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Journal articles on the topic 'Liver fat'

Author: Grafiati

Published: 4 June 2021

Last updated: 21 February 2023

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1

Koeckerling, David, Jeremy W. Tomlinson, and Jeremy F. Cobbold. "Fighting liver fat." Endocrine Connections 9, no. 7 (July 2020): R173—R186. http://dx.doi.org/10.1530/ec-20-0174.

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Non-alcoholic fatty liver disease is a chronic liver disease which is closely associated with components of the metabolic syndrome. Its high clinical burden results from the growing prevalence, inherent cardiometabolic risk and potential of progressing to cirrhosis. Patients with non-alcoholic fatty liver disease show variable rates of disease progression through a histological spectrum ranging from steatosis to steatohepatitis with or without fibrosis. The presence and severity of fibrosis are the most important prognostic factors in non-alcoholic fatty liver disease. This necessitates risk stratification of patients by fibrosis stage using combinations of non-invasive methods, such as composite scoring systems and/or transient elastography. A multidisciplinary approach to treatment is advised, centred on amelioration of cardiometabolic risk through lifestyle and pharmacological interventions. Despite the current lack of licensed, liver-targeted pharmacotherapy, several promising agents are undergoing late-phase clinical trials to complement standard management in patients with advanced disease. This review summarises the current concepts in diagnosis and disease progression of non-alcoholic liver disease, focusing on pragmatic approaches to risk assessment and management in both primary and secondary care settings.

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2

Rider, Oliver J., Rajarshi Banerjee, Jennifer J. Rayner, Ravi Shah, Venkatesh L. Murthy, Matthew D. Robson, and Stefan Neubauer. "Investigating a Liver Fat." Arteriosclerosis, Thrombosis, and Vascular Biology 36, no. 1 (January 2016): 198–203. http://dx.doi.org/10.1161/atvbaha.115.306561.

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3

Robinson, P. J. A. "Fat and the liver." Imaging 16, no. 4 (September 2004): 364–74. http://dx.doi.org/10.1259/imaging/26666175.

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4

Crunkhorn, Sarah. "Liver enzyme inflames fat." Nature Reviews Drug Discovery 17, no. 5 (April 20, 2018): 315. http://dx.doi.org/10.1038/nrd.2018.59.

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5

Kersten, Sander, and Michael Müller. "Dropping liver fat droplets." Hepatology 50, no. 2 (July 29, 2009): 645–47. http://dx.doi.org/10.1002/hep.23142.

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6

Bronson, Steven M., Brian Westwood, Katherine L. Cook, Nancy J. Emenaker, Mark C. Chappell, David D. Roberts, and David R. Soto-Pantoja. "Discrete Correlation Summation Clustering Reveals Differential Regulation of Liver Metabolism by Thrombospondin-1 in Low-Fat and High-Fat Diet-Fed Mice." Metabolites 12, no. 11 (October 28, 2022): 1036. http://dx.doi.org/10.3390/metabo12111036.

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Thrombospondin-1 (TSP1) is a matricellular protein with many important roles in mediating carcinogenesis, fibrosis, leukocyte recruitment, and metabolism. We have previously shown a role of diet in the absence of TSP1 in liver metabolism in the context of a colorectal cancer model. However, the metabolic implications of TSP1 regulation by diet in the liver metabolism are currently understudied. Therefore Discrete correlation summation (DCS) was used to re-interrogate data and determine the metabolic alterations of TSP1 deficiency in the liver, providing new insights into the role of TSP1 in liver injury and the progression of liver pathologies such as nonalcoholic fatty liver disease (NAFLD). DCS analysis provides a straightforward approach to rank covariance and data clustering when analyzing complex data sets. Using this approach, our previous liver metabolite data was re-analyzed by comparing wild-type (WT) and Thrombospondin-1 null (Thbs1−/−) mice, identifying changes driven by genotype and diet. Principal component analysis showed clustering of animals by genotype regardless of diet, indicating that TSP1 deficiency alters metabolite handling in the liver. High-fat diet consumption significantly altered over 150 metabolites in the Thbs1−/− livers versus approximately 90 in the wild-type livers, most involved in amino acid metabolism. The absence of Thbs1 differentially regulated tryptophan and tricarboxylic acid cycle metabolites implicated in the progression of NAFLD. Overall, the lack of Thbs1 caused a significant shift in liver metabolism with potential implications for liver injury and the progression of NAFLD.

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Zídková, J., J. Sajdok, K. Kontrová, A. Kotrbová-Kozak, T. Hanis, V. Zídek, and A. Fuíková. "Effects of oxidised dietary cod liver oil on the reproductive functions of Wistar rat." Czech Journal of Food Sciences 22, No. 3 (November 16, 2011): 108–20. http://dx.doi.org/10.17221/3414-cjfs.

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Weanling Wistar rats, males and females, were fed for 185 days with diets containing 15% of dietary fat in the form of a mixture of lard and partially oxidised cod liver oil. The proportion of cod liver oil in the dietary fat ranged from 0 to 100%, and the content of malonaldehyde from 0.3 to 19.6 mg/kg of the fat used. Animals fed with diets containing higher proportions of oxidised cod liver oil had higher concentrations of malonaldehyde in their livers. Serum lipid levels were lower in animals fed with higher proportions of cod liver oil than in animals fed control diets (milk fat or lard). The lowest concentration of serum lipid was found in the rats fed the diet containing half of its fat as fish oil. Increased intakes of cod liver oil resulted in lower body weight gains, weights of livers, kidneys, and weights of the reproductive organs. The relative weights of livers and kidneys/body weight were higher in the groups with higher intakes of cod liver oil. High intakes of cod liver oil led to a drastically impaired fertility of females, a decreased litter size, a higher postnatal mortality, and an increased incidence of morphologically abnormal spermatozoa in males.  

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8

Alanen, A., M. Komu, R. Leino, and S. Toikkanen. "MR and magnetisation transfer imaging in cirrhotic and fatty livers." Acta Radiologica 39, no. 4 (July 1998): 434–39. http://dx.doi.org/10.1080/02841859809172459.

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Purpose: To determine whether low-field MR fat/water separation and magnetisation transfer (MT) techniques are useful in studying the livers of patients with parenchymal liver diseases in vivo. Material and Methods: MR and MT imaging of the liver in 33 patients (14 with primary biliary cirrhosis, 15 with alcohol-induced liver disease, and 4 with fatty liver) was performed by means of the fat/water separation technique at 0.1 T. The relaxation time T1 and the MT contrast (MTC) parameter of liver and spleen tissue were measured, and the relative proton density fat content N(%) and MTC of the liver were calculated from the separate fat and water images. The value of N(%) was also compared with the percentage of fatty hepatocytes at histology. Results: The relaxation rate R1 of liver measured from the magnitude image, and the difference in the value of MTC measured from the water image compared with the one measured from the fat and water magnitude image, both depended linearly on the value of N(%). The value of N(%) correlated significantly with the percentage of the fatty hepatocytes. In in vivo fatty tissue, fat infiltration increased both the observed relaxation rate R1 and the measured magnetisation ratio (the steady state magnetisation Ms divided by the equilibrium magnetisation Mo, Ms/Mo) and consequently decreased the MT efficiency measured in a magnitude MR image. The amount of liver fibrosis did not correlate with the value of MTC measured after fat separation. Conclusion: Our results in studying fatty livers with MR imaging and the MT method show that the fat/water separation gives more reliable parametric results. Characterisation of liver cirrhosis by means of the MTC parameter is not reliable, even after fat separation.

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9

Green, Charlotte, and Leanne Hodson. "The Influence of Dietary Fat on Liver Fat Accumulation." Nutrients 6, no. 11 (November 10, 2014): 5018–33. http://dx.doi.org/10.3390/nu6115018.

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10

Yamada, Akiko, Kyoko K. Sato, Shigeki Kinuhata, Shinichiro Uehara, Ginji Endo, Yonezo Hikita, Wilfred Y. Fujimoto, Edward J. Boyko, and Tomoshige Hayashi. "Association of Visceral Fat and Liver Fat With Hyperuricemia." Arthritis Care & Research 68, no. 4 (March 24, 2016): 553–61. http://dx.doi.org/10.1002/acr.22729.

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11

Honap, Sailish, and Jude A. Oben. "Fat and Hidden Liver Cancer." Clinical Liver Disease 17, no. 2 (February 2021): 49–52. http://dx.doi.org/10.1002/cld.1011.

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12

Tsukamoto, Hide. "Fat paradox in liver disease." Keio Journal of Medicine 54, no. 4 (2005): 190–92. http://dx.doi.org/10.2302/kjm.54.190.

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13

Ferrarelli, Leslie K. "Fat, microRNAs, and liver disease." Science 360, no. 6390 (May 17, 2018): 748.14–750. http://dx.doi.org/10.1126/science.360.6390.748-n.

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14

Abdel Monem, Soad, Abdel Hamid Abaza, and Laila Gorrhoury. "Subcutaneous Fat in Liver Cirrhosis." Medical Journal of Ahmed Maher Teaching Hospital 1, no. 10 (December 1, 2012): 759–62. http://dx.doi.org/10.21608/mjam.2012.16795.

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15

Lee, Jae Young. "Ultrasound-Based Liver Fat Quantification." Ultrasound in Medicine & Biology 43 (2017): S151. http://dx.doi.org/10.1016/j.ultrasmedbio.2017.08.1493.

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16

Shah, Pankaj, Ananda Basu, and Robert Rizza. "Fat-induced liver insulin resistance." Current Diabetes Reports 3, no. 3 (May 2003): 214–18. http://dx.doi.org/10.1007/s11892-003-0066-1.

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17

Polavarapu, Abhishek D., Magda Daoud, Jobin Philipose, and Liliane Deeb. "Fat Burner Causing Liver Injury." American Journal of Gastroenterology 112 (October 2017): S1571. http://dx.doi.org/10.14309/00000434-201710001-02950.

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18

Fujisawa, Koichi, Taro Takami, Shoki Okubo, Yuto Nishimura, Yusaku Yamada, Keisuke Kondo, Toshihiko Matsumoto, Naoki Yamamoto, and Isao Sakaida. "Establishment of an Adult Medaka Fatty Liver Model by Administration of a Gubra-Amylin-Nonalcoholic Steatohepatitis Diet Containing High Levels of Palmitic Acid and Fructose." International Journal of Molecular Sciences 22, no. 18 (September 14, 2021): 9931. http://dx.doi.org/10.3390/ijms22189931.

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Among lifestyle-related diseases, fatty liver is the most common liver disease. To date, mammalian models have been used to develop methods for inhibiting fatty liver progression; however, new, more efficient models are expected. This study investigated the creation of a new model to produce fatty liver more efficiently than the high-fat diet medaka model that has been used to date. We compared the GAN (Gubra-Amylin nonalcoholic steatohepatitis) diet, which has been used in recent years to induce fatty liver in mice, and the high-fat diet (HFD). Following administration of the diets for three months, enlarged livers and pronounced fat accumulation was noted. The GAN group had large fat vacuoles and lesions, including ballooning, compared to the HFD group. The GAN group had a higher incidence of lesions. When fenofibrate was administered to the fatty liver model created via GAN administration and liver steatosis was assessed, a reduction in liver fat deposition was observed, and this model was shown to be useful in drug evaluations involving fatty liver. The medaka fatty liver model administered with GAN will be useful in future fatty liver research.

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19

Özbek, Sevan Çetin, Mendane Saka, Nesrin Turhan, Elvan Hortaç Iştar, Cenk Mirza, Nilüfer Bayraktar, and Mehtap Akçil Ok. "Protective Effects of Oral Lactobacillus rhamnosus on Liver Steatosis in Rats on High-Fat Diet." Current Topics in Nutraceutical Research 19, no. 3 (November 25, 2020): 353–58. http://dx.doi.org/10.37290/ctnr2641-452x.19:353-358.

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The purpose of this study was to investigate the effect of probiotic on fatty liver and metabolic endotoxemia in rats on high-fat diet. The rats were divided into three groups and fed one of the three diets (standard or control diet, high-fat diet, or high-fat+probiotic diet) for 16 weeks. At the end of this period, blood samples of the rats were taken and the liver tissue was removed for histopathology. There was an increase in the activities of both aspartate aminotransferase and alanine aminotransferase in the livers of rats on high-fat diet. However, only the rise in aspartate aminotransferase was blunted by incorporation of probiotics to the high-fat diet. Histopathological examination revealed 62.5% hepatosteatosis in high fat diet group and 12.5% in high-fat+probiotic diet group. In conclusion, the protective effect of probiotic supplement on liver steatosis caused by high-fat diet was histopathologically demonstrated; however, its effect on liver enzymes, inflammatory markers, and metabolic endotoxin was not observed. There is a need for further studies in terms of both dose and strain to recommend the use of probiotics in nonalcoholic fatty liver disease.

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20

McLeay, S. C., G. A. Morrish, T. K. Ponnuswamy, B. Devanand, M. Ramanathan, L. Venkatakrishnan, S. Ramalingam, and B. Green. "Noninvasive Quantification of Hepatic Steatosis: Relationship Between Obesity Status and Liver Fat Content." Open Obesity Journal 6, no. 1 (May 16, 2014): 16–24. http://dx.doi.org/10.2174/1876823701406010016.

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The aim of this study was to assess and compare fat content within the liver for normal (body mass index (BMI) < 25 kg/m2), overweight (25-30 kg/m2) and obese (≥ 30 kg/m2) subjects using a noninvasive, non-contrast computed tomography (CT) quantification method. Adult subjects aged 18-60 yrs scheduled to undergo CT examination of the abdominal region were recruited for this study, stratified across BMI categories. Liver volume, fat content, and lean liver volume were determined using CT methods. A total of 100 subjects were recruited, including 30 normal weight, 31 overweight, and 39 obese. Total liver volume increased with BMI, with mean values of 1138 ± 277, 1374 ± 331, and 1766 ± 389 cm3 for the normal, overweight, and obese, respectively (P < 0.001), which was due to an increase in both liver fat content and lean liver volume with BMI. Some obese subjects had no or minimal hepatic fat content. The prevalence of mild fatty liver in this study of 100 subjects was overestimated for all BMI categories using a range of qualitative diagnostic measures, with predicted prevalence of fatty liver in obese subjects ranging from 76.9% for liver-to-spleen ratio ≤ 1.1 to 89.7% for liver attenuation index (liver HU - spleen HU) ≤ 40, compared to 66.7% by quantification of fat content. Results show that total liver volume increases with BMI, however, not all obese subjects display fatty infiltration of the liver. CT quantification of liver fat content may be suitable for accurate diagnosis of hepatic steatosis in clinical practice and assessment of donor livers for transplantation.

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21

Patnana, Srikrishna, Srinivasa Chekuri, and Brian Borg. "Fatty Liver Is Not Always Fat in the Liver." American Journal of Gastroenterology 108 (October 2013): S329. http://dx.doi.org/10.14309/00000434-201310001-01106.

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22

Rosqvist, Fredrik, Joel Kullberg, Marcus Ståhlman, Jonathan Cedernaes, Kerstin Heurling, Hans-Erik Johansson, David Iggman, et al. "Overeating Saturated Fat Promotes Fatty Liver and Ceramides Compared With Polyunsaturated Fat: A Randomized Trial." Journal of Clinical Endocrinology & Metabolism 104, no. 12 (August 1, 2019): 6207–19. http://dx.doi.org/10.1210/jc.2019-00160.

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Abstract Context Saturated fatty acid (SFA) vs polyunsaturated fatty acid (PUFA) may promote nonalcoholic fatty liver disease by yet unclear mechanisms. Objective To investigate if overeating SFA- and PUFA-enriched diets lead to differential liver fat accumulation in overweight and obese humans. Design Double-blind randomized trial (LIPOGAIN-2). Overfeeding SFA vs PUFA for 8 weeks, followed by 4 weeks of caloric restriction. Setting General community. Participants Men and women who are overweight or have obesity (n = 61). Intervention Muffins, high in either palm (SFA) or sunflower oil (PUFA), were added to the habitual diet. Main Outcome Measures Lean tissue mass (not reported here). Secondary and exploratory outcomes included liver and ectopic fat depots. Results By design, body weight gain was similar in SFA (2.31 ± 1.38 kg) and PUFA (2.01 ± 1.90 kg) groups, P = 0.50. SFA markedly induced liver fat content (50% relative increase) along with liver enzymes and atherogenic serum lipids. In contrast, despite similar weight gain, PUFA did not increase liver fat or liver enzymes or cause any adverse effects on blood lipids. SFA had no differential effect on the accumulation of visceral fat, pancreas fat, or total body fat compared with PUFA. SFA consistently increased, whereas PUFA reduced circulating ceramides, changes that were moderately associated with liver fat changes and proposed markers of hepatic lipogenesis. The adverse metabolic effects of SFA were reversed by calorie restriction. Conclusions SFA markedly induces liver fat and serum ceramides, whereas dietary PUFA prevents liver fat accumulation and reduces ceramides and hyperlipidemia during excess energy intake and weight gain in overweight individuals.

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23

Nababan, Saut Horas Hatoguan, Seruni Tyas Khairunissa, Erni Erfan, Nafrialdi Nafrialdi, Ening Krisnuhoni, Irsan Hasan, and Rino Alvani Gani. "Choline-deficient High-fat Diet-induced Steatohepatitis in BALB/c Mice." Molecular and Cellular Biomedical Sciences 5, no. 2 (July 6, 2021): 74. http://dx.doi.org/10.21705/mcbs.v5i2.193.

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Background: Non-alcoholic steatohepatitis (NASH) is an expanding cause of chronic liver disease worldwide, including Indonesia, with higher risk progression to cirrhosis and hepatocellular carcinoma. Preclinical experiments using several mice models have been conducted to clarify its complex pathogenesis. This study was designed to investigate whether BALB/c mice on a choline-deficient high-fat diet can be used as a model for NASH. Materials and Methods: BALB/c male mice were fed choline-deficient L-amino acid-defined high-fat diet (CDAHFD) or a standard diet for six weeks. The body and liver weights, liver histology, and plasma biochemistry were analyzed. The relative expression levels of tumor necrosis factor (TNF)α, transforming growth factor (TGF)β1, collagen-1α1 (COL1α1), glutathione peroxidase 1 (GPx1), and uncoupling protein 2 (UCP2) genes in the livers were analyzed using a two-step real time-polymerase chain reaction. Liver fatty acids composition was analyzed using gas chromatography with flame ionization detector (GC-FID). Results: CDAHFD induced steatohepatitis in BALB/c mice with increased plasma levels of alanine aminotransferase. The liver of CDAHFD-fed BALB/c mice showed upregulated relative expression levels of TNFα, TGFβ1, COL1α1, GPx1, and UCP2 genes. The liver fatty acid analysis showed a significant accumulation of saturated fatty acids (SFAs) and an increased ratio of n-6/n-3 polyunsaturated fatty acids (PUFAs) in the livers of CDAHFD-fed BALB/c mice. Conclusion: This study suggests that CDAHFD can induce steatohepatitis in BALB/c mice and therefore may be used as NASH mice model.Keywords: steatohepatitis, fatty liver, choline-deficient high fat diet, BALB/c

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Westerbacka, Jukka, Katriina Lammi, Anna-Maija Häkkinen, Aila Rissanen, Irma Salminen, Antti Aro, and Hannele Yki-Järvinen. "Dietary Fat Content Modifies Liver Fat in Overweight Nondiabetic Subjects." Journal of Clinical Endocrinology & Metabolism 90, no. 5 (May 2005): 2804–9. http://dx.doi.org/10.1210/jc.2004-1983.

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25

XING, XUEKUN, HUI WAN, and LAN ZHAO. "CCL2 affects fat metabolism in liver regeneration by regulating ADRP expression." Medycyna Weterynaryjna 76, no. 11 (2020): 652–55. http://dx.doi.org/10.21521/mw.6467.

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This study aimed to elucidate the effect of chemokine (c-c motif) ligand 2 (CCL2) on fat metabolism in liver regeneration. CCL2 shRNA expression plasmids were constructed and transfected into rats using hydraulic transgenic technology. Transfection efficiency was measured using a fluorescence microscope. We also measured serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) to test liver functioning. The weights of regenerative livers were recorded and the liver index was calculated. We used immunohistochemistry to determine the expression of PCNA, and used western blot to measure expression levels of adipose differentiation related protein (ADRP). After transfection of pGenesil-1.0-ccl2 into the liver, expression levels of green fluorescent protein were 35% at 6 h, and the liver index as well as levels of ALT, AST, PCNA, and ADRP were all lower than those in the group that underwent partial hepatectomy. We conclude that CCL2 may affect fat metabolism in liver regeneration by inhibiting the expression of ADRP.

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Nguyen-Duy, Thanh-Binh, Milton Z. Nichaman, Timothy S. Church, Steven N. Blair, and Robert Ross. "Visceral fat and liver fat are independent predictors of metabolic risk factors in men." American Journal of Physiology-Endocrinology and Metabolism 284, no. 6 (June 1, 2003): E1065—E1071. http://dx.doi.org/10.1152/ajpendo.00442.2002.

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We examined the independent associations among abdominal adipose tissue (AT), liver fat, cardiorespiratory fitness (CRF), and lipid variables in 161 Caucasian men who had a wide variation in adiposity. We measured AT and liver fat by computed tomography and CRF by a maximal exercise test on a treadmill. Visceral AT remained a significant ( P ≤ 0.05) predictor of plasma triglycerides (TG), high-density-lipoprotein cholesterol (HDL-C), and total cholesterol (TC)/HDL-C ratio (TC/HDL-C) after statistical control for abdominal subcutaneous AT, CRF, and alcohol consumption. Abdominal subcutaneous AT was not a significant ( P ≥ 0.05) correlate of any lipid variable after control for visceral AT and CRF. Furthermore, subdivision of subcutaneous AT into deep and superficial depots did not alter these observations. Visceral AT was the strongest correlate of liver fat and remained so after control for abdominal subcutaneous AT, CRF, and alcohol consumption ( r = −0.34, P < 0.01). In contrast, abdominal subcutaneous AT and CRF were not significant ( P > 0.10) correlates of liver fat after control for visceral AT. Visceral AT remained a significant ( P < 0.01) correlate of TG, HDL-C, and TC/HDL-C independent of liver fat. However, liver fat was also a significant correlate ( P ≤ 0.05) of fasting glucose and TG independent of visceral AT. These observations reinforce the importance of visceral obesity in the pathogenesis of dyslipidemia in men, and they suggest that visceral AT and liver fat carry independent health risk.

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Soofi, Abdul, Katherine I. Wolf, Egon J. Ranghini, Mohammad A. Amin, and Gregory R. Dressler. "The kielin/chordin-like protein KCP attenuates nonalcoholic fatty liver disease in mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 311, no. 4 (October 1, 2016): G587—G598. http://dx.doi.org/10.1152/ajpgi.00165.2016.

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Nonalcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disease and is increasing with the rising rate of obesity in the developed world. Signaling pathways known to influence the rate of lipid deposition in liver, known as hepatic steatosis, include the transforming growth factor (TGF) superfamily, which function through the SMAD second messengers. The kielin/chordin-like protein (KCP) is a large secreted protein that can enhance bone morphogenetic protein signaling while suppressing TGF-β signaling in cells and in genetically modified mice. In this report, we show that aging KCP mutant ( Kcp −/−) mice are increasingly susceptible to developing hepatic steatosis and liver fibrosis. When young mice are put on a high-fat diet, Kcp −/− mice are also more susceptible to developing liver pathology, compared with their wild-type littermates. Furthermore, mice that express a Pepck-KCP transgene ( Kcp Tg) in the liver are resistant to developing liver pathology even when fed a high-fat diet. Analyses of liver tissues reveal a significant reduction of P-Smad3, consistent with a role for KCP in suppressing TGF-β signaling. Transcriptome analyses show that livers from Kcp −/− mice fed a normal diet are more like wild-type livers from mice fed a high-fat diet. However, the KCP transgene can suppress many of the changes in liver gene expression that are due to a high-fat diet. These data demonstrate that shifting the TGF-β signaling paradigm with the secreted regulatory protein KCP can significantly alter the liver pathology in aging mice and in diet-induced NAFLD.

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Lind, Lars, Samira Salihovic, Ulf Risérus, Joel Kullberg, Lars Johansson, Håkan Ahlström, Jan W. Eriksson, and Jan Oscarsson. "The Plasma Metabolomic Profile is Differently Associated with Liver Fat, Visceral Adipose Tissue, and Pancreatic Fat." Journal of Clinical Endocrinology & Metabolism 106, no. 1 (October 30, 2020): e118-e129. http://dx.doi.org/10.1210/clinem/dgaa693.

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Abstract Context Metabolic differences between ectopic fat depots may provide novel insights to obesity-related diseases. Objective To investigate the plasma metabolomic profiles in relation to visceral adipose tissue (VAT) volume and liver and pancreas fat percentages. Design Cross-sectional. Setting Multicenter at academic research laboratories. Patients Magnetic resonance imaging (MRI) was used to assess VAT volume, the percentage of fat in the liver and pancreas (proton density fat fraction [PDFF]) at baseline in 310 individuals with a body mass index ≥ 25 kg/m2 and with serum triglycerides ≥ 1.7 mmol/l and/or type 2 diabetes screened for inclusion in the 2 effect of omega-3 carboxylic acid on liver fat content studies. Intervention None. Main Outcome Measure Metabolomic profiling with mass spectroscopy enabled the determination of 1063 plasma metabolites. Results Thirty metabolites were associated with VAT volume, 31 with liver PDFF, and 2 with pancreas PDFF when adjusting for age, sex, total body fat mass, and fasting glucose. Liver PDFF and VAT shared 4 metabolites, while the 2 metabolites related to pancreas PDFF were unique. The top metabolites associated with liver PDFF were palmitoyl-palmitoleoyl-GPC (16:0/16:1), dihydrosphingomyelin (d18:0/22:0), and betaine. The addition of these metabolites to the Liver Fat Score improved C-statistics significantly (from 0.776 to 0.861, P = 0.0004), regarding discrimination of liver steatosis. Conclusion Liver PDFF and VAT adipose tissue shared several metabolic associations, while those were not shared with pancreatic PDFF, indicating partly distinct metabolic profiles associated with different ectopic fat depots. The addition of 3 metabolites to the Liver Fat Score improved the prediction of liver steatosis.

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Matikainen, Niina, Sakari Mänttäri, Jukka Westerbacka, Satu Vehkavaara, Nina Lundbom, Hannele Yki-Järvinen, and Marja-Riitta Taskinen. "Postprandial Lipemia Associates with Liver Fat Content." Journal of Clinical Endocrinology & Metabolism 92, no. 8 (August 1, 2007): 3052–59. http://dx.doi.org/10.1210/jc.2007-0187.

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Abstract Context/Objective: Postprandial lipemia and low adiponectin represent novel risk factors for vascular disease. This study aimed to determine whether liver fat content and adiponectin are predictors of postprandial triglyceride (TG)-rich lipoproteins (TRL). Patients/Interventions: Twenty-nine men were allocated into subgroups with either low (≤5%) or high (>5%) liver fat measured with magnetic resonance proton spectroscopy. Subjects underwent an oral fat tolerance test with measurements of postprandial TG, cholesterol, apolipoprotein B-48 (apoB-48), and apoB-100 in TRL fractions, a euglycemic hyperinsulinemic clamp, and determination of abdominal fat volumes by magnetic resonance imaging. Results: Subjects with high liver fat displayed increased response of postprandial lipids in plasma, chylomicron, and very-low-density lipoprotein 1 (VLDL1) (Svedberg flotation rate 60–400) fractions. Liver fat correlated positively with postprandial responses (area under the curve) of TG (r = 0.597; P = 0.001), cholesterol (r = 0.546; P = 0.002), apoB-48 (r = 0.556; P = 0.002), and apoB-100 (r = 0.42; P = 0.023) in the VLDL1 fraction. Respective incremental areas under the curve correlated significantly with liver fat. Fasting adiponectin levels were inversely correlated with both postprandial lipids and liver fat content. Liver fat remained the only independent correlate in a multiple linear regression analysis for chylomicron and VLDL1 responses. Conclusions: Liver fat content is a close correlate of postprandial lipids predicting the responses of TRL in chylomicrons and VLDL1 better than measures of glucose metabolism or body adiposity. Low adiponectin concentration is closely linked to high liver fat content and impaired TRL metabolism. High liver fat content associated with postprandial lipemia represents potential risk factors for cardiovascular disease.

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Ramírez-Vélez, Robinson, Mikel Izquierdo, Jorge Correa-Bautista, María Correa-Rodríguez, Jacqueline Schmidt-RioValle, Emilio González-Jiménez, and Katherine González-Jiménez. "Liver Fat Content and Body Fat Distribution in Youths with Excess Adiposity." Journal of Clinical Medicine 7, no. 12 (December 7, 2018): 528. http://dx.doi.org/10.3390/jcm7120528.

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This study had two main objectives: To examine the association between body fat distribution and non-alcoholic fatty liver disease (NAFLD) and liver fat content, and to determine whether the relationship between NAFLD and regional body fat distribution, with respect to liver fat content in youths with excess adiposity, is independent of cardiorespiratory fitness (CRF) and a healthy diet. Liver fat content (controlled attenuation parameter (CAP)), body fat distribution (body mass index (BMI) z-score, waist circumference, waist-to-height ratio, fat mass/height, body fat percentage, total fat mass, android-to-gynoid fat mass ratio, visceral adipose tissue (VAT), and lean mass index, determined by dual-energy X-ray absorptiometry (DXA)), CRF (20-m shuttle-run test), and healthy diet (adherence to the Mediterranean diet by KIDMED questionnaire) were measured in 126 adolescents (66% girls) aged between 11 and 17 years. Participants were assigned to two groups according to the presence or absence of hepatic steatosis (CAP values ≥225 dB/m or <225 dB/m of liver fat, respectively). Considering the similar total fat values for the two groups (>30% by DXA), youths with NAFLD had higher fat distribution parameters than those without NAFLD, regardless of sex, age, puberty stage, lean mass index, CRF, and healthy diet (p < 0.01). In the non-NAFLD group, the association between hepatic fat and fat distribution parameters presented a similar pattern, although the association was statistically insignificant after adjusting for a potential confounding variable (ps > 0.05), except for the case of VAT. Body fat distribution parameters were higher in youths with NAFLD compared to those without NAFLD. Additionally, body fat distribution showed a significant association with liver fat content as assessed by CAP in youths with NAFLD independent of CRF and adherence to the Mediterranean diet, supporting the notion that upper body fat distribution might play a pivotal role in the development of NAFLD in adolescents. These results may have implications for the clinical management of youths with excess adiposity given the high prevalence of NAFLD in children and young adults.

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Bianchi-Santamaria, Stefanelli, Cembran, Gobbi, Peschiera, Vannini, and Santamaria. "Hepatic Subcellular Storage of Beta-Carotene in Rats Following Diet Supplementation." International Journal for Vitamin and Nutrition Research 69, no. 1 (January 1, 1999): 3–7. http://dx.doi.org/10.1024/0300-9831.69.1.3.

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Beta-carotene (BC) storage was measured in liver and its subcellular fractions (plasma membranes, mitochondria, microsomes and nuclei) of rats fed BC added to diet. The BC supplementation dose was about 350 mg/week/rat. After 15 weeks of this supplementation, rats were killed and their livers were immediately excised and processed to obtain total liver tissue and its subcellular fractions. Their BC contents were measured by HPLC as pmols/mg protein. Intact BC was found to be stored in all the above subcellular fractions, thus showing that BC is probably taken up by liver cell lipid moiety. Interestingly, the mean BC concentrations in plasma membranes and mitochondria were significantly higher than that in total liver tissue. Our data confirmed that rodents are a good animal model for the study of BC metabolism and its effects on several pathologies, and cancer prevention and treatment in humans in spite of the fact that rodents are classified as white-fat animals because of their poor BC absorption and storage in fat and blood plasma, whereas humans are classified as yellow-fat organisms because of their opposite behavior in BC uptake and organ distribution.

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Kotronen, Anna, Satu Vehkavaara, Anneli Seppälä-Lindroos, Robert Bergholm, and Hannele Yki-Järvinen. "Effect of liver fat on insulin clearance." American Journal of Physiology-Endocrinology and Metabolism 293, no. 6 (December 2007): E1709—E1715. http://dx.doi.org/10.1152/ajpendo.00444.2007.

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A fatty liver is associated with fasting hyperinsulinemia, which could reflect either impaired insulin clearance or hepatic insulin action. We determined the effect of liver fat on insulin clearance and hepatic insulin sensitivity in 80 nondiabetic subjects [age 43 ± 1 yr, body mass index (BMI) 26.3 ± 0.5 kg/m2]. Insulin clearance and hepatic insulin resistance were measured by the euglycemic hyperinsulinemic (insulin infusion rate 0.3 mU·kg−1·min−1for 240 min) clamp technique combined with the infusion of [3-3H]glucose and liver fat by proton magnetic resonance spectroscopy. During hyperinsulinemia, both serum insulin concentrations and increments above basal remained ∼40% higher ( P < 0.0001) in the high (15.0 ± 1.5%) compared with the low (1.8 ± 0.2%) liver fat group, independent of age, sex, and BMI. Insulin clearance (ml·kg fat free mass−1·min−1) was inversely related to liver fat content ( r = −0.52, P < 0.0001), independent of age, sex, and BMI ( r = −0.37, P = 0.001). The variation in insulin clearance due to that in liver fat (range 0–41%) explained on the average 27% of the variation in fasting serum (fS)-insulin concentrations. The contribution of impaired insulin clearance to fS-insulin concentrations increased as a function of liver fat. This implies that indirect indexes of insulin sensitivity, such as homeostatic model assessment, overestimate insulin resistance in subjects with high liver fat content. Liver fat content correlated significantly with fS-insulin concentrations adjusted for insulin clearance ( r = 0.43, P < 0.0001) and with directly measured hepatic insulin sensitivity ( r = −0.40, P = 0.0002). We conclude that increased liver fat is associated with both impaired insulin clearance and hepatic insulin resistance. Hepatic insulin sensitivity associates with liver fat content, independent of insulin clearance.

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Liangpunsakul, Suthat, and Bin Gao. "Alcohol and fat promote steatohepatitis: a critical role for fat-specific protein 27/CIDEC." Journal of Investigative Medicine 64, no. 6 (June 24, 2016): 1078–81. http://dx.doi.org/10.1136/jim-2016-000204.

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Alcoholic liver disease (ALD) is a major public health problem worldwide and is the leading cause of end-stage liver disease. While the ultimate control of ALD will require the prevention of alcohol abuse, better understanding of the mechanisms of alcohol-induced liver injury may lead to treatments of fatty liver, alcoholic hepatitis, and prevention or delay of occurrence of cirrhosis. The elucidation and the discovery of several new concepts in ALD pathogenesis have raised our understanding on the complex mechanisms and the potential in developing the new strategies for therapeutic benefits. In this review, we provide the most up-to-date information on the basic molecular mechanisms focusing on the role of fat-specific protein 27/CIDEC in the pathogenesis of ALD.

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Harisankar, Chidambaram Natrajan Balasubramanian. "Focal Fat Sparing of the Liver." Clinical Nuclear Medicine 39, no. 7 (July 2014): e359-e361. http://dx.doi.org/10.1097/rlu.0b013e31829b2657.

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35

Waxman, David J., and Rhonda D. Kineman. "Sex matters in liver fat regulation." Science 378, no. 6617 (October 21, 2022): 252–53. http://dx.doi.org/10.1126/science.ade7614.

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36

Vinaixa, Carmen, Nazia Selzner, and Marina Berenguer. "Fat and liver transplantation: clinical implications." Transplant International 31, no. 8 (June 25, 2018): 828–37. http://dx.doi.org/10.1111/tri.13288.

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37

Kotronen, Anna, Jukka Westerbacka, Robert Bergholm, Kirsi H. Pietiläinen, and Hannele Yki-Järvinen. "Liver Fat in the Metabolic Syndrome." Journal of Clinical Endocrinology & Metabolism 92, no. 9 (September 1, 2007): 3490–97. http://dx.doi.org/10.1210/jc.2007-0482.

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38

Olefsky, Jerrold M. "Fat Talks, Liver and Muscle Listen." Cell 134, no. 6 (September 2008): 914–16. http://dx.doi.org/10.1016/j.cell.2008.09.001.

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39

Stein, Theodore A., Gerard P. Burns, Burton E. Tropp, and Leslie Wise. "Hepatic fat accumulation during liver regeneration." Journal of Surgical Research 39, no. 4 (October 1985): 338–43. http://dx.doi.org/10.1016/0022-4804(85)90112-x.

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40

Mezey, Esteban. "Dietary fat and alcoholic liver disease." Hepatology 28, no. 4 (October 1998): 901–5. http://dx.doi.org/10.1002/hep.510280401.

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41

Rudnick, David A. "Trimming the fat from liver regeneration." Hepatology 42, no. 5 (November 2005): 1001–3. http://dx.doi.org/10.1002/hep.20931.

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42

Friedman, Mark I., James E. Koch, Grazyna Graczyk-Milbrandt, Patricia M. Ulrich, and Mary D. Osbakken. "High-fat diet prevents eating response and attenuates liver ATP decline in rats given 2,5-anhydro-d-mannitol." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 3 (March 1, 2002): R710—R714. http://dx.doi.org/10.1152/ajpregu.00156.2001.

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Administration of the fructose analog 2,5-anhydro-d-mannitol (2,5-AM) stimulates eating in rats fed a low-fat diet but not in those fed a high-fat diet that enhances fatty acid oxidation. The eating response to 2,5-AM treatment is apparently triggered by a decrease in liver ATP content. To assess whether feeding a high-fat diet prevents the eating response to 2,5-AM by attenuating the decrease in liver ATP, we examined the effects of the analog on food intake, liver ATP content, and hepatic phosphate metabolism [using in vivo 31P-NMR spectroscopy (NMRS)]. Injection (intraperitoneal) of 300 mg/kg 2,5-AM increased food intake in rats fed a high-carbohydrate/low-fat diet, but not in those fed high-fat/low-carbohydrate (HF/LC) food. Liver ATP content decreased in all rats given 2,5-AM compared with saline, but it decreased about half as much in rats fed the HF/LC diet. NMRS on livers of anesthetized rats indicated that feeding the HF/LC diet attenuates the effects of 2,5-AM on liver ATP by reducing phosphate trapping. These results suggest that rats consuming a high-fat diet do not increase food intake after injection of 2,5-AM, because the analog is not sufficiently phosphorylated and therefore fails to decrease liver energy status below a level that generates a signal to eat.

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Musso, Giovanni, Roberto Gambino, Marilena Durazzo, and Maurizio Cassader. "Noninvasive assessment of liver disease severity with liver fat score and CK-18 in NAFLD: Prognostic value of liver fat equation goes beyond hepatic fat estimation." Hepatology 51, no. 2 (August 25, 2009): 715–17. http://dx.doi.org/10.1002/hep.23255.

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44

Yamane, Takuya, Miyuki Kozuka, Yoshio Yamamoto, Yoshihisa Nakano, Takenori Nakagaki, Iwao Ohkubo, and Hiroyoshi Ariga. "Effectiveness of aronia berries for reduction of mild fibrosis and gene expression analysis in livers from mice fed a high-fat diet with aronia berries." Functional Foods in Health and Disease 6, no. 3 (March 18, 2016): 144. http://dx.doi.org/10.31989/ffhd.v6i3.245.

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Background: Aronia berries have many potential effects on health, including an antioxidant effect, effect for antimutagenesis, hepatoprotection and cardioprotection, an antidiabetic effect and inhibition of cancer cell proliferation. Previous human studies have shown that aronia juice may be useful for treatment of obesity disorders.Objective: To reveal relationship between beneficial effect and the gene expression change by aronia berries, we analyzed mice livers using RNA sequencing and RT-qPCR.Method: At 28 days after starting a normal diet, a high fat diet and a high-fat diet containing 10% freeze-dried aronia berries, serum was obtained from veins of mice after isoflurane anesthesia, and liver tissues were isolated and weighed. Triglyceride, total cholesterol and LDL cholesterol levels were measured and total RNAs were extracted. cDNA libraries were prepared according to Illumina protocols and sequenced using an Illumina HiSeq2500 to perform 100 paired-end sequencing. RNA-sequence reads mapping was performed using a DNA nexus. Gene expression analysis was performed. The liver tissue specimens were fixed and embedded in paraffin. After 5-mm-thick paraffin sections had been cut, they were stained with hematoxylin-eosin using the standard procedure and also with Sirius Red.Results: In this study, we found that mild fibrosis induced by a high-fat diet was reduced in livers of mice fed a high-fat diet containing aronia berries. RNA sequencing and RT-qPCR analyses revealed that gene expression levels of Igfbp1 and Gadd45g were increased in livers from mice fed a high-fat diet containing aronia berries. Furthermore, results of an enzyme-linked immunoassay showed that a secreted protein levels of FABP1 and FABP4 were reduced in serum from mice fed a high-fat diet containing aronia berries. The results suggest that aronia berries have beneficial effects on mild fibrosis in liver.Conclusion: Aronia berries have a beneficial effect on liver fibrosis. The recovery from liver fibrosis is associated with expression levels of Gadd45g and Igfbp1 in the liver. The beneficial effects of aronia berries on liver fibrosis reduce the risk of liver cancer diseases and insulin resistance, resulting in reduction of serum FABP1 and FABP4 levels.Keywords: aronia; fibrosis; liver; Igfbp1; Gadd45g

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Power Guerra, Nicole, Luisa Müller, Kristin Pilz, Annika Glatzel, Daniel Jenderny, Deborah Janowitz, Brigitte Vollmar, and Angela Kuhla. "Dietary-Induced Low-Grade Inflammation in the Liver." Biomedicines 8, no. 12 (December 9, 2020): 587. http://dx.doi.org/10.3390/biomedicines8120587.

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The literature describes a close correlation between metabolic disorders and abnormal immune responses, like low-grade inflammation (LGI), which may be one mechanistic link between obesity and various comorbidities, including non-alcoholic fatty liver disease (NAFLD). In our study, we investigated the influence of dietary composition on obesity-derived LGI in the liver. We used a dietary induced obesity mouse model of C57BL/6J mice fed with high fat diet (HFD, 60% fat, 20% protein, 20% carbohydrates) and two different controls. One was rich in carbohydrates (10% fat, 20% protein, 70% carbohydrates), further referred to as the control diet (CD), and the other one is referred to as the standard diet (SD), with a more balanced macronutrient content (9% fat, 33% protein, 58% carbohydrates). Our results showed a significant increased NAFLD activity score in HFD compared to both controls, but livers of the CD group also differed in their macroscopic appearance from healthy livers. Hepatic fat content showed significantly elevated cholesterol concentrations in the CD group. Histologic analysis of the cellular immune response in the liver showed no difference between HFD and CD and expression analysis of immunologic mediators like interleukin (IL)-1β, IL-6, IL-10 and tumor necrosis factor alpha also point towards a pro-inflammatory response to CD, comparable to LGI in HFD. Therefore, when studying diet-induced obesity with a focus on inflammatory processes, we encourage researchers to carefully select controls and not use a control diet disproportionally rich in carbohydrates.

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Crabtree, Christopher, Madison Kackley, Alexandru Buga, Brandon Fell, Richard LaFountain, Parker Hyde, Teryn Sapper, et al. "Comparison of Ketogenic Diets with and without Ketone Salts versus a Low-Fat Diet: Liver Fat Responses in Overweight Adults." Nutrients 13, no. 3 (March 17, 2021): 966. http://dx.doi.org/10.3390/nu13030966.

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Ketogenic diets (KDs) often contain high levels of saturated fat, which may increase liver fat, but the lower carbohydrate intake may have the opposite effect. Using a controlled feeding design, we compared liver fat responses to a hypocaloric KD with a placebo (PL) versus an energy-matched low-fat diet (LFD) in overweight adults. We also examined the added effect of a ketone supplement (KS). Overweight adults were randomized to a 6-week KD (KD + PL) or a KD with KS (KD + KS); an LFD group was recruited separately. All diets were estimated to provide 75% of energy expenditure. Weight loss was similar between groups (p > 0.05). Liver fat assessed by magnetic resonance imaging decreased after 6 week (p = 0.004) with no group differences (p > 0.05). A subset with nonalcoholic fatty liver disease (NAFLD) (liver fat > 5%, n = 12) showed a greater reduction in liver fat, but no group differences. In KD participants with NAFLD, 92% of the variability in change in liver fat was explained by baseline liver fat (p < 0.001). A short-term hypocaloric KD high in saturated fat does not adversely impact liver health and is not impacted by exogenous ketones. Hypocaloric low-fat and KDs can both be used in the short-term to significantly reduce liver fat in individuals with NAFLD.

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47

Hodson, Leanne, Fredrik Rosqvist, and Siôn A. Parry. "The influence of dietary fatty acids on liver fat content and metabolism." Proceedings of the Nutrition Society 79, no. 1 (April 3, 2019): 30–41. http://dx.doi.org/10.1017/s0029665119000569.

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Non-alcoholic fatty liver disease encompasses a spectrum of conditions from hepatic steatosis through to cirrhosis; obesity is a known risk factor. The liver plays a major role in regulating fatty acid metabolism and perturbations in intrahepatic processes have potential to impact on metabolic health. It remains unclear why intra-hepatocellular fat starts to accumulate, but it likely involves an imbalance between fatty acid delivery to the liver, fatty acid synthesis and oxidation within the liver and TAG export from the liver. As man spends the majority of the day in a postprandial rather than postabsorptive state, dietary fatty acid intake should be taken into consideration when investigating why intra-hepatic fat starts to accumulate. This review will discuss the impact of the quantity and quality of dietary fatty acids on liver fat accumulation and metabolism, along with some of the potential mechanisms involved. Studies investigating the role of dietary fat in liver fat accumulation, although surprisingly limited, have clearly demonstrated that it is total energy intake, rather than fat intake per se, that is a key mediator of liver fat content; hyperenergetic diets increase liver fat whilst hypoenergetic diets decrease liver fat content irrespective of total fat content. Moreover, there is now, albeit limited evidence emerging to suggest the composition of dietary fat may also play a role in liver fat accumulation, with diets enriched in saturated fat appearing to increase liver fat content to a greater extent when compared with diets enriched in unsaturated fats.

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48

Shen, Li-Shan, Quan-Xi Li, Xiao-Wen Luo, Hui-Jun Tang, You-Jie Tang, Wen-Jie Tang, and Ruo-Mi Guo. "Quantification of Liver Fat Content after Radiofrequency Ablation for Liver Cancer: Correlation with Hepatic Perfusion Disorders." Diagnostics 11, no. 11 (November 18, 2021): 2137. http://dx.doi.org/10.3390/diagnostics11112137.

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Purpose: To quantitatively investigate the correlation between liver fat content and hepatic perfusion disorders (HPD) after radiofrequency ablation (RFA) for liver cancer using magnetic resonance imaging (MRI)-determined proton density fat fraction (PDFF). Materials and methods: A total of 150 liver cancer patients underwent liver MRI examination within one month after RFA and at four months after RFA. According to the liver fat content, they were divided into non-, mild, moderate, and severe fatty liver groups. The liver fat content and hepatic perfusion disorders were determined using PDFF images and dynamic contrast-enhanced MRI images. The relationship between the liver fat content and HPD was investigated. Results: At the first postoperative MRI examination, the proportion of patients in the nonfatty liver group with hyperperfused foci (11.11%) was significantly lower than that in the mild (30.00%), moderate (42.86%), and severe fatty liver (56.67%) groups (p < 0.05), whereas the proportions of patients with hypoperfused foci (6.67%, 7.5%, 5.71%, and 6.67%, respectively) were not significantly different among the four groups (p > 0.05). In the nonfatty liver group, the liver fat content was not correlated with hyperperfusion abnormalities or hypoperfusion abnormalities. By contrast, in the three fatty liver groups, the liver fat content was correlated with hyperperfusion abnormalities but was not correlated with hypoperfusion abnormalities. At the second postoperative MRI examination, six patients in the nonfatty liver group were diagnosed with fatty liver, including two patients with newly developed hyperperfusion abnormalities and one patient whose hypoperfusion abnormality remained the same as it was in the first postoperative MRI examination. Conclusion: There was a high correlation between the liver fat content and hyperperfusion abnormalities after RFA for liver cancer. The higher the liver fat content was, the higher the was risk of hyperperfusion abnormalities. However, there was little correlation between liver fat content and hypoperfusion abnormalities, and the increase in postoperative liver fat content did not induce or alter the presence of hypoperfused foci.

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SALIMNIA, TANAZ, NARAYANA R GANDHAM, MICHELLE ANDRIACCHI, and SANJAY DOGRA. "FAT-BURNER FIASCO: ACUTE LIVER FAILURE SECONDARY TO FAT-BURNER SUPPLEMENTS." Chest 162, no. 4 (October 2022): A777. http://dx.doi.org/10.1016/j.chest.2022.08.613.

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50

Fan, Jian-Gao, and Geoffrey C. Farrell. "VAT fat is bad for the liver, SAT fat is not!" Journal of Gastroenterology and Hepatology 23, no. 6 (June 2008): 829–32. http://dx.doi.org/10.1111/j.1440-1746.2008.05474.x.

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