic Conditions." Journal of Biological Chemistry 287, no. 15 (February 23, 2012): 12578–88. http://dx.doi.org/10.1074/jbc.m111.309559.
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Hepatic fat accumulation resulting from increased de novo fatty acid synthesis leads to hepatic steatosis and hepatic insulin resistance. We have shown previously that acetyl-CoA carboxylase 2 (Acc2−/−) mutant mice, when fed a high-fat (HF) or high-fat, high-carbohydrate (HFHC) diet, are protected against diet-induced obesity and maintained whole body and hepatic insulin sensitivity. To determine the effect of an ACC2 deletion on hepatic fat metabolism, we studied the regulation of the enzymes involved in the lipogenic pathway under Western HFHC dietary and de novo lipogenic conditions. After completing the HFHC regimen, Acc2−/− mutant mice were found to have lower body weight, smaller epididymal fat pads, lower blood levels of nonesterified fatty acids and triglycerides, and higher hepatic cholesterol than wild-type mice. Significant up-regulation of lipogenic enzymes and an elevation in hepatic peroxisome proliferator-activated receptor-γ (PPAR-γ) protein were found in Acc2−/− mutant mice under de novo lipogenic conditions. The increase in lipogenic enzyme levels was accompanied by up-regulation of the transcription factors, sterol regulatory element-binding proteins 1 and 2, and carbohydrate response element-binding protein. In contrast, hepatic levels of the PPAR-γ and PPAR-α proteins were significantly lower in the Acc2−/− mutant mice fed an HFHC diet. When compared with wild-type mice fed the same diet, Acc2−/− mutant mice exhibited a similar level of AKT but with a significant increase in pAKT. Hence, deleting ACC2 ameliorates the metabolic syndrome and protects against fatty liver despite increased de novo lipogenesis and dietary conditions known to induce obesity and diabetes.
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Ghanim, Husam, Chang Ling Sia, Kelly Korzeniewski, Teekam Lohano, Sanaa Abuaysheh, Anuritha Marumganti, Ajay Chaudhuri, and Paresh Dandona. "A Resveratrol and Polyphenol Preparation Suppresses Oxidative and Inflammatory Stress Response to a High-Fat, High-Carbohydrate Meal." Endocrinology 152, no. 3 (February 2, 2011): 1193–94. http://dx.doi.org/10.1210/endo.152.3.zee1193b.
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Abstract Background: High-fat, high-carbohydrate (HFHC) meals are known to induce oxidative and inflammatory stress, an increase in plasma endotoxin concentrations, and an increase in the expression of suppressor of cytokine signaling-3 (SOCS-3). Hypothesis: The intake of a nutritional supplement containing resveratrol and muscadine grape polyphenols reduces HFHC meal-induced oxidative and inflammatory stress and stimulates the activity of the antioxidant transcription factor, Nrf-2, and its downstream targets. Methods: Ten normal, healthy subjects were given a 930-kcal HFHC meal either with placebo or with the supplement. Indices of oxidative stress, inflammation, Nrf-2 binding activity, the concentrations of endotoxin (lipopolysaccharide) and lipoprotein binding protein (LBP), and the expression of TLR-4, CD14, IL-1β, TNFα, SOCS-3, Keap-1, NQO-1, and GST-P1 were measured. Results: The intake of the supplement suppressed the meal-induced elevations of plasma endotoxin and LBP concentrations, the expression of p47phox, TLR-4, CD14, SOCS-3, IL-1β, and Keap-1, while enhancing Nrf-2 binding activity and the expression of NQO-1 and GST-P1 genes. Conclusion: A supplement containing resveratrol and muscadine polyphenols reduces the magnitude of oxidative stress, increase in lipopolysaccharide and LBP and TLR-4, CD14, IL-1β and SOCS-3 expression after an HFHC meal. It also stimulates specific Nrf-2 activity and induces the expression of the related antioxidant genes, NQO-1 and GST-P1. These results demonstrate the acute antioxidant and antiinflammatory effects of resveratrol and polyphenolic compounds in humans in the postprandial state.
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Morrow, Nadya M., Natasha A. Trzaskalski, Antonio A. Hanson, Evgenia Fadzeyeva, Dawn E. Telford, Sanjiv S. Chhoker, Brian G. Sutherland, Jane Y. Edwards, Murray W. Huff, and Erin E. Mulvihill. "Nobiletin Prevents High-Fat Diet-Induced Dysregulation of Intestinal Lipid Metabolism and Attenuates Postprandial Lipemia." Arteriosclerosis, Thrombosis, and Vascular Biology 42, no. 2 (February 2022): 127–44. http://dx.doi.org/10.1161/atvbaha.121.316896.
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Objective: Nobiletin is a dietary flavonoid that improves insulin resistance and atherosclerosis in mice with metabolic dysfunction. Dysregulation of intestinal lipoprotein metabolism contributes to atherogenesis. The objective of the study was to determine if nobiletin targets the intestine to improve metabolic dysregulation in both male and female mice. Approach and Results: Triglyceride-rich lipoprotein (TRL) secretion, intracellular triglyceride kinetics, and intestinal morphology were determined in male and female LDL (low-density lipoprotein) receptor knockout ( Ldlr –/– ), and male wild-type mice fed a standard laboratory diet or high-fat, high-cholesterol (HFHC) diet ± nobiletin using an olive oil gavage, radiotracers, and electron microscopy. Nobiletin attenuated postprandial TRL levels in plasma and enhanced TRL clearance. Nobiletin reduced fasting jejunal triglyceride accumulation through accelerated TRL secretion and lower jejunal fatty acid synthesis with no impact on fatty acid oxidation. Fasting-refeeding experiments revealed that nobiletin led to higher levels of phosphorylated AKT (protein kinase B) and FoxO1 (forkhead box O1) and normal Srebf1c expression indicating increased insulin sensitivity. Intestinal length and weight were diminished by HFHC feeding and restored by nobiletin. Both fasting and postprandial plasma GLP-1 (glucagon-like peptide-1; and likely GLP-2) were elevated in response to nobiletin. Treatment with a GLP-2 receptor antagonist, GLP-2(3-33), reduced villus length in HFHC-fed mice but did not impact TRL secretion in any diet group. In contrast to males, nobiletin did not improve postprandial lipid parameters in female mice. Conclusions: Nobiletin opposed the effects of the HFHC diet by normalizing intestinal de novo lipogenesis through improved insulin sensitivity. Nobiletin prevents postprandial lipemia because the enhanced TRL clearance more than compensates for increased TRL secretion.
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Singh, Vijay P., Melanie A. Fontaine, Rabban Mangat, Janelle M. Fouhse, Abdoulaye Diane, Benjamin P. Willing, and Spencer D. Proctor. "High Vaccenic Acid Content in Beef Fat Attenuates High Fat and High Carbohydrate Western Diet Induced Changes in Lipid Metabolism and Gut Microbiota in Pigs." Microorganisms 9, no. 12 (December 6, 2021): 2517. http://dx.doi.org/10.3390/microorganisms9122517.
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High-fat diets (HFD) have been shown to induce substantial shifts in intestinal microbial community composition and activity which are associated with adverse metabolic outcomes. Furthermore, changes in microbial composition are affected by fatty acid composition; saturated, monounsaturated (MUFA), and industrial trans fats (iTFA) adversely affect microbial diversity while polyunsaturated fats (PUFA) have been shown to have neutral effects. The effects of naturally occurring trans fats on gut microbial composition are unknown. Vaccenic acid (VA) is the most abundant naturally occurring trans fat (abundant in meat and dairy), can be elevated by altering a cow’s diet, and has been shown to have hypolipidemic effects. The aim of this study was to determine how variations of VA content in beef fat affect gut microbial composition, insulin resistance, and lipid metabolism in pigs. Low birth weight (LBW) and control pigs were fed a control or high-fat, high-carbohydrate (HFHC) diet supplemented with beef fat containing either high or low VA levels for 7 weeks. An adapted modified oral glucose tolerance test and fat challenge test were performed at 9 weeks of age following implantation of jugular catheters. Impacts on microbial composition were assessed using 16S rRNA gene amplicon sequencing. The HFHC diet containing beef fat rich in VA had a mild insulin sensitizing effect (p < 0.05, slope of curve), increased plasma HDL cholesterol (p < 0.05, +28%), reduced postprandial plasma TG (p < 0.05), and showed protection from HFHC-induced changes to gut microbial composition in LBW pigs as compared to HFHC diet containing standard beef fat. This is the first study to show effects of natural trans fats on gut dysbiosis; further studies are needed to elucidate mechanisms.
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Birulina, Yu G., I. V. Petrova, V. V. Ivanov, E. E. Buyko, R. R. Shaibekova, A. V. Grigoreva, I. V. Kovalev, A. V. Nosarev, and S. V. Gusakova. "Changes in Red Blood Cell Membrane Properties: The Role of Metabolic Syndrome Components." International Journal of Biology and Biomedical Engineering 15 (June 21, 2021): 228–33. http://dx.doi.org/10.46300/91011.2021.15.26.
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Metabolic syndrome (MetS) is a cluster of metabolic, hormonal and hemodynamic disorders that contribute to a change in the structural and functional status of erythrocytes and contribute to dysregulation of their cation transport function, where Ca2+ -dependent potassium channels (KCa channels) play an important role. A MetS model was performed using male Wistar rats, which were divided into control and experimental groups. Rats in the control group were fed standard rat chow. Rats in the experimental group were exposed to a high-fat and high-carbohydrate (HFHC) diet for 12 weeks. The data obtained indicate that the HFHC diet led to obesity, high blood pressure, hyperglycemia, impaired glucose tolerance, and dyslipidemia. The level of glutathione (GSH) decreased in the erythrocytes of rats suffering from MetS, but the level of malondialdehyde (MDA) increased. It was shown that the amplitude of the membrane potential of erythrocytes of rats with MetS changed depending on the acting agent: when stimulated with calcium ionophore A23187 it decreased, when the redox system ascorbat –phenazine methosulfate was used, it increased compared to the control group. The data obtained indicate that a HFHC diet leads to changes in the physical and chemical properties of the erythrocyte membrane.
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Hardy, A. B., N. Wijesekara, I. Genkin, K. J. Prentice, A. Bhattacharjee, D. Kong, F. Chimienti, and M. B. Wheeler. "Effects of high-fat diet feeding on Znt8-null mice: differences between β-cell and global knockout of Znt8." American Journal of Physiology-Endocrinology and Metabolism 302, no. 9 (May 1, 2012): E1084—E1096. http://dx.doi.org/10.1152/ajpendo.00448.2011.
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Genomewide association studies have linked a polymorphism in the zinc transporter 8 (Znt8) gene to higher risk of developing type 2 diabetes. Znt8 is highly expressed in pancreatic β-cells where it is involved in the regulation of zinc transport into granules. However, Znt8 is also expressed in other tissues including α-cells, where its function is as yet unknown. Previous work demonstrated that mice lacking Znt8 globally were more susceptible to diet-induced obesity (Lemaire et al., Proc Natl Acad Sci USA 106: 14872–14877, 2009; Nicolson et al., Diabetes 58: 2070–2083, 2009). Therefore, the main goal of this study was to examine the physiological impact of β-cell-specific Znt8 deficiency in mice during high-fat high-calorie (HFHC) diet feeding. For these studies, we used β-cell-specific Znt8 knockout (Ins2Cre:Znt8loxP/loxP) and whole body Znt8 knockout (Cre-:Znt8−/−) mice placed on a HFHC diet for 16 wk. Ins2Cre:Znt8loxP/loxP mice on HFHC diet had similar body weights throughout the study but displayed impaired insulin biosynthesis and secretion and were glucose intolerant compared with littermate control Ins2Cre mice. In contrast, Cre-:Znt8−/− mice became remarkably obese, hyperglycemic, hyperinsulinemic, insulin resistant, and glucose intolerant compared with littermate control Cre- mice. These data show that β-cell Znt8 alone does not considerably aggravate weight gain and glucose intolerance during metabolic stress imposed by an HFHC diet. However, global loss of Znt8 is involved in exacerbating diet-induced obesity and resulting insulin resistance, and this may be due to the loss of Znt8 activity in a tissue other than the β-cell. Thus, our data suggest that Znt8 contributes to the risk of developing type 2 diabetes through β-cell- and non-β-cell-specific effects.
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Pereira, Evelyn Nunes Goulart da Silva, Beatriz Peres de Araujo, Karine Lino Rodrigues, Raquel Rangel Silvares, Carolina Souza Machado Martins, Edgar Eduardo Ilaquita Flores, Caroline Fernandes-Santos, and Anissa Daliry. "Simvastatin Improves Microcirculatory Function in Nonalcoholic Fatty Liver Disease and Downregulates Oxidative and ALE-RAGE Stress." Nutrients 14, no. 3 (February 8, 2022): 716. http://dx.doi.org/10.3390/nu14030716.
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Increased reactive oxidative stress, lipid peroxidation, inflammation, and fibrosis, which contribute to tissue damage and development and progression of nonalcoholic liver disease (NAFLD), play important roles in microcirculatory disorders. We investigated the effect of the modulatory properties of simvastatin (SV) on the liver and adipose tissue microcirculation as well as metabolic and oxidative stress parameters, including the advanced lipoxidation end product–receptors of advanced glycation end products (ALE-RAGE) pathway. SV was administered to an NAFLD model constructed using a high-fat–high-carbohydrate diet (HFHC). HFHC caused metabolic changes indicative of nonalcoholic steatohepatitis; treatment with SV protected the mice from developing NAFLD. SV prevented microcirculatory dysfunction in HFHC-fed mice, as evidenced by decreased leukocyte recruitment to hepatic and fat microcirculation, decreased hepatic stellate cell activation, and improved hepatic capillary network architecture and density. SV restored basal microvascular blood flow in the liver and adipose tissue and restored the endothelium-dependent vasodilatory response of adipose tissue to acetylcholine. SV treatment restored antioxidant enzyme activity and decreased lipid peroxidation, ALE-RAGE pathway activation, steatosis, fibrosis, and inflammatory parameters. Thus, SV may improve microcirculatory function in NAFLD by downregulating oxidative and ALE-RAGE stress and improving steatosis, fibrosis, and inflammatory parameters.
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Wu, Cheng, Ming Wang, and Hui Shi. "Cholesterol Promotes Colorectal Cancer Growth by Activating the PI3K/AKT Pathway." Journal of Oncology 2022 (April 29, 2022): 1–7. http://dx.doi.org/10.1155/2022/1515416.
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Globally, the incidence of colorectal cancer (CRC) increases each year, with an unhealthy diet representing one of the major pathogenic risk factors for CRC. Cholesterol is a vital dietary ingredient required to maintain the normal function of the body; however, disturbances in cholesterol levels have been discovered to exert a significant role in tumorigenesis. The present study is aimed at investigating the role of cholesterol in the occurrence of CRC. Briefly, CRC model mice were established through an intraperitoneal injection of azoxyemethane (AOM) and were subsequently either fed a normal diet (ND), high-fat diet (HFD), or high-fat high-cholesterol diet (HFHC). Furthermore, in vitro experiments were performed following the treatment of SW480 and HCT116 cells with cholesterol, and the cell viability and colony formation rate of CRC cells were analyzed. The findings identified that cholesterol levels were increased in CRC tissues compared with adjacent normal tissues. In contrast, the serum levels of cholesterol were decreased in patients with CRC compared with the healthy controls; however, no significant differences were observed in the cholesterol levels between stage I + II and stage III + IV patients with CRC. Notably, CRC model mice fed with an HFD or HFHC recorded a larger body weight compared with those mice fed a ND; however, no significant differences were reported in the number of tumors formed in each group. Furthermore, the tumor size in the HFHC group was discovered to be increased compared with the ND and HFD groups, and HGD and the pathological morphology were the most pronounced in the HFHC group. Moreover, mice in the HFHC group presented the highest ratio of Ki-67-positive staining and the lowest ratio of TUNEL-positive staining compared with those in the two other groups. Cholesterol treatment also increased the cell viability and clonality of SW480 and HCT116 cells. In addition, the protein expression levels of phosphorylated-AKT were upregulated in cholesterol-induced CRC cells and tissues, whereas the treatment with BAY80-6946 attenuated the cholesterol-induced increases in the cell viability, colony formation ability, and tumor size. In conclusion, the findings of the present study suggested that cholesterol may stimulate the progression of CRC by activating the PI3K/AKT signaling pathway; however, cholesterol may not affect the number of tumors formed in CRC. In addition, cholesterol was discovered to mainly affect the advanced stages of CRC rather than the early stages.
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Malhotra, Pooja, Costica Aloman, Aparna Ankireddy, Hani Khadra, Kohtaro Ooka, Ravinder K. Gill, Seema Saksena, Pradeep K. Dudeja, and Waddah A. Alrefai. "Overactivation of intestinal sterol response element-binding protein 2 promotes diet-induced nonalcoholic steatohepatitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 313, no. 5 (November 1, 2017): G376—G385. http://dx.doi.org/10.1152/ajpgi.00174.2017.
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Nonalcoholic fatty liver disease (NAFLD) is characterized by lipid accumulation in the liver that may progress to hepatic fibrosis and nonalcoholic steatohepatitis (NASH). Mechanisms underlying NAFLD and NASH are not yet fully understood. Dietary cholesterol was recently shown to be a risk factor for the development of NASH, suggesting a role for intestinal handling of cholesterol. One important regulator of cholesterol homeostasis is the sterol response element-binding protein-2 (SREBP-2) transcription factor. We tested the hypothesis that the overactivation of intestinal SREBP-2 increases the susceptibility to diet-induced NASH. A transgenic mouse model with intestine-specific overexpression of active SREBP-2 (ISR2 mice) driven by villin promoter was used. ISR2 mice and their wild-type littermates were fed a regular chow diet or a high-fat, high-cholesterol (HFHC) diet (15% fat, 1% cholesterol) for 15 wk. Results showed that HFHC feeding to ISR2 mice caused hepatic inflammation with increased levels of proinflammatory cytokines. Histological examination demonstrated extensive fibrosis after a HFHC diet associated with a perivascular as well as pericellular collagen deposits in ISR2 mice compared with wild-type littermates. The severe hepatic inflammation and advanced fibrosis in ISR2 mice was not associated with a difference in lipid accumulation in ISR2 mice compared with wild type littermates after HFHC feeding. These data indicate that overactivation of intestinal SREBP2 promotes diet-induced hepatic inflammation with features of human NASH resulting in rapid severe fibrosis and provide a novel link between regulatory processes of intestinal cholesterol and progression of fatty liver. NEW & NOTEWORTHY The current study highlights the role of overactivation of intestinal SREBP-2 transcription factor in the progression of hepatic fibrosis associated with diet-induced NASH. Mice with intestine-specific overexpression of SREBP-2 demonstrated more inflammation and severe fibrosis in the liver in response to 15 wk of being fed a high-cholesterol, high-fat diet as compared with their wild-type littermates. These data demonstrate a novel link between intestinal regulatory processes of cholesterol metabolism and the pathogenesis of fatty liver diseases.
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He, Kai, Xuegang Li, Yubo Xiao, Yang Yong, Zaiqi Zhang, Shuping Li, Taimei Zhou, Daqing Yang, Pincao Gao, and Xiaoliang Xin. "Hypolipidemic effects of Myrica rubra extracts and main compounds in C57BL/6j mice." Food & Function 7, no. 8 (2016): 3505–15. http://dx.doi.org/10.1039/c6fo00623j.
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The present study evaluated the antihyperlipidemic activity of myricetin, myricetrin, the alcohol fraction (AF) and the ethyl acetate fraction (EF) obtained from the bark of Myrica rubra (MR) in high-fat and high-cholesterol (HFHC) induced hyperlipidemic C57BL/6j mice.
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Li, Rui, Ruitong Liu, Lei Chen, Guiping Wang, Liqiang Qin, Zengli Yu, and Zhongxiao Wan. "Microbiota from Exercise Mice Counteracts High-Fat High-Cholesterol Diet-Induced Cognitive Impairment in C57BL/6 Mice." Oxidative Medicine and Cellular Longevity 2023 (January 20, 2023): 1–17. http://dx.doi.org/10.1155/2023/2766250.
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Gut microbes may be the critical mediators for the cognitive enhancing effects of exercise. Via fecal microbiota transplantation (FMT), this study is aimed at determining the mechanism of how voluntary exercise improved learning and memory ability impairment post a high-fat, high-cholesterol (HFHC) diet. The learning and memory abilities assessed via the Morris water maze in the FMT recipient group of voluntary exercising mice were improved compared to sedentary group. 16S rRNA gene sequencing results indicated that exercise-induced changes in gut microbiota distribution were transmissible, mainly in terms of elevated Lactobacillus, Lactobacillus, and Eubacterium nodatum, as well as decreased Clostrida_UCG-014 and Akkermansia after FMT. The neuroprotective effects of FMT were mainly related to the improved insulin signaling pathway (IRS2/PI3K/AKT) and mitochondrial function; inhibition of AQP4; decreased p-Tau at serine 396 and 404; increased BDNF, PSD95, and synaptophysin in the hippocampus; and also decreased HDAC2 and HDAC3 protein expressions in the nuclear and cytoplasmic fractions of the hippocampus. The findings of qRT-PCR suggested that exercise-induced gut microbes, on the one hand, elevated GPR109A and decreased GPR43 and TNF-α in the hippocampus. On the other hand, it increased GPR109A and GPR41 expressions in the proximal colon tissue. In addition, total short-chain fatty acid (SCFA), acetic acid, propionic acid, isobutyric acid, valeric acid, and isovaleric acid contents were also elevated in the cecum. In conclusion, exercise-induced alterations in gut microbiota play a decisive role in ameliorating HFHC diet-induced cognitive deficits. FMT treatment may be a new considerable direction in ameliorating cognitive impairment induced by exposure to HFHC diet.
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Ribas, Vicent, Laura Conde de la Rosa, David Robles, Susana Núñez, Paula Segalés, Naroa Insausti-Urkia, Estel Solsona-Vilarrasa, José C. Fernández-Checa, and Carmen García-Ruiz. "Dietary and Genetic Cholesterol Loading Rather Than Steatosis Promotes Liver Tumorigenesis and NASH-Driven HCC." Cancers 13, no. 16 (August 13, 2021): 4091. http://dx.doi.org/10.3390/cancers13164091.
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The association of nonalcoholic steatohepatitis (NASH) with obesity and type 2 diabetes is a major determinant factor for the continued rise of NASH-driven HCC. Unfortunately, the mechanisms underlying the progression from NASH to HCC are not well-understood. Steatosis is characterized by the accumulation of different lipid species, and cholesterol has emerged as an important player in NASH development, which has been shown to promote NASH-driven HCC. However, recent findings indicated a tumor suppressor role of cholesterol in liver carcinogenesis and HCC development. Thus, we examined the contribution of hepatic steatosis with or without cholesterol accumulation induced by dietary or genetic approaches in liver tumorigenesis and whether the role of cholesterol in NASH-driven HCC is species-dependent. While diethylnitrosamine (DEN) treatment to rats or mice fed a choline-deficient diet decreased the hepatic steatosis, feeding an atherogenic diet enriched in cholesterol potentiated the liver tumor markers. Similar effects were observed in DEN-treated transgenic SREBP-2 mice but not wild-type (WT) mice fed a regular chow diet. Remarkably, long-term feeding of a high-fat high-cholesterol diet (HFHC) but not a high-fat diet (HFD) to WT mice caused severe NASH with spontaneous progression to HCC. A similar outcome was observed in MUP-uPA transgenic mice fed a HFHC diet, which resulted in increased liver tumors and expression of the genes involved in the immune checkpoints. Ezetimibe treatment ameliorated chronic liver disease and, more importantly, tumor multiplicity in HFHC-fed MUP-uPA mice or DEN-treated WT mice. Thus, these results revealed a differential role of steatosis and cholesterol in NASH-driven HCC and indicated that the tumor-promoter role of cholesterol is species-independent and associated with impaired immunosurveillance.
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Arman, Tarana, Katherine D. Lynch, Michelle L. Montonye, Michael Goedken, and John D. Clarke. "Sub-Chronic Microcystin-LR Liver Toxicity in Preexisting Diet-Induced Nonalcoholic Steatohepatitis in Rats." Toxins 11, no. 7 (July 9, 2019): 398. http://dx.doi.org/10.3390/toxins11070398.
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Microcystin-LR (MCLR) is a hepatotoxic cyanotoxin reported to cause a phenotype similar to nonalcoholic steatohepatitis (NASH). NASH is a common progressive liver disease that advances in severity due to exogenous stressors such as poor diet and toxicant exposure. Our objective was to determine how sub-chronic MCLR toxicity affects preexisting diet-induced NASH. Sprague-Dawley rats were fed one of three diets for 10 weeks: control, methionine and choline deficient (MCD), or high fat/high cholesterol (HFHC). After six weeks of diet, animals received vehicle, 10 µg/kg, or 30 µg/kg MCLR via intraperitoneal injection every other day for the final 4 weeks. Incidence and severity scoring of histopathology endpoints suggested that MCLR toxicity drove NASH to a less fatty and more fibrotic state. In general, expression of genes involved in de novo lipogenesis and fatty acid esterification were altered in favor of decreased steatosis. The higher MCLR dose increased expression of genes involved in fibrosis and inflammation in the control and HFHC groups. These data suggest MCLR toxicity in the context of preexisting NASH may drive the liver to a more severe phenotype that resembles burnt-out NASH.
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Xin, Xin, Yue Jin, Xin Wang, Beiyu Cai, Ziming An, Yi-Yang Hu, and Qin Feng. "A Combination of Geniposide and Chlorogenic Acid Combination Ameliorates Nonalcoholic Steatohepatitis in Mice by Inhibiting Kupffer Cell Activation." BioMed Research International 2021 (May 13, 2021): 1–11. http://dx.doi.org/10.1155/2021/6615881.
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The incidence of nonalcoholic steatohepatitis (NASH) is increasing worldwide. Activation of Kupffer cells (KCs) is central to the development of diet-induced NASH. We investigated whether a combination of two active chemical components, geniposide and chlorogenic acid (GC), at a specific ratio (67 : 1), ameliorates diet-induced NASH and the underlying mechanisms involved. C57BL/6J mice exposed to a high-fat and high-cholesterol (HFHC) diet containing cholesterol, choline, and high-sugar drinking water, as well as RAW264.7 cells stimulated with lipopolysaccharide (LPS) were studied. The combination exerted a therapeutic effect on HFHC-induced NASH in mice. Simultaneously, GC was found to reduce the expression of cytokines secreted by hepatic macrophages, including tumor necrosis factor-α (TNF-α), interleukin-1α (IL-1α), IL-1β, IL-6, monocyte chemotactic protein 1 (MCP-1), and granulocyte-macrophage colony-stimulating factor (GM-CSF). Moreover, GC reduced the number of KCs expressing F4/80. Furthermore, TNF-α, inducible nitric oxide synthase (INOS), IL-1β, and IL-6 mRNA and TNF-α protein expression levels were suppressed upon GC treatment in RAW264.7 cells. Our findings suggest that GC has a strong anti-inflammatory effect in NASH, and this effect can be attributed to the suppression of KC activity in the liver.
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Wurdianing, Indrawati, SA Nugraheni, and Zen Rahfiludin. "Efek ekstrak daun sirsak (Annona muricata Linn) terhadap profil lipid tikus putih jantan (Rattus Norvegicus)." Jurnal Gizi Indonesia (The Indonesian Journal of Nutrition) 3, no. 1 (December 1, 2014): 7–12. http://dx.doi.org/10.14710/jgi.3.1.96-101.
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Background: Lipid profile effects is a risk factor for Coronary Heart Disease. Soursop leaves (Annona muricata L) isa traditional medicine plant containing metabolic compounds that contribute to the improvement of the lipid profile.Objective: To determine the effects of soursop leaves extract on lipid profile (total cholesterol, LDL cholesterol, HDLcholesterol and triglyceride).Methods: An experimental study using randomized pre-posttest with control group design. Sample consisted of 28 maleWistar rats, were divided into four groups. The control group (K) was only given High Fat High Cholesterol (HFHC)diet and treatment groups (P1, P2, P3) were given a HFHC diet plus Annona muricata L extract with doses of 100, 200and 300 mg/kgBB per day for 28 days respectively. Data were analyzed by Wilcoxon test, Kruskal-Wallis and MannWhitney.Results: The mean total cholesterol level significantly decreased in the treatment group P1 (p = 0.028) from 60.7 mg/dl(47.6-75.3) to 45.5 mg/dl (38.4-62.4). Mean HDL cholesterol level significantly increased in the treatment group P2(p=0.043) from 26.0 mg/dl (19.7-35.3) to 27.9 mg/dl (18.8-38.0). The mean levels of LDL cholesterol and triglyceridedecreased but not significantly.Conclusion: The administration of Annona muricata L extract can decrease total cholesterol and increase HDLcholesterol significantly.
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van Bennekum, Ariëtte M., David V. Nguyen, Georg Schulthess, Helmut Hauser, and Michael C. Phillips. "Mechanisms of cholesterol-lowering effects of dietary insoluble fibres: relationships with intestinal and hepatic cholesterol parameters." British Journal of Nutrition 94, no. 3 (September 2005): 331–37. http://dx.doi.org/10.1079/bjn20051498.
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Fibres with a range of abilities to perturb cholesterol homeostasis were used to investigate how the serum cholesterol-lowering effects of insoluble dietary fibres are related to parameters of intestinal cholesterol absorption and hepatic cholesterol homeostasis in mice. Cholestyramine, chitosan and cellulose were used as examples of fibres with high, intermediate and low bile acid-binding capacities, respectively. The serum cholesterol levels in a control group of mice fed a high fat/high cholesterol (HFHC) diet for 3 weeks increased about 2-fold to 4·3 mm and inclusion of any of these fibres at 7·5 % of the diet prevented this increase from occurring. In addition, the amount of cholesterol accumulated in hepatic stores due to the HFHC diet was reduced by treatment with these fibres. The three kinds of fibres showed similar hypocholesterolaemic activity; however, cholesterol depletion of liver tissue was greatest with cholestyramine. The mechanisms underlying the cholesterol-lowering effect of cholestyramine were (1) decreased cholesterol (food) intake, (2) decreased cholesterol absorption efficiency, and (3) increased faecal bile acid and cholesterol excretion. The latter effects can be attributed to the high bile acid-binding capacity of cholestyramine. In contrast, incorporation of chitosan or cellulose in the diet reduced cholesterol (food) intake, but did not affect either intestinal cholesterol absorption or faecal sterol output. The present study provides strong evidence that above all satiation and satiety effects underlie the cholesterol-lowering properties of insoluble dietary fibres with moderate or low bile acid-binding capabilities.
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Akinnuga, Akinjide Moses, Angezwa Siboto, Bongiwe Khumalo, Ntethelelo Hopewell Sibiya, Phikelelani Ngubane, and Andile Khathi. "Bredemolic Acid Ameliorates Selected Liver Function Biomarkers in a Diet-Induced Prediabetic Rat Model." Canadian Journal of Gastroenterology and Hepatology 2020 (February 20, 2020): 1–9. http://dx.doi.org/10.1155/2020/2475301.
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Background. Prediabetes is an intermediary hyperglycaemic state that precedes type 2 diabetes mellitus (T2DM) in which abnormal metabolism of glucose and lipids occurs in organs such as the liver. Evidence has shown that, about 70% of T2DM patients develop hepatic dysfunction which is found to begin during the prediabetic stage. Bredemolic acid, a pentacyclic triterpene, has been found to improve insulin sensitivity in diet-induced prediabetic rats. The effects of this compound on liver function, however, are unknown. This study was therefore designed to investigate the effects of BA on liver function in high fat-high carbohydrate (HFHC) diet-induced prediabetic rats. Methods. Thirty-six (36) male rats that weigh 150 g–180 g were divided into two groups, the non-prediabetic (n = 6) and the prediabetic groups (n = 30) that were fed normal diet (ND) and HFHC diet, respectively. The prediabetic rats were further subdivided into five groups (n = 6) and treated with either BA (80 mg/kg) or metformin (MET, 500 mg/kg) every third day for 12 weeks. After 12 weeks, blood samples and the liver were collected for biochemical analysis. Results. The induction of prediabetes resulted in increased release of liver enzymes (AST and ALT), increased liver glycogen and triglyceride, lipid peroxidation, and decreased sterol regulatory element-binding protein (SREBP1c) and antioxidant enzymes. However, the administration of BA decreased liver enzyme concentrations, decreased hepatic oxidative stress, and improved antioxidant enzymes such as SOD and GPx. Conclusion. BA administration improved liver function in diet-induced prediabetic rats in the presence or absence of dietary intervention.
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McGettigan, Brett M., Rachel H. McMahan, and Hugo R. Rosen. "The transcriptional response of Kupffer Cells to fat and cholesterol is non-canonical and distinct from bone-marrow derived macrophages." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 197.15. http://dx.doi.org/10.4049/jimmunol.198.supp.197.15.
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Abstract Diets high in fat and cholesterol can cause hepatic lipid accumulation and inflammation known as non-alcoholic steatohepatitis (NASH). Liver macrophages putatively drive disease by responding to PAMPS/DAMPS and producing pro-inflammatory cytokines. However, recent studies show that there are two principle subsets of macrophages in a NASH liver: Tissue-resident macrophages that are embryonically derived (Kupffer Cells; KCs) and infiltrating macrophages that are adult-derived from bone marrow (IMs). Furthermore, the role that each subset plays in disease pathogenesis is unclear. We FACS sorted the KC (F4/80hiCD11blow) and IM subsets (F4/80lowCD11bhi) from mice fed a high fat/cholesterol (HFHC) diet as well as those from healthy controls. RNA was extracted and gene expression was analyzed using RNA sequencing techniques. HFHC mice had a prominent IM population that was absent in controls. IMs were the primary producers of cytokines and chemokines. KCs did not upregulate pro-inflammatory cytokines in response to dietary fat and cholesterol, yet upstream analysis revealed that lipid metabolism and bile acid signaling pathways were more active than IMs. 3,617 genes were differentially expressed KCs, while 3,421 genes were differentially expressed in IMs. Genes known to be expressed by restorative macrophages were enriched in KCs (CD163, MARCO, TIMD4, MMP12, MMP13), while pro-inflammatory and M1 genes predominated in the IM population (TNF, SPP1, CXCL2, CCL2, S100A8). In conclusion, bone marrow-derived macrophages have a transcriptional profile consistent with the previously reported role of liver macrophages in NASH pathogenesis. However, Kupffer Cells respond to dietary stress in a non-canonical manner.
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Hwang, Sun Mi, Jin Sook Kim, Yun Jung Lee, Jung Joo Yoon, So Min Lee, Dae Gill Kang, and Ho Sub Lee. "Anti-Diabetic Atherosclerosis Effect of Prunella vulgaris in db/db Mice with Type 2 Diabetes." American Journal of Chinese Medicine 40, no. 05 (January 2012): 937–51. http://dx.doi.org/10.1142/s0192415x12500693.
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Diabetes mellitus is the leading cause of vascular complications such as atherosclerosis. This study was designed to investigate whether Prunella vulgaris (APV) would inhibit diabetic atherosclerosis in db/db mice with type 2 diabetes. The db/db mice were treated with high fat/high cholesterol (HFHC) diet and an aqueous extract of APV (100 and 200 mg/kg/day) for eight weeks to examine the long-term effect on metabolic abnormalities and diabetic atherosclerosis. APV treatment markedly lowered blood glucose and systolic blood pressure. The db/db mice experienced an increase in blood urea nitrogen as well as a decrease of creatinine clearance, the latter of which was restored by treatment with APV. Treatment with APV markedly decreased total plasma cholesterol, triglyceride, and LDL-cholesterol and also increased the HDL-cholesterol. In addition, malondialdehyde and TGF-β1 were decreased by treatment of APV. On the other hand, total NO level was decreased in db/db mice. However, the NO level was increased by treatment with APV, suggesting an association with vascular dysfunction. Vascular relaxation of aortic rings by acetylcholine or SNP-inducement was ameliorated by APV in a dose-dependent manner. Damage of vascular intima and hypertrophic of media were observed in db/db mice; however its dysfunction was improved by the treatment of APV. APV treatment significantly reduced the aortic expressions of ICAM-1, VCAM-1, ET-1, and nitrotyrosine. Furthermore, expression of eNOS in aortic was remarkably increased by APV treatment. Taken together, APV suppressed hyperglycemia and diabetic vascular dysfunction in HFHC diet-db/db mice. The present data suggest that Prunella vulgaris may prevent development of diabetic atherosclerosis.
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Ehlers, Kerstin, Tina Brand, Adina Bangert, Hans Hauner, and Helmut Laumen. "Postprandial activation of metabolic and inflammatory signalling pathways in human peripheral mononuclear cells." British Journal of Nutrition 111, no. 12 (February 28, 2014): 2167–75. http://dx.doi.org/10.1017/s0007114514000208.
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High-fat, high-carbohydrate (HFHC) meals induce an inflammatory response in mononuclear cells (MNC). Here, we studied the interaction between metabolic and inflammatory signalling pathways by the measurement of postprandial effects of three different test meals on intracellular Akt, S6 kinase (S6K)/mammalian target of rapamycin and NF-κB signalling in human MNC. We recruited six healthy, lean individuals. Each individual ingested three different meals in the morning separated by at least 3 d: a HFHC meal; an oral lipid-tolerance test meal; a healthy breakfast. Blood samples were obtained before and 1, 2, 4, 6 and 8 h after ingestion. Plasma insulin and IL-6 levels were measured. Intracellular metabolic and inflammatory signalling pathways were assessed by measuring the phosphorylation of Akt kinase and S6K, the degradation of inhibitory κB-α (IκB-α) protein and the DNA binding activity of NF-κB in MNC. mRNA expression levels of the Akt and NF-κB target genes Mn superoxide dismutase (MnSOD), CC-chemokine-receptor 5 (CCR5), intercellular adhesion molecule 1 (ICAM-1) and plasminogen activator inhibitor-1 (PAI-1) were measured by quantitative RT-PCR. We found a positive correlation of Akt phosphorylation with NF-κB activation (NF-κB binding activity: r 0·4500, P= 0·0003; IκB-α protein levels: r − 0·5435, P< 0·0001), a negative correlation of plasma insulin levels with NF-κB binding activity (r − 0·3993, P= 0·0016) and a positive correlation of plasma insulin levels with S6K activation (r 0·4786, P< 0·0001). The activation of Akt and pro-inflammatory NF-κB signalling was supported by the up-regulation of the respective target genes MnSOD and CCR5. In conclusion, the present data suggest a postprandial interaction between the metabolic and inflammatory signalling pathways Akt and NF-κB in MNC.
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Pavithra, S., Parida Subhashree, D. G. Kishor Kumar, K. S. Suhas, Sagar M. Patel, Monalisa Sahoo, Thakur Uttam Singh, and Dinesh Kumar. "High Fat High Cholesterol (HFHC) Diet Alters Liver and Uterine Histopathology in Late Pregnant Rats." Indian Journal of Veterinary Pathology 46, no. 2 (2022): 136–40. http://dx.doi.org/10.5958/0973-970x.2022.00022.0.
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Huang, Yudai, Meng-Fu Tsai, Rajrajeshwari Thorat, Di Xiao, Xuhuiqun Zhang, Amandeep Sandhu, Indika Edirisinghe, and Britt Burton-Freeman. "Acute Effect of Herbs and Spices Intake on Endothelial Function and Metabolic Markers in Overweight or Obese Adults." Current Developments in Nutrition 5, Supplement_2 (June 2021): 324. http://dx.doi.org/10.1093/cdn/nzab037_034.
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Abstract Objectives Herbs and Spices (H/S) contain an array of bioactive compounds with purported health benefits. This study investigated the effect of acute H/S intake on vascular and metabolic health indicators, including flow-mediated vasodilation (FMD), glucose control and inflammatory markers over 24 h in overweight or obese individuals. Methods In this randomized, single-blinded, 4-arm, 24-h, crossover clinical trial, subjects (n = 25, age 37 ± 15 years, BMI 28.5 ± 2.8 kg/m2, mean ± SD) consumed a high-fat and high-carbohydrate (HFHC) challenge meal (about 810 kcal) without (control) or with three different combinations of commercially-available H/S: Italian herbs (rosemary, basil, thyme, oregano, and parsley), cinnamon, or pumpkin pie spice (cinnamon, ginger, nutmeg, and allspice) on four separate days at least three days apart. Meals provided 35% of subjects energy to maintain weight and 1 g H/S per 135 kcal. FMD and blood samples were collected at 0, 2, 4, 5.5, 7, and 24 h for endpoint analysis (additional blood samples at 0.5 and 1 h for insulin/glucose). Mixed-model analysis of repeated measures via PROC MIXED PC-SAS 9.4 was performed on primary and secondary outcome variables. FMD was the primary outcome. Results The addition of H/S in HFHC meals significantly reduced postprandial insulin concentrations over 7 h compared to control (P = 0.03) with no significant decrease in glucose (P = 0.17) compared to the control meal. A significant interaction between H/S and age (P = 0.003) suggested benefits of H/S on insulinemia in individuals 41–65 years. Preliminary analysis showed significant effects of test meal (P < 0.05) on plasma interleukin-6 (IL-6). FMD assessment revealed increased %FMD 24 h after H/S consumption compared to the control meal (P = 0.04), suggesting a possible effect of gut microbial-derived H/S bioactive metabolites, which is under study. Conclusions This study demonstrated the vascular and metabolic effects of meals differing in herbs and spices. Herbs and spices may improve vascular function after 24 h consumption and have different potencies on metabolic indices in different age groups in overweight or obese individuals. Funding Sources This project was funded by McCormick Science Institute.
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Hupa-Breier, Katharina Luise, Janine Dywicki, Björn Hartleben, Freya Wellhöner, Benjamin Heidrich, Richard Taubert, Young-Seon Elisabeth Mederacke, et al. "Dulaglutide Alone and in Combination with Empagliflozin Attenuate Inflammatory Pathways and Microbiome Dysbiosis in a Non-Diabetic Mouse Model of NASH." Biomedicines 9, no. 4 (March 30, 2021): 353. http://dx.doi.org/10.3390/biomedicines9040353.
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Dysregulation of glucose homeostasis plays a major role in the pathogenesis of non-alcoholic steatohepatitis (NASH) as it activates proinflammatory and profibrotic processes. Beneficial effects of antiglycemic treatments such as GLP-1 agonist or SGLT-2 inhibitor on NASH in patients with diabetes have already been investigated. However, their effect on NASH in a non-diabetic setting remains unclear. With this aim, we investigated the effect of long-acting GLP1-agonist dulaglutide and SGLT-2 inhibitor empagliflozin and their combination in a non-diabetic mouse model of NASH. C57BL/6 mice received a high-fat-high-fructose (HFHC) diet with a surplus of cholesterol for 16 weeks. After 12 weeks of diet, mice were treated with either dulaglutide, empagliflozin or their combination. Dulaglutide alone and in combination with empagliflozin led to significant weight loss, improved glucose homeostasis and diminished anti-inflammatory and anti-fibrotic pathways. Combination of dulaglutide and empagliflozin further decreased MoMFLy6CHigh and CD4+Foxp3+ T cells. No beneficial effects for treatment with empagliflozin alone could be shown. While no effect of dulaglutide or its combination with empaglifozin on hepatic steatosis was evident, these data demonstrate distinct anti-inflammatory effects of dulaglutide and their combination with empagliflozin in a non-diabetic background, which could have important implications for further treatment of NASH.
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Srichomphu, Pratthana, Jintanaporn Wattanathorn, Wipawee Thukham-mee, and Supaporn Muchimapura. "Anxiety, Insomnia, and Memory Impairment in Metabolic Syndrome Rats Are Alleviated by the Novel Functional Ingredients from Anacardium occidentale." Antioxidants 11, no. 11 (November 7, 2022): 2203. http://dx.doi.org/10.3390/antiox11112203.
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Despite an increase in the coexistence of metabolic syndrome (MetS) and psychological disorders, together with their great impact on socio-economic burdens, no protective strategies that focus on these situations are available. Due to the role of oxidative stress in the pathophysiology of metabolic syndrome (MetS) and psychological disorders, we hypothesized that substances possessing antioxidant activity such as the novel functional ingredients from Anacardium occidentale (AO) could mitigate common psychological disorders in MetS rats. Male Wistar rats, weighing 200–250 g, were induced with MetS through a 12-week high-fat and high-cholesterol diet (HFHC). Then, they were given AO orally via a gastric gavage needle at doses of 1, 10 and 100 mg/kg BW for 14 days. Spatial memory, anxiety, depression, and sleep behaviors, together with changes in oxidative stress status and neurotransmitters, were assessed. All doses of AO significantly improved memory, anxiety, and sleep, together with the suppression of oxidative stress, AChE, and GABA-T in the cerebral cortex and hippocampus. These results suggest the protective effect of AO against anxiety, insomnia, and memory impairment that coexist with the MetS condition via an improvement in oxidative stress and the functions of the cholinergic and GABAergic systems. However, this benefit requires clinical confirmation.
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Wang, Yue, Yulong Han, Fangni Chai, Hongmei Xiang, Tao Huang, Shuming Kou, Bing Han, Xiaobao Gong, and Xiaoli Ye. "The antihypercholesterolemic effect of columbamine from Rhizoma Coptidis in HFHC-diet induced hamsters through HNF-4α/FTF-mediated CYP7A1 activation." Fitoterapia 115 (December 2016): 111–21. http://dx.doi.org/10.1016/j.fitote.2016.09.019.
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Barros, Érico Luiz Damasceno, Shelon Cristina Souza Pinto, Alvaro Henrique Borges, Mateus Rodrigues Tonetto, Roger Phillip Ellwood, Ian Pretty, and Matheus Coelho Bandéca. "Toothpaste Prevents Debonded Brackets on Erosive Enamel." Scientific World Journal 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/468582.
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This study evaluated the effect of high fluoride dentifrice on the bond strength of brackets after erosive challenge. Eighty-four enamel specimens were divided into seven groups(n=12): WN (distilled water/no acid challenge), W3C (distilled water/3 cycles of acid challenge), and W6C (distilled water/6 cycles of acid challenge) were not submitted to dentifrice treatment. Groups RF3C (regular fluoride dentifrice/3 cycles of acid challenge) and RF6C (regular fluoride dentifrice/6 cycles of acid challenge) were treated with dentifrices containing 1450 μg F−/g and HF3C (high fluoride dentifrice/3 cycles of acid challenge) and HF6C (high fluoride dentifrice/6 cycles of acid challenge) were with 5000 μg F−/g. Acid challenges were performed for seven days. After bond strength test, there was no significant difference among groups submitted to 3 cycles of acid challenge(P>0.05). Statistically significant difference was found between the regular and high fluoride dentifrices after 6 cycles of acid challenge (<0.05). Similar areas of adhesive remaining were found among control groups and among groups W6C, RF3C, RF6C, HF3C, and HF6C. The high fluoride dentifrice was able to prevent the reduction of bond strength values of brackets submitted to acid challenge. Clinical relevance: the high fluoride toothpaste prevents debonded brackets on erosive enamel.
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Kim, Da Eun, Bo Yoon Chang, Byeong Min Jeon, Jong In Baek, Sun Chang Kim, and Sung Yeon Kim. "SGL 121 Attenuates Nonalcoholic Fatty Liver Disease through Adjusting Lipid Metabolism Through AMPK Signaling Pathway." International Journal of Molecular Sciences 21, no. 12 (June 25, 2020): 4534. http://dx.doi.org/10.3390/ijms21124534.
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A ginsenoside F2-enhanced mixture (SGL 121) increases the content of ginsenoside F2 by biotransformation. In the present study, we investigated the effect of SGL 121 on nonalcoholic fatty liver disease (NAFLD) in vitro and in vivo. High-fat, high-carbohydrate-diet (HFHC)-fed mice were administered SGL 121 for 12 weeks to assess its effect on improving NAFLD. In HepG2 cells, SGL 121 acted as an antioxidant, a hepatoprotectant, and had an anti-lipogenic effect. In NAFLD mice, SGL 121 significantly improved body fat mass; levels of hepatic triglyceride (TG), hepatic malondialdehyde (MDA), serum total cholesterol (TC), high-density lipoprotein (HDL), and low-density lipoprotein (LDL); and activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). In HepG2 cells, induced by oxidative stress, SGL 121 increased cytoprotection, inhibited reactive oxygen species (ROS) production, and increased antioxidant enzyme activity. SGL 121 activated the Nrf2/HO-1 signaling pathway and improved lipid accumulation induced by free fatty acids (FFA). Sterol regulatory element-binding protein-1 (SREBP-1) and fatty acid synthase (FAS) expression was significantly reduced in NAFLD-induced liver and HepG2 cells treated with SGL 121. Moreover, SGL 121 activated adenosine monophosphate-activated protein kinase (AMPK), which plays an important role in the regulation of lipid metabolism. The effect of SGL 121 on the improvement of NAFLD seems to be related to its antioxidant effects and activation of AMPK. In conclusion, SGL 121 can be potentially used for the treatment of NAFLD.
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Akinnuga, Akinjide Moses, Angezwa Siboto, Bongiwe Khumalo, Ntethelelo Hopewell Sibiya, Phikelelani Ngubane, and Andile Khathi. "Bredemolic Acid Improves Cardiovascular Function and Attenuates Endothelial Dysfunction in Diet-Induced Prediabetes: Effects on Selected Markers." Cardiovascular Therapeutics 2020 (February 11, 2020): 1–9. http://dx.doi.org/10.1155/2020/1936406.
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Prediabetes is an intermediate hyperglycaemic state which has been associated with cardiovascular dysfunction. However, cardiovascular dysfunction is not only caused by intermediate hyperglycaemia but also endothelial dysfunction, inflammation, and oxidative stress associated with prediabetes. Bredemolic acid (BA), an isomer of maslinic acid, has been reported to ameliorate the intermediate hyperglycaemia found in prediabetes; however, the effects of this triterpene on cardiovascular function have not yet been determined. Therefore, this study investigated the effects of BA on cardiovascular function in diet-induced prediabetic rats. Thirty-six male rats that weighed 150–180 g were divided into two groups, the non-prediabetic (n = 6) and the prediabetic groups (n = 30), which were fed normal diet (ND) and HFHC diet, respectively. The prediabetic rats were further subdivided into five groups (n = 6) and treated with either BA (80 mg/kg) or metformin (MET, 500 mg/kg) every third day for 12 weeks. After 12 weeks, blood samples and the heart were collected for biochemical analysis. The untreated prediabetic rats showed a significant increase in body mass index (BMI), waist circumference (WC), blood pressure, heart rate, lipid profile, lipid peroxidation, and inflammatory markers with significant decrease in endothelial function and antioxidant biomarkers by comparison with the non-prediabetic animals. The administration of BA significantly improved cardiovascular functions such as blood pressure, heart rate, and endothelial function. There was also a significant decrease in BMI, WC, lipid profile, lipid peroxidation, and inflammation with a concomitant increase in antioxidant capacity. BA administration improved cardiovascular function by attenuation of oxidative stress, inflammatory, and endothelial dysfunction markers.
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Soran, Ozlem, Ileana L. Pina, Gervasio A. Lamas, Kimberly Huck, Octaviano Roges, Virginia Schneider, Sheryl F. Kelsey, and Arthur M. Feldman. "The Heart Failure Home Care (HFHC) Trial : A Multicenter, Randomized, Controlled Trial of a Computer Based Telephonic Heart Failure Monitoring System: Design and Methods." Journal of Cardiac Failure 9, no. 5 (October 2003): S113. http://dx.doi.org/10.1016/s1071-9164(03)00339-7.
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Akinnuga, Akinjide Moses, Angezwa Siboto, Bongiwe Khumalo, Ntethelelo Hopewell Sibiya, Phikelelani Ngubane, and Andile Khathi. "Ameliorative Effects of Bredemolic Acid on Markers Associated with Renal Dysfunction in a Diet-Induced Prediabetic Rat Model." Oxidative Medicine and Cellular Longevity 2020 (June 22, 2020): 1–12. http://dx.doi.org/10.1155/2020/2978340.
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Recently, studies have shown that renal dysfunction is associated not only with overt diabetes but also with the preceding stage known as prediabetes. Diet and pharmacological interventions are the therapeutic approaches to managing prediabetes, but the compliance in combining the two interventions is low. Hence, the efficacy of pharmacological intervention is reduced without diet modification. In our previous study, we established that bredemolic acid (BA) ameliorated glucose homeostasis via increased GLUT 4 expression in the skeletal muscle of prediabetic rats in the absence of diet intervention. However, the effects of bredemolic acid on renal function in prediabetic condition are unknown. Therefore, this study was aimed at investigating the ameliorative effects of bredemolic acid on renal dysfunction in a diet-induced prediabetic rat model. Thirty-six Sprague-Dawley male rats (150–180 g) were divided into two groups: the nonprediabetic (n=6) and prediabetic (n=30) groups which were fed normal diet (ND) and high-fat high-carbohydrate (HFHC) diet, respectively, for 20 weeks. After the 20th week, the prediabetic groups were subdivided into prediabetic control (PD) and 4 other prediabetic groups which were treated with either BA (80 mg/kg) or metformin (MET, 500 mg/kg) for further 12 weeks (21st to 32nd). Plasma, urine, and kidney samples were collected for biochemical analysis. The untreated prediabetic (PD) rats presented increased fluid intake and urine output; increased creatinine, urea, and uric acid plasma concentrations; albuminuria; proteinuria; sodium retention; potassium loss; increased aldosterone and kidney injury molecule (KIM-1) concentration; and increased urinary podocin mRNA expression. However, BA administration attenuated the renal markers and oxidative stress and decreased the urinary podocin mRNA expression. In conclusion, BA administration, regardless of diet modification, attenuates renal dysfunction in an experimentally induced prediabetic state.
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Banerjee, G., A. K. Ray, F. Askarian, and E. Ringø. "Characterisation and identification of enzyme-producing autochthonous bacteria from the gastrointestinal tract of two Indian air-breathing fish." Beneficial Microbes 4, no. 3 (September 1, 2013): 277–84. http://dx.doi.org/10.3920/bm2012.0051.
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Characterisation and identification of autochthonous enzyme-producing bacteria isolated from the proximal intestine and distal intestine of two species of Indian air-breathing fish, murrel (Channa punctatus) and stinging catfish (Heteropneustes fossilis), were investigated using conventional culture technique. Population levels of proteolytic strains were highest in the digestive tract of stinging catfish. In both species, the viable counts of amylase-producing bacteria were somewhat higher than cellulase-producing bacteria. Among the gut bacteria isolated, 8 strains (4 from murrel and 4 from stinging catfish) were selected as potent enzyme-producers on the basis of quantitative enzyme assays. All these strains were Gram-positive rods, but only four isolates (CPF4, CPH6, CPH7 and HFH4) were capable of forming endospores. The tested bacteria grew in wide range of temperatures and pH. The strains were further identified by 16S rRNA gene sequence analysis. Two strains, CPF3 (isolated from murrel) and HFH4 (isolated from stinging catfish) showed high similarity to Bacillus sp., strain HFH7 (isolated from the stinging catfish) was most closely related to Bacillus subtilis, while five strains belonged to Bacillus licheniformis. Based on the results of the present study, we suggest that incorporation of autochthonous enzyme-producing bacteria in aquafeeds merits further investigations.
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Park, Man-Young, Jong-Hoon Son, Sang-Woo Kang, and Shi-Woo Rhee. "Comparison of (hexafluoroacetylacetonate)Cu(vinyltrimethylsilane) and (hexafluoroacetylacetonate)Cu(allyltrimethylsilane) for metalorganic chemical vapor deposition of copper." Journal of Materials Research 14, no. 3 (March 1999): 975–79. http://dx.doi.org/10.1557/jmr.1999.0129.
Full textAbstract:
For the metalorganic chemical vapor deposition (MOCVD) of copper, (hfac)Cu(VTMS) (hfac = hexafluoroacetylacetonate, VTMS = vinyltrimethylsilane) and (hfac)Cu(ATMS) (ATMS = allyltrimethylsilane) were compared, and the effect of L ligand in (hfac)Cu–L was examined. It was found by 1H-NMR (nuclear magnetic resonance) that the thermal stability of (hfac)Cu(VTMS) was better than that of (hfac)Cu(ATMS) due to the relatively weak Cu–ATMS bond. From in situ Fourier transform infrared spectroscopy (FTIR) experiments, the formation of Cu(hfac)2, the product of disproportion reaction of Cu(hfac), was observed in the gas phase and (hfac)Cu(ATMS) was found to be more reactive to form Cu(hfac)2. The minimum temperature for the deposition of copper films from (hfac)Cu(ATMS) was as low as 60 °C, which was about 70 °C lower than from (hfac)Cu(VTMS). The grain size of the film deposited with (hfac)Cu(ATMS) was substantially larger than that with (hfac)Cu(VTMS), which showed that the chemical reactivity of the precursor had an influence on the microstructure along with the deposition temperature.