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1
Kim, Hyun Uk. "Lipid Metabolism in Plants." Plants 9, no. 7 (July 9, 2020): 871. http://dx.doi.org/10.3390/plants9070871.
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In plants, lipids function in a variety of ways. Lipids are a major component of biological membranes and are used as a compact energy source for seed germination. Fatty acids, the major lipids in plants, are synthesized in plastid and assembled by glycerolipids or triacylglycerols in endoplasmic reticulum. The metabolism of fatty acids and triacylglycerols is well studied in most Arabidopsis model plants by forward and reverse genetics methods. However, research on the diverse functions of lipids in plants, including various crops, has yet to be completed. The papers of this Special Issue cover the core of the field of plant lipid research on the role of galactolipids in the chloroplast biogenesis from etioplasts and the role of acyltransferases and transcription factors involved in fatty acid and triacylglycerol synthesis. This information will contribute to the expansion of plant lipid research.
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Nichols, Frank, and Baliram Maraj. "Relationship between Hydroxy Fatty Acids and Prostaglandin E2 in Gingival Tissue." Infection and Immunity 66, no. 12 (December 1, 1998): 5805–11. http://dx.doi.org/10.1128/iai.66.12.5805-5811.1998.
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ABSTRACT Bacterial hydroxy fatty acids and alpha-hydroxy fatty acids have been demonstrated in complex lipid extracts of subgingival plaque and gingival tissue. However, little is known about the relationship between these hydroxy fatty acids in plaque and gingival tissues or the significance of these complex lipids in promoting inflammatory periodontal disease. The present study determined the percentages of ester-linked and amide-linked hydroxy fatty acids in complex lipids recovered from plaque and gingival tissue samples and the relationship between bacterial hydroxy fatty acids and alpha-hydroxy fatty acids in the lipid extracts. To evaluate a potential role for these hydroxy fatty acids in inflammatory periodontal disease, gingival tissue samples were examined for a relationship between prostaglandin E2 (PGE2) and hydroxy fatty acids recovered in gingival lipid. This investigation demonstrated that alpha-hydroxy fatty acids are only ester linked in plaque lipids but are largely amide linked in gingival tissue lipids. Furthermore, the level of alpha-hydroxy fatty acid in gingival lipid is directly related to the level of the bacterial hydroxy fatty acid 3-OHiso-branched C17:0 (3-OH iC17:0) in the same lipid extract. However, the relationship between hydroxy fatty acids in gingival lipids does not parallel the fatty acid relationship observed in plaque lipids. Finally, alpha-hydroxy fatty acid levels in gingival tissue lipids correlate directly with the recovery of PGE2 in the same tissue samples. These results demonstrate that alpha-hydroxy fatty acid levels in gingival lipids are directly related to both 3-OH iC17:0 bacterial lipid levels and PGE2 levels. These results indicate that in periodontal tissues there are unusual host-parasite interactions involving penetration of bacterial lipid in association with an altered gingival lipid metabolism and prostaglandin synthesis.
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Poitelon, Yannick, Ashley M. Kopec, and Sophie Belin. "Myelin Fat Facts: An Overview of Lipids and Fatty Acid Metabolism." Cells 9, no. 4 (March 27, 2020): 812. http://dx.doi.org/10.3390/cells9040812.
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Myelin is critical for the proper function of the nervous system and one of the most complex cell–cell interactions of the body. Myelination allows for the rapid conduction of action potentials along axonal fibers and provides physical and trophic support to neurons. Myelin contains a high content of lipids, and the formation of the myelin sheath requires high levels of fatty acid and lipid synthesis, together with uptake of extracellular fatty acids. Recent studies have further advanced our understanding of the metabolism and functions of myelin fatty acids and lipids. In this review, we present an overview of the basic biology of myelin lipids and recent insights on the regulation of fatty acid metabolism and functions in myelinating cells. In addition, this review may serve to provide a foundation for future research characterizing the role of fatty acids and lipids in myelin biology and metabolic disorders affecting the central and peripheral nervous system.
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Valença, Isabel, Ana Rita Ferreira, Marcelo Correia, Sandra Kühl, Carlo van Roermund, Hans R. Waterham, Valdemar Máximo, Markus Islinger, and Daniela Ribeiro. "Prostate Cancer Proliferation Is Affected by the Subcellular Localization of MCT2 and Accompanied by Significant Peroxisomal Alterations." Cancers 12, no. 11 (October 27, 2020): 3152. http://dx.doi.org/10.3390/cancers12113152.
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Reprogramming of lipid metabolism directly contributes to malignant transformation and progression. The increased uptake of circulating lipids, the transfer of fatty acids from stromal adipocytes to cancer cells, the de novo fatty acid synthesis, and the fatty acid oxidation support the central role of lipids in many cancers, including prostate cancer (PCa). Fatty acid β-oxidation is the dominant bioenergetic pathway in PCa and recent evidence suggests that PCa takes advantage of the peroxisome transport machinery to target monocarboxylate transporter 2 (MCT2) to peroxisomes in order to increase β-oxidation rates and maintain the redox balance. Here we show evidence suggesting that PCa streamlines peroxisome metabolism by upregulating distinct pathways involved in lipid metabolism. Moreover, we show that MCT2 is required for PCa cell proliferation and, importantly, that its specific localization at the peroxisomal membranes is essential for this role. Our results highlight the importance of peroxisomes in PCa development and uncover different cellular mechanisms that may be further explored as possible targets for PCa therapy.
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Abulnaja, Khalid O., and John L. Harwood. "Effect of a Safener Towards Thiocarbamates on Plant Lipid Metabolism." Zeitschrift für Naturforschung C 46, no. 9-10 (October 1, 1991): 931–33. http://dx.doi.org/10.1515/znc-1991-9-1035.
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Abstract It has been found that various thiocarbamate herbicides, known to alter surface wax and cutin synthesis, inhibit the elongation of fatty acids. We have proposed this as a mode of action of such compounds. Because it is believed that the sulphoxide metabolites of thiocarbamates are the active intermediates, we have examined the action of 1-aminobenzotriazole (an inhibitor of sulphoxide formation) on the inhibition of very long-chain fatty acid biosynthesis. In all tissues tested, aminobenzotriazole was able to block the specific inhibitory effect of thiocarbamates on fatty acid elongation. These results add further support to our proposal that fatty acid elongation is a sensitive target site for thiocarbamate herbicides in plants.
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Cheng, Xiang, Feng Geng, Yaogang Zhong, Zhihua Tian, Meixia Pan, Chunming Cheng, Craig Horbinski, Xiaokui Mo, Xianlin Han, and Deliang Guo. "CBMT-29. PROMOTING FATTY ACID STORAGE BY DIACYLGLYCEROL-ACYLTRANSFERASE 1 PROTECTS GLIOBLASTOMA AGAINST OXIDATIVE STRESS AND MAINTAINS LIPID HOMEOSTASIS FOR RAPID TUMOR GROWTH." Neuro-Oncology 21, Supplement_6 (November 2019): vi39. http://dx.doi.org/10.1093/neuonc/noz175.151.
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Abstract Fatty acids are essential building blocks and energy substrates of lipids in cells. They constitute the major structural components of membrane lipids, i.e., glycerophospholipids and sphingolipids, and also serve as an important energy resource. Whereas excess fatty acids or dysregulation of fatty acid metabolism causes lipotoxicity, leading to severe cell damage. We previously identified that lipid metabolism is dramatically altered in glioblastoma (GBM), especially fatty acid synthesis, which is greatly elevated in various types of cancers. However, how tumor cells prevent excessive fatty acids accumulation from inducing lipotoxicity has rarely been studied. We recently identified that GBM greatly upregulates diacylglycerol-acyltransferase 1 (DGAT1) to direct excess fatty acids into triglycerides and lipid droplets to prevent oxidative stress. Inhibiting DGAT1 disrupts lipid homeostasis and shifts excessive fatty acids moving into mitochondria for oxidation, resulting in a high level of reactive oxygen species (ROS), mitochondrial damage, cytochrome c release and apoptosis. Inhibiting carnitine palmitoyltransferase to reduce fatty acids shuttling into mitochondria significantly decreases ROS and rescues cell death caused by DGAT1 inhibition. Xenograft models show that genetic or pharmacological inhibition of DGAT1 blocks lipid droplet formation, induces tumor cell apoptosis and markedly suppresses GBM tumor growth. Together, our study demonstrates that DGAT1 upregulation protects GBM from oxidative damage and maintains lipid homeostasis by facilitating excess fatty acids storage. Our data further show that targeting DGAT1 specifically induces lipotoxicity in tumor cells, while sparing normal brain, which is a very promising therapeutic strategy antagonizing GBM and has a high potential to shift current paradigm in treating GBM.
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Wu, Jiayue, Linlin Peng, Shubin Dong, Xiaofei Xia, and Liangcheng Zhao. "Transcriptome analysis of Chelidonium majus elaiosomes and seeds provide insights into fatty acid biosynthesis." PeerJ 7 (May 3, 2019): e6871. http://dx.doi.org/10.7717/peerj.6871.
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Background Elaiosomes are specialized fleshy and edible seed appendages dispersed by ants. Lipids are the primary components of elaiosomes. Chelidonium majus is a well-known plant, the seeds of which are dispersed by ants. Previous studies have identified the presence of primary fatty acids in its elaiosomes and seeds. However, the molecular mechanisms underlying fatty acid biosynthesis in elaiosomes remain unknown. Methods In order to gain a comprehensive transcriptional profile of the elaiosomes and seeds of C. majus, and understand the expression patterns of genes associated with fatty acid biosynthesis, four different developmental stages, including the flower-bud (Ch01), flowering (Ch02), young seed (Ch03), and mature seed (Ch04) stages, were chosen to perform whole-transcriptome profiling through the RNA-seq technology (Illumina NGS sequencing). Results A total of 63,064 unigenes were generated from 12 libraries. Of these, 7,323, 258, and 11,540 unigenes were annotated with 25 Cluster of Orthologous Groups, 43 Gene Ontology terms, and 373 Kyoto Encyclopedia of Genes and Genomes pathways, respectively. In addition, 322 genes were involved in lipid transport and metabolism, and 508 genes were involved in the lipid metabolism pathways. A total of 41 significantly differentially expressed genes (DEGs) involved in the lipid metabolism pathways were identified, most of which were upregulated in Ch03 compared to Ch02, indicating that fatty acid biosynthesis primarily occurs during the flowering to the young seed stages. Of the DEGs, acyl-ACP thioesterases, acyl carrier protein desaturase (DESA1), and malonyl CoA-ACP transacylase were involved in palmitic acid synthesis; stearoyl-CoA desaturase and DESA1 were involved in oleic acid synthesis, and acyl-lipid omega-6 desaturase was involved in linoleic acid synthesis.
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Moibi, J. A., R. J. Christopherson, and E. K. Okine. "In vivo and in vitro lipogenesis and aspects of metabolism in ovines: Effect of environmental temperature and dietary lipid supplementation." Canadian Journal of Animal Science 80, no. 1 (March 1, 2000): 59–67. http://dx.doi.org/10.4141/a99-049.
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Twenty-four wether lambs were randomly allocated to six treatments to investigate the effect of temperature and dietary lipid supplements on fatty acid synthesis and metabolic activity in sheep. The treatments consisted of four groups exposed to either cold (0 °C) or warm temperature (+23 °C) and given ad libitum access to either a control barley-based diet or with lipid supplementation. Two other groups were placed on the dietary regimen at 0 °C, but pair-fed to intake of animals in the +23 °C environment. At 5 wk, fatty acid synthesis was measured by [1-14C]acetate incorporation into tissue lipids. Cold exposure and dietary lipid supplementation had no effect (P > 0.05) on in vivo fatty acid synthesis rates in either longissimus dorsi or the liver. In both subcutaneous and mesenteric adipose tissue depots, the rate of acetate incorporation into tissue lipid was not significantly affected by cold exposure. In the perirenal fat depot, cold exposure increased (P < 0.05) the rate of fatty acid synthesis, while lipid supplementation decreased (P < 0.05) the rate in all tissue adipose depots. In vitro, mesenteric and perirenal adipose tissues from cold pair-fed animals had higher (P < 0.05) rates of fatty acid synthesis compared to tissues from animals in the warm environment. However, there was no effect of dietary lipid supplementation in these two fat depots. Metabolic heat production, and energy and nitrogen excretion by animals were increased (P < 0.05) by cold exposure while lipid supplementation had the opposite effect (P < 0.05). The relationship between average daily gain and feed intake was linear at both warm and cold environments, but with higher (P < 0.05) average daily gain at all levels of intake in the cold compared to the warm environment. Results indicate that both environment and diet regulate metabolic activity in sheep. However, there were differences in lipogenic response by tissues to the treatments. Key words: Environmental temperature, dietary lipid, fatty acid synthesis, metabolic rate, sheep
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Cazzolli, R., D. L. Craig, T. J. Biden, and C. Schmitz-Peiffer. "Inhibition of glycogen synthesis by fatty acid in C2C12 muscle cells is independent of PKC-α, -ε, and -θ." American Journal of Physiology-Endocrinology and Metabolism 282, no. 6 (June 1, 2002): E1204—E1213. http://dx.doi.org/10.1152/ajpendo.00487.2001.
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We have previously shown that glycogen synthesis is reduced in lipid-treated C2C12 skeletal muscle myotubes and that this is independent of changes in glucose uptake. Here, we tested whether mitochondrial metabolism of these lipids is necessary for this inhibition and whether the activation of specific protein kinase C (PKC) isoforms is involved. C2C12 myotubes were pretreated with fatty acids and subsequently stimulated with insulin for the determination of glycogen synthesis. The carnitine palmitoyltransferase-1 inhibitor etomoxir, an inhibitor of β-oxidation of acyl-CoA, did not protect against the inhibition of glycogen synthesis caused by the unsaturated fatty acid oleate. In addition, although oleate caused translocation, indicating activation, of individual PKC isoforms, inhibition of PKC by pharmacological agents or adenovirus-mediated overexpression of dominant negative PKC-α, -ε, or -θ mutants was unable to prevent the inhibitory effects of oleate on glycogen synthesis. We conclude that neither mitochondrial lipid metabolism nor activation of PKC-α, -ε, or -θ plays a role in the direct inhibition of glycogen synthesis by unsaturated fatty acids.
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Li, Tiangang, and John Y. L. Chiang. "Regulation of Bile Acid and Cholesterol Metabolism by PPARs." PPAR Research 2009 (2009): 1–15. http://dx.doi.org/10.1155/2009/501739.
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Bile acids are amphipathic molecules synthesized from cholesterol in the liver. Bile acid synthesis is a major pathway for hepatic cholesterol catabolism. Bile acid synthesis generates bile flow which is important for biliary secretion of free cholesterol, endogenous metabolites, and xenobiotics. Bile acids are biological detergents that facilitate intestinal absorption of lipids and fat-soluble vitamins. Recent studies suggest that bile acids are important metabolic regulators of lipid, glucose, and energy homeostasis. Agonists of peroxisome proliferator-activated receptors (PPARα, PPARγ, PPARδ) regulate lipoprotein metabolism, fatty acid oxidation, glucose homeostasis and inflammation, and therefore are used as anti-diabetic drugs for treatment of dyslipidemia and insulin insistence. Recent studies have shown that activation of PPARαalters bile acid synthesis, conjugation, and transport, and also cholesterol synthesis, absorption and reverse cholesterol transport. This review will focus on the roles of PPARs in the regulation of pathways in bile acid and cholesterol homeostasis, and the therapeutic implications of using PPAR agonists for the treatment of metabolic syndrome.
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Kytikova, O. Yu, T. P. Novgorodtseva, Yu K. Denisenko, and D. A. Kovalevsky. "Metabolic and Genetic Determinants of Lipid Metabolism Disruption in Non-Alcoholic Fatty Liver Disease." Russian Journal of Gastroenterology, Hepatology, Coloproctology 30, no. 2 (May 6, 2020): 15–25. http://dx.doi.org/10.22416/1382-4376-2020-30-2-15-25.
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Aim. To present literature data on the metabolic and genetic mechanisms of impaired fatty acid (FA) synthesis in the development and progression of non-alcoholic fatty liver disease (NAFLD).General findings. NAFLD is a widespread disease progressing from steatosis to non-alcoholic steatohepatitis (NASH), increasing the risk of cirrhosis, liver failure and hepatocellular carcinoma. Progression of NAFLD and the development of NASH are closely related to lipid metabolism disorders caused not only by insufficient alimentary intake of fatty acids, but also by a decrease in the efficiency of their endogenous processing. The regulation of fatty acid metabolism involves enzymes desaturase (FADS1, FADS2) and elongase (ELOVL2 and ELOVL5) fatty acids. Desaturases are encoded by the FADS1 and FADS2 genes for fatty acid desaturases. Polymorphisms in the genes of fatty acid desaturases determine the effectiveness of PUFA endogenous processing. Violations in the activity of FADS1 and FADS2 and their genes are accompanied by dysregulation of the metabolic pathway involved in the biosynthesis of fatty acids. This leads to the damage of cell membranes, whose main components are represented by phospholipids. The progression of NAFLD is associated with the powerful toxicity of lipids released in the liver parenchyma upon the loss of the cell biomembrane integrity.Conclusions. Further research into the NAFLD genetic mechanisms regulating the metabolism of fatty acids appears to be promising for a deeper understanding of the pathogenesis of this multifactorial disease.
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Lee, Ji-Yoon, Won Kon Kim, Kwang-Hee Bae, Sang Chul Lee, and Eun-Woo Lee. "Lipid Metabolism and Ferroptosis." Biology 10, no. 3 (March 2, 2021): 184. http://dx.doi.org/10.3390/biology10030184.
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Ferroptosis is a type of iron-dependent regulated necrosis induced by lipid peroxidation that occurs in cellular membranes. Among the various lipids, polyunsaturated fatty acids (PUFAs) associated with several phospholipids, such as phosphatidylethanolamine (PE) and phosphatidylcholine (PC), are responsible for ferroptosis-inducing lipid peroxidation. Since the de novo synthesis of PUFAs is strongly restricted in mammals, cells take up essential fatty acids from the blood and lymph to produce a variety of PUFAs via PUFA biosynthesis pathways. Free PUFAs can be incorporated into the cellular membrane by several enzymes, such as ACLS4 and LPCAT3, and undergo lipid peroxidation through enzymatic and non-enzymatic mechanisms. These pathways are tightly regulated by various metabolic and signaling pathways. In this review, we summarize our current knowledge of how various lipid metabolic pathways are associated with lipid peroxidation and ferroptosis. Our review will provide insight into treatment strategies for ferroptosis-related diseases.
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Park, Hyeon Young, Hye Suk Kang, and Seung-Soon Im. "Recent insight into the correlation of SREBP-mediated lipid metabolism and innate immune response." Journal of Molecular Endocrinology 61, no. 3 (October 2018): R123—R131. http://dx.doi.org/10.1530/jme-17-0289.
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Fatty acids are essential nutrients that contribute to several intracellular functions. Fatty acid synthesis and oxidation are known to be regulated by sterol regulatory element-binding proteins (SREBPs), which play a pivotal role in the regulation of cellular triglyceride synthesis and cholesterol biogenesis. Recent studies point to a multifunctional role of SREBPs in the pathogenesis of metabolic diseases, such as obesity, type II diabetes and cancer as well as in immune responses. Notably, fatty acid metabolic intermediates are involved in energy homeostasis and pathophysiological conditions. In particular, intracellular fatty acid metabolism affects an inflammatory response, thereby influencing metabolic diseases. The objective of this review is to summarize the recent advances in our understanding of the dual role of SREBPs in both lipid metabolism and inflammation-mediated metabolic diseases.
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Nonogaki, K., X. M. Pan, A. H. Moser, J. Shigenaga, I. Staprans, N. Sakamoto, C. Grunfeld, and K. R. Feingold. "LIF and CNTF, which share the gp130 transduction system, stimulate hepatic lipid metabolism in rats." American Journal of Physiology-Endocrinology and Metabolism 271, no. 3 (September 1, 1996): E521—E528. http://dx.doi.org/10.1152/ajpendo.1996.271.3.e521.
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We determined the effects of leukemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF) on lipid metabolism in intact rats. Administration of LIF and CNTF increased serum triglycerides in a dose-dependent manner with peak values at 2 h. The effects of LIF and CNTF on serum cholesterol were very small, and serum glucose was unaffected. Both LIF and CNTF stimulated hepatic triglyceride secretion, hepatic de novo fatty acid synthesis, and lipolysis. Pretreatment with phenylisopropyl adenosine, which inhibits lipolysis, partially inhibited LIF- and CNTF-induced hypertriglyceridemia. Interleukin-4, which inhibits cytokine-induced hepatic fatty acid synthesis, also partially inhibited LIF- and CNTF-induced hypertriglyceridemia. These results indicate that both lipolysis and de novo fatty acid synthesis play a role in providing fatty acids for the increase in hepatic triglyceride secretion. Neither indomethacin nor adrenergic receptor antagonists affected the hypertriglyceridemia. The combination of LIF plus CNTF showed no additive effects consistent with the action of both cytokines through the gp130 transduction system. Thus LIF and CNTF have similar effects on lipid metabolism; they join a growing list of cytokines that stimulate hepatic triglyceride secretion and may mediate the changes in lipid metabolism that accompany the acute phase response.
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Ko, Seong-Hee, and Hyun-Sook Kim. "Menopause-Associated Lipid Metabolic Disorders and Foods Beneficial for Postmenopausal Women." Nutrients 12, no. 1 (January 13, 2020): 202. http://dx.doi.org/10.3390/nu12010202.
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Menopause is clinically diagnosed as a condition when a woman has not menstruated for one year. During the menopausal transition period, there is an emergence of various lipid metabolic disorders due to hormonal changes, such as decreased levels of estrogens and increased levels of circulating androgens; these may lead to the development of metabolic syndromes including cardiovascular diseases and type 2 diabetes. Dysregulation of lipid metabolism affects the body fat mass, fat-free mass, fatty acid metabolism, and various aspects of energy metabolism, such as basal metabolic ratio, adiposity, and obesity. Moreover, menopause is also associated with alterations in the levels of various lipids circulating in the blood, such as lipoproteins, apolipoproteins, low-density lipoproteins (LDLs), high-density lipoproteins (HDL) and triacylglycerol (TG). Alterations in lipid metabolism and excessive adipose tissue play a key role in the synthesis of excess fatty acids, adipocytokines, proinflammatory cytokines, and reactive oxygen species, which cause lipid peroxidation and result in the development of insulin resistance, abdominal adiposity, and dyslipidemia. This review discusses dietary recommendations and beneficial compounds, such as vitamin D, omega-3 fatty acids, antioxidants, phytochemicals—and their food sources—to aid the management of abnormal lipid metabolism in postmenopausal women.
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Lira, Fábio S., Luiz C. Carnevali, Nelo E. Zanchi, Ronaldo VT Santos, Jean Marc Lavoie, and Marília Seelaender. "Exercise Intensity Modulation of Hepatic Lipid Metabolism." Journal of Nutrition and Metabolism 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/809576.
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Lipid metabolism in the liver is complex and involves the synthesis and secretion of very low density lipoproteins (VLDL), ketone bodies, and high rates of fatty acid oxidation, synthesis, and esterification. Exercise training induces several changes in lipid metabolism in the liver and affects VLDL secretion and fatty acid oxidation. These alterations are even more conspicuous in disease, as in obesity, and cancer cachexia. Our understanding of the mechanisms leading to metabolic adaptations in the liver as induced by exercise training has advanced considerably in the recent years, but much remains to be addressed. More recently, the adoption of high intensity exercise training has been put forward as a means of modulating hepatic metabolism. The purpose of the present paper is to summarise and discuss the merit of such new knowledge.
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Hernández, M. Luisa, Elena Lima-Cabello, Juan de D. Alché, José M. Martínez-Rivas, and Antonio J. Castro. "Lipid Composition and Associated Gene Expression Patterns during Pollen Germination and Pollen Tube Growth in Olive (Olea europaea L.)." Plant and Cell Physiology 61, no. 7 (May 8, 2020): 1348–64. http://dx.doi.org/10.1093/pcp/pcaa063.
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Abstract Pollen lipids are essential for sexual reproduction, but our current knowledge regarding lipid dynamics in growing pollen tubes is still very scarce. Here, we report unique lipid composition and associated gene expression patterns during olive pollen germination. Up to 376 genes involved in the biosynthesis of all lipid classes, except suberin, cutin and lipopolysaccharides, are expressed in olive pollen. The fatty acid profile of olive pollen is markedly different compared with other plant organs. Triacylglycerol (TAG), containing mostly C12–C16 saturated fatty acids, constitutes the bulk of olive pollen lipids. These compounds are partially mobilized, and the released fatty acids enter the β-oxidation pathway to yield acetyl-CoA, which is converted into sugars through the glyoxylate cycle during the course of pollen germination. Our data suggest that fatty acids are synthesized de novo and incorporated into glycerolipids by the ‘eukaryotic pathway’ in elongating pollen tubes. Phosphatidic acid is synthesized de novo in the endomembrane system during pollen germination and seems to have a central role in pollen tube lipid metabolism. The coordinated action of fatty acid desaturases FAD2–3 and FAD3B might explain the increase in linoleic and alpha-linolenic acids observed in germinating pollen. Continuous synthesis of TAG by the action of diacylglycerol acyltransferase 1 (DGAT1) enzyme, but not phosphoplipid:diacylglycerol acyltransferase (PDAT), also seems plausible. All these data allow for a better understanding of lipid metabolism during the olive reproductive process, which can impact, in the future, on the increase in olive fruit yield and, therefore, olive oil production.
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Fuchs, Michael. "III. Regulation of bile acid synthesis: past progress and future challenges." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 4 (April 1, 2003): G551—G557. http://dx.doi.org/10.1152/ajpgi.00468.2002.
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Bile acids, amphipathic detergent-like molecules synthesized from cholesterol, are highly conserved by means of enterohepatic circulation. They participate in the generation of bile flow and biliary lipid secretion and also promote absorption of fat-soluble vitamins and lipids. Conversion of cholesterol to bile acids represents a quantitatively important route to eliminate cholesterol from the body. Regulation of bile acid synthesis involves a complex and interrelated group of transcription regulators that link bile acid synthesis to cholesterol and fatty acid metabolism. Targeting key steps of bile acid synthetic pathways as well as the metabolic network that maintains homeostatic levels of lipids should provide exciting novel opportunities for the treatment of cardiovascular and liver diseases.
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Mika, Adriana, Alicja Pakiet, Aleksandra Czumaj, Zbigniew Kaczynski, Ivan Liakh, Jarek Kobiela, Adrian Perdyan, Krystian Adrych, Wojciech Makarewicz, and Tomasz Sledzinski. "Decreased Triacylglycerol Content and Elevated Contents of Cell Membrane Lipids in Colorectal Cancer Tissue: A Lipidomic Study." Journal of Clinical Medicine 9, no. 4 (April 12, 2020): 1095. http://dx.doi.org/10.3390/jcm9041095.
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Recent evidence suggests that lipid composition in cancer tissues may undergo multiple alterations. However, no comprehensive analysis of various lipid groups in colorectal cancer (CRC) tissue has been conducted thus far. To address the problem in question, we determined the contents of triacylglycerols (TG), an energetic substrate, various lipids necessary for cell membrane formation, among them phospholipids (phosphatidylcholine, phosphatidylethanolamine), sphingolipids (sphingomyelin) and cholesterol (free, esterified and total), and fatty acids included in complex lipids. 1H-nuclear magnetic resonance (1H-NMR) and gas chromatography-mass spectrometry (GC-MS) were used to analyze the lipid composition of colon cancer tissue and normal large intestinal mucosa from 25 patients. Compared with normal tissue, cancer tissues had significantly lower TG content, along with elevated levels of phospholipids, sphingomyelin, and cholesterol. Moreover, the content of oleic acid, the main component of TG, was decreased in cancer tissues, whereas the levels of saturated fatty acids and polyunsaturated fatty acids (PUFAs), which are principal components of polar lipids, were elevated. These lipidome rearrangements were associated with the overexpression of genes associated with fatty acid oxidation, and the synthesis of phospholipids and cholesterol. These findings suggest that reprogramming of lipid metabolism might occur in CRC tissue, with a shift towards increased utilization of TG for energy production and enhanced synthesis of membrane lipids, necessary for the rapid proliferation of cancer cells.
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Umpleby, A. Margot. "HORMONE MEASUREMENT GUIDELINES: Tracing lipid metabolism: the value of stable isotopes." Journal of Endocrinology 226, no. 3 (June 4, 2015): G1—G10. http://dx.doi.org/10.1530/joe-14-0610.
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Labelling molecules with stable isotopes to create tracers has become a gold-standard method to study the metabolism of lipids and lipoproteins in humans. There are a range of techniques which use stable isotopes to measure fatty acid flux and oxidation, hepatic fatty synthesis, cholesterol absorption and synthesis and lipoprotein metabolism in humans. Stable isotope tracers are safe to use, enabling repeated studies to be undertaken and allowing studies to be undertaken in children and pregnant women. This review provides details of the most appropriate tracers to use, the techniques which have been developed and validated for measuring different aspects of lipid metabolism and some of the limitations of the methodology.
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Molnár, T., J. Biró, C. Hancz, R. Romvári, D. Varga, P. Horn, and A. Szabó. "Fatty acid profile of fillet, liver and mesenteric fat in tilapia (<i>Oreochromis niloticus</i>) fed vegetable oil supplementation in the finishing period of fattening." Archives Animal Breeding 55, no. 2 (October 10, 2012): 194–205. http://dx.doi.org/10.5194/aab-55-194-2012.
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Abstract. Tilapia (Oreochromis niloticus) previously reared on a commercial feed were shifted to 3 experimental diets with added 5 % of soybean, linseed oil or fish oils, for 42 days as a finishing diet, according to literature recommendations. Fillet, liver and mesenteric fat total lipid fatty acid composition was determined and evaluated taking health and dietary recommendations into consideration. It was found that dietary vegetable oil fatty acids are effectively incorporated into tilapia hepatic and muscular total lipids, but have no pronounced effect on further fatty acid metabolism, in particular on the n-3 fatty acids. Liver was found to sensitively indicate elevated dietary lipid intake, as proven by its higher, most probably endogenous palmitate synthesis. Based on our results the application of vegetable oils to partially substitute fish oil for tilapia can be recommended in relation to the most important dietary lipid quality indicators.
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Rayner, Katey J., Carlos Fernández-Hernando, and Kathryn J. Moore. "MicroRNAs regulating lipid metabolism in atherogenesis." Thrombosis and Haemostasis 107, no. 04 (2012): 642–47. http://dx.doi.org/10.1160/th11-10-0694.
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SummaryMicroRNAs have emerged as important post-transcriptional regulators of lipid metabolism, and represent a new class of targets for therapeutic intervention. Recently, microRNA-33a and b (miR-33a/b) were discovered as key regulators of metabolic programs including cholesterol and fatty acid homeostasis. These intronic microRNAs are embedded in the sterol response element binding protein genes, SREBF2 and SREBF1, which code for transcription factors that coordinate cholesterol and fatty acid synthesis. By repressing a variety of genes involved in cholesterol export and fatty acid oxidation, including ABCA1, CROT, CPT1, HADHB and PRKAA1, miR-33a/b act in concert with their host genes to boost cellular sterol levels. Recent work in animal models has shown that inhibition of these small non-coding RNAs has potent effects on lipoprotein metabolism, including increasing plasma high-density lipo-protein (HDL) and reducing very low density lipoprotein (VLDL) triglyce-rides. Furthermore, other microRNAs are being discovered that also target the ABCA1 pathway, including miR-758, suggesting that miRNAs may work cooperatively to regulate this pathway. These exciting findings support the development of microRNA antagonists as potential therapeutics for the treatment of dyslipidaemia, atherosclerosis and related metabolic diseases.
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Liu, Lei, Chunyan Fu, and Fuchang Li. "Acetate Affects the Process of Lipid Metabolism in Rabbit Liver, Skeletal Muscle and Adipose Tissue." Animals 9, no. 10 (October 14, 2019): 799. http://dx.doi.org/10.3390/ani9100799.
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Short-chain fatty acids (SCFAs) (a microbial fermentation production in the rabbit gut) have an important role in many physiological processes, which may be related to the reduced body fat of rabbits. In the present experiment, we study the function of acetate (a major SCFA in the rabbit gut) on fat metabolism. Ninety rabbits (40 days of age) were randomly divided into three groups: a sham control group (injection of saline for four days); a group experiencing subcutaneous injection of acetate for four days (2 g/kg BM per day, one injection each day, acetate); and a pair-fed sham treatment group. The results show that acetate-inhibited lipid accumulation by promoting lipolysis and fatty acid oxidation and inhibiting fatty acid synthesis. Activated G protein-coupled receptor 41/43, adenosine monophosphate activated protein kinase (AMPK) and extracellular-signal-regulated kinase (ERK) 1/2 signal pathways were likely to participate in the regulation in lipid accumulation of acetate. Acetate reduced hepatic triglyceride content by inhibiting fatty acid synthesis, enhancing fatty acid oxidation and lipid output. Inhibited peroxisome proliferator-activated receptor α (PPARα) and activated AMPK and ERK1/2 signal pathways were related to the process in liver. Acetate reduced intramuscular triglyceride level via increasing fatty acid uptake and fatty acid oxidation. PPARα was associated with the acetate-reduced intracellular fat content.
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Guschina, Irina A., Natalia Ninkina, Andrei Roman, Mikhail V. Pokrovskiy, and Vladimir L. Buchman. "Triple-Knockout, Synuclein-Free Mice Display Compromised Lipid Pattern." Molecules 26, no. 11 (May 21, 2021): 3078. http://dx.doi.org/10.3390/molecules26113078.
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Recent studies have implicated synucleins in several reactions during the biosynthesis of lipids and fatty acids in addition to their recognised role in membrane lipid binding and synaptic functions. These are among aspects of decreased synuclein functions that are still poorly acknowledged especially in regard to pathogenesis in Parkinson’s disease. Here, we aimed to add to existing knowledge of synuclein deficiency (i.e., the lack of all three family members), with respect to changes in fatty acids and lipids in plasma, liver, and two brain regions in triple synuclein-knockout (TKO) mice. We describe changes of long-chain polyunsaturated fatty acids (LCPUFA) and palmitic acid in liver and plasma, reduced triacylglycerol (TAG) accumulation in liver and non-esterified fatty acids in plasma of synuclein free mice. In midbrain, we observed counterbalanced changes in the relative concentrations of phosphatidylcholine (PC) and cerebrosides (CER). We also recorded a notable reduction in ethanolamine plasmalogens in the midbrain of synuclein free mice, which is an important finding since the abnormal ether lipid metabolism usually associated with neurological disorders. In summary, our data demonstrates that synuclein deficiency results in alterations of the PUFA synthesis, storage lipid accumulation in the liver, and the reduction of plasmalogens and CER, those polar lipids which are principal compounds of lipid rafts in many tissues. An ablation of all three synuclein family members causes more profound changes in lipid metabolism than changes previously shown to be associated with γ-synuclein deficiency alone. Possible mechanisms by which synuclein deficiency may govern the reported modifications of lipid metabolism in TKO mice are proposed and discussed.
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Jiang, Y., X. D. Liao, M. Xie, J. Tang, S. Y. Qiao, Z. G. Wen, and S. S. Hou. "Dietary threonine supplementation improves hepatic lipid metabolism of Pekin ducks." Animal Production Science 59, no. 4 (2019): 673. http://dx.doi.org/10.1071/an17633.
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The present study was conducted to evaluate the regulatory role of threonine (Thr) on hepatic lipid metabolism by determining the effects of dietary Thr concentration on lipid deposition and on genes related to lipid expression in the liver of Pekin duck. In total, 240 1-day-old ducklings were randomly allocated according to the average bodyweight to one of five dietary treatments with six replicate cages of eight birds per cage for each treatment. Birds were fed diets with 0.52%, 0.59%, 0.66%, 0.73% and 0.80% Thr (as-fed basis) from 1 to 21 days of age respectively. The results showed that dietary Thr supplementation increased average daily gain (P < 0.0001), average daily feed intake (P < 0.0001) and abdominal fat percentage (P < 0.04), while it decreased feed to gain ratio (P < 0.0001), the hepatic contents of total lipid (P < 0.003) and triglycerides (P < 0.003) of Pekin ducks. However, dietary Thr supplementation had no influence (P > 0.05) on the concentration of hepatic cholesterol, and plasma amino acids and biochemical parameters of Pekin ducks. Moreover, Thr-unsupplemented control diet upregulated (P < 0.05) hepatic gene expression related to lipid uptake (fatty acid-binding protein, apolipoprotein A4, lipoprotein lipase), fatty acid synthesis (sterol regulatory element-binding protein 1c, malic enzyme), fatty acid β-oxidation (peroxisome proliferator-activated receptor α, fatty acyl– coenzyme A (CoA) oxidase), ketogenesis (hydroxymethylglutaryl–CoA synthase 1, and acetyl–CoA synthetase1), responsive genes to amino acid deficiency (general control non-derepressible 2 (GCN2), GCN1, eukaryotic initiation factor 2α, impact RWD domain protein (IMPACT)), and triglyceride transport (apolipoprotein B) of Pekin ducks. In addition, dietary Thr deficiency had no effect on the expression of stearoyl CoA desaturase, fatty acid synthase, and ATP–citrate lyase in the liver of Pekin ducks. It is suggested that dietary Thr supplementation improved hepatic lipid metabolism of Pekin ducks by regulating lipid synthesis, transport and oxidation.
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Herzberg, Gene R. "The 1990 Borden Award Lecture Dietary regulation of fatty acid and triglyceride metabolism." Canadian Journal of Physiology and Pharmacology 69, no. 11 (November 1, 1991): 1637–47. http://dx.doi.org/10.1139/y91-242.
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The level of circulating triacylglycerols is determined by the balance between their delivery into the plasma and their removal from it. Plasma triacylglycerols are derived either from dietary fat as chylomicrons or from endogenous hepatic synthesis as very low density lipoproteins. Their removal occurs through the action of lipoprotein lipase after which the fatty acids are either stored in adipose tissue or oxidized, primarily in skeletal muscle and heart. The composition of the diet has been shown to influence many of these processes. Hepatic fatty acid synthesis and triacylglycerol secretion are affected by the quantity and composition of dietary fat, carbohydrate, and protein. Polyunsaturated but not saturated fats reduce hepatic fatty acid synthesis by decreasing the amount of the lipogenic enzymes needed for de novo fatty acid synthesis. Dietary fish oils are particularly effective at reducing both fatty acid synthesis and triacylglycerol secretion and as a result are hypotriacylglycerolemic, particularly in hypertriacylglycerolemic individuals. In addition, dietary fish oils can increase the oxidation of fatty acids and lead to increased activity of lipoprotein lipase in skeletal muscle and heart. It appears that the hypotriacylglycerolemic effect of dietary fish oils is mediated by effects on both synthesis and removal of circulating triacylglycerols.Key words: lipid, fish oil, fructose, liver, adipose tissue, oxidation.
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Okuliarova, Monika, Valentina Sophia Rumanova, Katarina Stebelova, and Michal Zeman. "Dim Light at Night Disturbs Molecular Pathways of Lipid Metabolism." International Journal of Molecular Sciences 21, no. 18 (September 21, 2020): 6919. http://dx.doi.org/10.3390/ijms21186919.
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Dim light at night (dLAN) is associated with metabolic risk but the specific effects on lipid metabolism have only been evaluated to a limited extent. Therefore, to explore whether dLAN can compromise lipid metabolic homeostasis in healthy individuals, we exposed Wistar rats to dLAN (~2 lx) for 2 and 5 weeks and analyzed the main lipogenic pathways in the liver and epididymal fat pad, including the control mechanisms at the hormonal and molecular level. We found that dLAN promoted hepatic triacylglycerol accumulation, upregulated hepatic genes involved in de novo synthesis of fatty acids, and elevated glucose and fatty acid uptake. These observations were paralleled with suppressed fatty acid synthesis in the adipose tissue and altered plasma adipokine levels, indicating disturbed adipocyte metabolic function with a potential negative impact on liver metabolism. Moreover, dLAN-exposed rats displayed an elevated expression of two peroxisome proliferator-activated receptor family members (Pparα and Pparγ) in the liver and adipose tissue, suggesting the deregulation of important metabolic transcription factors. Together, our results demonstrate that an impaired balance of lipid biosynthetic pathways caused by dLAN can increase lipid storage in the liver, thereby accounting for a potential linking mechanism between dLAN and metabolic diseases.
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Konstantynowicz-Nowicka, Berk, Chabowski, Kasacka, Bielawiec, Łukaszuk, and Harasim-Symbor. "High-Fat Feeding in Time-Dependent Manner Affects Metabolic Routes Leading to Nervonic Acid Synthesis in NAFLD." International Journal of Molecular Sciences 20, no. 15 (August 5, 2019): 3829. http://dx.doi.org/10.3390/ijms20153829.
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Nonalcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in the liver. The disturbances in the fatty acid composition of stored lipids are more important than the lipid species itself, which may influence the overall effect caused by these molecules. Thus, uncovering time-dependent changes in the fatty acid composition of accumulated lipid fractions after a high fat diet seems to be a new marker of NAFLD occurrence. The experiments were conducted on high fat fed Wistar rats. The blood and liver samples were collected at the end of each experimental week and used to assess the content of lipid fractions and their fatty acid composition by gas liquid chromatography. The expression of proteins from lipid metabolism pathways and of fatty acid exporting proteins were detected by Western blotting. In the same high fat feeding period, decreased de novo lipogenesis, increased β-oxidation and lipid efflux were demonstrated. The observed effects may be the first liver protective mechanisms against lipotoxicity. Nevertheless, such effects were still not sufficient to prevent the liver from proinflammatory lipid accumulation. Moreover, the changes in liver metabolic pathways caused the plasma nervonic acid concentration in sphingomyelin to decrease simultaneously with NAFLD development, which may be a steatosis occurrence prognostic marker.
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Pellerin, Laurence, Lorry Carrié, Carine Dufau, Laurence Nieto, Bruno Ségui, Thierry Levade, Joëlle Riond, and Nathalie Andrieu-Abadie. "Lipid metabolic Reprogramming: Role in Melanoma Progression and Therapeutic Perspectives." Cancers 12, no. 11 (October 27, 2020): 3147. http://dx.doi.org/10.3390/cancers12113147.
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Metabolic reprogramming contributes to the pathogenesis and heterogeneity of melanoma. It is driven both by oncogenic events and the constraints imposed by a nutrient- and oxygen-scarce microenvironment. Among the most prominent metabolic reprogramming features is an increased rate of lipid synthesis. Lipids serve as a source of energy and form the structural foundation of all membranes, but have also emerged as mediators that not only impact classical oncogenic signaling pathways, but also contribute to melanoma progression. Various alterations in fatty acid metabolism have been reported and can contribute to melanoma cell aggressiveness. Elevated expression of the key lipogenic fatty acid synthase is associated with tumor cell invasion and poor prognosis. Fatty acid uptake from the surrounding microenvironment, fatty acid β-oxidation and storage also appear to play an essential role in tumor cell migration. The aim of this review is (i) to focus on the major alterations affecting lipid storage organelles and lipid metabolism. A particular attention has been paid to glycerophospholipids, sphingolipids, sterols and eicosanoids, (ii) to discuss how these metabolic dysregulations contribute to the phenotype plasticity of melanoma cells and/or melanoma aggressiveness, and (iii) to highlight therapeutic approaches targeting lipid metabolism that could be applicable for melanoma treatment.
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YICHOY, M., T. T. DUARTE, A. DE CHATTERJEE, T. L. MENDEZ, K. Y. AGUILERA, D. ROY, S. ROYCHOWDHURY, S. B. ALEY, and S. DAS. "Lipid metabolism inGiardia: a post-genomic perspective." Parasitology 138, no. 3 (September 30, 2010): 267–78. http://dx.doi.org/10.1017/s0031182010001277.
Full textAbstract:
SUMMARYGiardia lamblia, a protozoan parasite, infects a wide variety of vertebrates, including humans. Studies indicate that this anaerobic protist possesses a limited ability to synthesize lipid moleculesde novoand depends on supplies from its environment for growth and differentiation. It has been suggested that most lipids and fatty acids are taken up by endocytic and non-endocytic pathways and are used byGiardiafor energy production and membrane/organelle biosynthesis. The purpose of this article is to provide an update on recent progress in the field of lipid research of this parasite and the validation of lipid metabolic pathways through recent genomic information. Based on current cellular, biochemical and genomic data, a comprehensive pathway has been proposed to facilitate our understanding of lipid and fatty acid metabolism/syntheses in this waterborne pathogen. We envision that the current review will be helpful in identifying targets from the pathways that could be used to design novel therapies to control giardiasis and related diseases.
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Schindler, Maria, Mareike Pendzialek, Alexander Navarrete Santos, Torsten Plösch, Stefanie Seyring, Jacqueline Gürke, Elisa Haucke, Julia Miriam Knelangen, Bernd Fischer, and Anne Navarrete Santos. "Maternal Diabetes Leads to Unphysiological High Lipid Accumulation in Rabbit Preimplantation Embryos." Endocrinology 155, no. 4 (April 1, 2014): 1498–509. http://dx.doi.org/10.1210/en.2013-1760.
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According to the “developmental origin of health and disease” hypothesis, the metabolic set points of glucose and lipid metabolism are determined prenatally. In the case of a diabetic pregnancy, the embryo is exposed to higher glucose and lipid concentrations as early as during preimplantation development. We used the rabbit to study the effect of maternal diabetes type 1 on lipid accumulation and expression of lipogenic markers in preimplantation blastocysts. Accompanied by elevated triglyceride and glucose levels in the maternal blood, embryos from diabetic rabbits showed a massive intracellular lipid accumulation and increased expression of fatty acid transporter 4, fatty acid–binding protein 4, perilipin/adipophilin, and maturation of sterol-regulated element binding protein. However, expression of fatty acid synthase, a key enzyme for de novo synthesis of fatty acids, was not altered in vivo. During a short time in vitro culture of rabbit blastocysts, the accumulation of lipid droplets and expression of lipogenic markers were directly correlated with increasing glucose concentration, indicating that hyperglycemia leads to increased lipogenesis in the preimplantation embryo. Our study shows the decisive effect of glucose as the determining factor for fatty acid metabolism and intracellular lipid accumulation in preimplantation embryos.
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RAMLI, Umi S., Darren S. BAKER, Patti A. QUANT, and John L. HARWOOD. "Control mechanisms operating for lipid biosynthesis differ in oil-palm (Elaeis guineensis Jacq.) and olive (Olea europaea L.) callus cultures." Biochemical Journal 364, no. 2 (June 1, 2002): 385–91. http://dx.doi.org/10.1042/bj20010202.
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As a prelude to detailed flux control analysis of lipid synthesis in plants, we have examined the latter in tissue cultures from two important oil crops, olive (Olea europaea L.) and oil palm (Elaeis guineensis Jacq.). Temperature was used to manipulate the overall rate of lipid formation in order to characterize and validate the system to be used for analysis. With [1-14C]acetate as a precursor, an increase in temperature from 20 to 30°C produced nearly a doubling of total lipid labelling. This increase in total lipids did not change the radioactivity in the intermediate acyl-(acyl carrier protein) or acyl-CoA pools, indicating that metabolism of these pools did not exert any significant constraint for overall synthesis. In contrast, there were some differences in the proportional labelling of fatty acids and of lipid classes at the two temperatures. The higher temperature caused a decrease in polyunsaturated fatty acid labelling and an increase in the proportion of triacylglycerol labelling in both calli. The intermediate diacylglycerol was increased in olive, but not in oil palm. Overall the data indicate the suitability of olive and oil-palm cultures for the study of lipid synthesis and indicate that de novo fatty acid synthesis may exert more flux control than complex lipid assembly. In olive, diacylglycerol acyltransferase may exert significant flux control when lipid synthesis is rapid.
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Lee, Ju-Young, Kwang-Hyeon Liu, Yunhi Cho, and Kun-Pyo Kim. "Enhanced Triacylglycerol Content and Gene Expression for Triacylglycerol Metabolism, Acyl-Ceramide Synthesis, and Corneocyte Lipid Formation in the Epidermis of Borage Oil Fed Guinea Pigs." Nutrients 11, no. 11 (November 18, 2019): 2818. http://dx.doi.org/10.3390/nu11112818.
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Triacylglycerol (TAG) metabolism is related to the acyl-ceramide (Cer) synthesis and corneocyte lipid envelope (CLE) formation involved in maintaining the epidermal barrier. Prompted by the recovery of a disrupted epidermal barrier with dietary borage oil (BO: 40.9% linoleic acid (LNA) and 24.0% γ-linolenic acid (GLA)) in essential fatty acid (EFA) deficiency, lipidomic and transcriptome analyses and subsequent quantitative RT-PCR were performed to determine the effects of borage oil (BO) on TAG content and species, and the gene expression related to overall lipid metabolism. Dietary BO for 2 weeks in EFA-deficient guinea pigs increased the total TAG content, including the TAG species esterified LNA, GLA, and their C20 metabolized fatty acids. Moreover, the expression levels of genes in the monoacylglycerol and glycerol-3-phosphate pathways, two major pathways of TAG synthesis, increased, along with those of TAG lipase, acyl-Cer synthesis, and CLE formation. Dietary BO enhanced TAG content, the gene expression of TAG metabolism, acyl-Cer synthesis, and CLE formation.
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Yuskiv, L. L., and I. D. Yuskiv. "The lipid metabolism in carp during invasion by the tapeworn Bothriocephalus acheilognathi." Regulatory Mechanisms in Biosystems 11, no. 2 (April 16, 2020): 214–19. http://dx.doi.org/10.15421/022031.
Full textAbstract:
The changes in total lipids, their fatty acid composition and the ratio of individual classes were established in tissues of the intestine, hepatopancreas and skeletal muscles of carp (Cyprinus carpio Linnaeus, 1758), with body weight 14.5–20.5 g, at different rates of invasion by Bothriocephalus acheilognathi (Yamaguti, 1934) helminth, which belongs to the family Bothriocephalidae, of the Pseudophyllidae order, of the Cestoda class. The examined carp was divided into three groups: first group of fish was free from intestinal helminths of B. acheilognathi (control); second group of fish was weakly infected with helminths (intensity of invasion is 1–3 helminths per fish); the third group of fish was highly infected (the invasion intensity is 4 worms and more per fish). Our results showed that fish infected with helminth B. acheilognathi compared to uninfected fish had reduced total lipid level in the gut due to phospholipids, triacylglycerols, and also lipids were characterized by lower content of linoleic, linolenic, arachidonic, penta- and hexanoic fatty acids; decrease in the level of unsaturated and increase in the content of saturated fatty acids, which leads to an increase of the saturation factor. During the infection of carp with B. acheilognathi in the hepatopancreas, the content of total lipids, structural lipids – phospholipids and reserve energy sources – triacylglycerols is probably reduced, and lipids are characterized by a high content of saturated fatty acids (С14:0, С16:0, С18:0) and lower content of unsaturated: arachidonic (С20:4), linolenic (С18:3) and linoleic acid (С18:2), which is associated with a decrease in the source for the synthesis of a number of polyunsaturated fatty acids, especially docosahexaenoic (С22:6). The total content of lipids, triacylglycerols, free fatty acids and phospholipids in skeletal muscle of carp during the Bothriocephalus invasion decreased and the content of free cholesterol, mono- and triacylglycerols increased. Helminth B. acheilognathi has the effect of reducing the total lipids of the skeletal muscle content of С18-, С20-, С22-polyunsaturated fatty acids and increasing the content of saturated (С14:0, С16:0, С18:0) and monounsaturated (С16:1, С18:1) fatty acids. The obtained results prove that the parasite B. acheilognathi in the intestine of the carp significantly affects the nutrition processes of the host depending on the intensity of the damage by helminths, which is accompanied by impaired lipid metabolism.
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Holub, Bruce J., Diana J. Philbrick, Anwar Parbtani, and William F. Clark. "Dietary lipid modification of renal disorders and ether phospholipid metabolism." Biochemistry and Cell Biology 69, no. 7 (July 1, 1991): 485–89. http://dx.doi.org/10.1139/o91-072.
Full textAbstract:
The formation of arachidonic acid derived eicosanoids, including thromboxane A2 and leukotriene B4, as well as platelet-activating factor (1-O-alkyl-2-acetyl-glycerophosphocholine), has been implicated in various renal pathophysiologies. Alteration of the fatty acid composition of membrane phospholipids in platelets, the glomerulus, and inflammatory cells, and of 1-O-alkyl-2-acyl-glycerophosphocholine (platelet-activating factor precursor) can be attained by dietary lipid modifications (e.g., consumption of fish oil containing n – 3 polyunsaturated fatty acids). These changes have been associated with an attenuation in renal disease progression and modifications in the synthesis and actions-interactions of eicosanoids, cytokines, and platelet-activating factor.Key words: renal disorders, omega-3, platelet-activating factor, eicosanoids, cytokines.
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Chen, Li, Hao Yu, Shengping Yang, Yunfang Qian, and Jing Xie. "Study on the Mechanism of Cold Tolerance of the Strain Shewanella putrefaciens WS13 Through Fatty Acid Metabolism." Nanoscience and Nanotechnology Letters 11, no. 12 (December 1, 2019): 1718–23. http://dx.doi.org/10.1166/nnl.2019.3055.
Full textAbstract:
In order to investigate the cold tolerance mechanism of Shewanella, the whole genome of strain Shewanella putrefaciens WS13 was used to study the comparative genome related to cold tolerance of Shewanella . By comparing and analyzing the key enzymes involved in the process of lipid synthesis with those of other psychrophilic and non-psychrophilic bacteria, the results showed that in S. putrefaciens WS13, the genes fabA, fabB, fabD, fabF, fabG, fabH and fabZ, as the key enzymes of fatty acid synthesis, were found in the target strain, but the gene fabI did not exist in the type II fatty acid synthesis pathway. However, due to the absence of the key enzyme fabI gene, the synthesis process of saturated fatty acids will be blocked, and the pathway of unsaturated fatty acid synthesis still exists, which leads to the bacteria Shewanella start to synthesize a large number of unsaturated fatty acids, thus increasing the synthesis of unsaturated fatty acids and reducing the synthesis of saturated fatty acids. It is precisely because unsaturated fatty acids have lower phase transition temperature than that saturated fatty acids have, which can increase the fluidity of biofilm, so that Shewanella has better cold adaptability than that other bacteria have. It is a complex biological process for microorganisms to adapt to the environment, and the biosynthesis of fatty acids is only one aspect. However, the mechanism of cold adaptation of Shewanella in other aspects remains to be further discussed.
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Catalá, Angel. "Five Decades with Polyunsaturated Fatty Acids: Chemical Synthesis, Enzymatic Formation, Lipid Peroxidation and Its Biological Effects." Journal of Lipids 2013 (2013): 1–19. http://dx.doi.org/10.1155/2013/710290.
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I have been involved in research on polyunsaturated fatty acids since 1964 and this review is intended to cover some of the most important aspects of this work. Polyunsaturated fatty acids have followed me during my whole scientific career and I have published a number of studies concerned with different aspects of them such as chemical synthesis, enzymatic formation, metabolism, transport, physical, chemical, and catalytic properties of a reconstructed desaturase system in liposomes, lipid peroxidation, and their effects. The first project I became involved in was the organic synthesis of [1-14C] eicosa-11,14-dienoic acid, with the aim of demonstrating the participation of that compound as a possible intermediary in the biosynthesis of arachidonic acid “in vivo.” From 1966 to 1982, I was involved in several projects that study the metabolism of polyunsaturated fatty acids. In the eighties, we studied fatty acid binding protein. From 1990 up to now, our laboratory has been interested in the lipid peroxidation of biological membranes from various tissues and different species as well as liposomes prepared with phospholipids rich in PUFAs. We tested the effect of many antioxidants such as alpha tocopherol, vitamin A, melatonin and its structural analogues, and conjugated linoleic acid, among others.
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Barakat, H. A., G. L. Dohm, N. Shukla, R. H. Marks, M. Kern, J. W. Carpenter, and R. S. Mazzeo. "Influence of age and exercise training on lipid metabolism in Fischer-344 rats." Journal of Applied Physiology 67, no. 4 (October 1, 1989): 1638–42. http://dx.doi.org/10.1152/jappl.1989.67.4.1638.
Full textAbstract:
The influence of training on fatty acid and glyceride synthesis by liver and adipose tissue homogenates of young and old Fischer-344 rats was examined. Four groups of rats (10 animals/group) were studied: young untrained, young trained, old untrained, and old trained. Training of each group was for 10 wk at 75% maximal O2 uptake. Young rats were killed at 6 mo of age and old rats were killed at 27 mo of age. Fatty acid synthesis was assessed by measuring the activities of acetyl-CoA carboxylase, fatty acid synthase, ATP citrate-lyase, "malic" enzyme, and glucose-6-phosphate dehydrogenase. Glyceride synthesis was evaluated by determining the rate of incorporation of [14C]glycerol 3-phosphate into lipids. In addition, lipoprotein lipase activity was measured in acetone-ether powders of adipose tissue from the four groups of rats. In liver, training had no effect on fatty acid or glyceride synthesis in either group. However, aging caused a significant decrease in the activities of four of the lipogenic enzymes but had no effect on glyceride synthesis. Training caused an increase in fatty acid synthase and glyceride synthesis in adipose tissue, and aging decreased lipoprotein lipase activity. It was concluded that training enhances the synthetic capacity of lipids by adipose tissue but that aging had a more profound effect in that the activities of the enzymes involved in these processes were lower in the old rats. Furthermore, the decreased activity of lipoprotein lipase in the older rats may explain the higher plasma triglyceride levels that were observed in these animals.
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Shih, Lu-Min, Hsiang-Yu Tang, Ke-Shiuan Lynn, Cheng-Yu Huang, Hung-Yao Ho, and Mei-Ling Cheng. "Stable Isotope-Labeled Lipidomics to Unravel the Heterogeneous Development Lipotoxicity." Molecules 23, no. 11 (November 2, 2018): 2862. http://dx.doi.org/10.3390/molecules23112862.
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Non-alcoholic fatty liver disease (NAFLD) as a global health problem has clinical manifestations ranging from simple non-alcoholic fatty liver (NAFL) to non-alcoholic steatohepatitis (NASH), cirrhosis, and cancer. The role of different types of fatty acids in driving the early progression of NAFL to NASH is not understood. Lipid overload causing lipotoxicity and inflammation has been considered as an essential pathogenic factor. To correlate the lipid profiles with cellular lipotoxicity, we utilized palmitic acid (C16:0)- and especially unprecedented palmitoleic acid (C16:1)-induced lipid overload HepG2 cell models coupled with lipidomic technology involving labeling with stable isotopes. C16:0 induced inflammation and cell death, whereas C16:1 induced significant lipid droplet accumulation. Moreover, inhibition of de novo sphingolipid synthesis by myriocin (Myr) aggravated C16:0 induced lipoapoptosis. Lipid profiles are different in C16:0 and C16:1-treated cells. Stable isotope-labeled lipidomics elucidates the roles of specific fatty acids that affect lipid metabolism and cause lipotoxicity or lipid droplet formation. It indicates that not only saturation or monounsaturation of fatty acids plays a role in hepatic lipotoxicity but also Myr inhibition exasperates lipoapoptosis through ceramide in-direct pathway. Using the techniques presented in this study, we can potentially investigate the mechanism of lipid metabolism and the heterogeneous development of NAFLD.
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Pelster, B., J. R. Bailey, and W. R. Driedzic. "The fate of14C infused into the swim bladder of the American eel,Anguilla rostrata." Canadian Journal of Zoology 75, no. 1 (January 1, 1997): 116–21. http://dx.doi.org/10.1139/z97-015.
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The present study analyses the capability of swim-bladder tissue of the American eel (Anguilla rostrata) to incorporate either intermediates of glucose metabolism or blood-borne fatty acids into the swim-bladder lipid fraction. At 29.9 ± 6.0 nmol∙min−1∙g−1wet mass, the activity of acyl-CoA synthetase was about 10-fold higher than the activity of acetyl-CoA carboxylase, a key enzyme required for de novo fatty acid synthesis. The level of fatty acid synthase activity was too low to be detected by the enzymatic test used. When the swim bladder was perfused for 1 h with medium containing 5 mmol∙L−1glucose as the only fuel, 11.5 ± 3.3 nmol glucose∙g−1tissue was incorporated into the lipid pool. When, in addition to 5 mmol∙L−1glucose, 1.1 mmol∙L−1acetate was added to the perfusate, incorporation of acetate into the lipid pool was 3.06 ± 1.14 nmol acetate∙g−1tissue. When 0.41 mmol∙L−1palmitate was added to the glucose-containing perfusate, 144.5 ± 24.2 nmol palmitate∙g−1tissue was incorporated into the lipid pool. These results demonstrate that de novo synthesis of lipids in swim-bladder tissue is only possible at a very low rate and cannot explain the difference in numbers of carbon atoms entering and leaving the swim-bladder wall. Blood-borne fatty acids, however, can be readily taken up and incorporated into swim-bladder lipids.
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Smith, S. A. "Peroxisome proliferator-activated receptors and the regulation of mammalian lipid metabolism." Biochemical Society Transactions 30, no. 6 (November 1, 2002): 1086–90. http://dx.doi.org/10.1042/bst0301086.
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Peroxisome proliferator-activated receptors (PPARs) are members of the superfamily of ligand-activated nuclear transcription factors. Three PPAR subtypes, PPARα, PPARδ (PPARβ) and PPARγ, have been described in mammals. The tissue distribution of PPARs is heterogeneous: PPARα is highly expressed in liver and skeletal muscle, PPARγ is preferentially expressed in adipose tissues, and PPARδ is expressed in most cell types with relative abundance. Unlike most receptors, PPARs show low ligand specificity, being activated by many long-chain saturated and unsaturated fatty acids, or by eicosanoids. PPARs are transcriptionally active as heterodimeric complexes with the retinoid X receptor and bind to specific recognition sequences in the regulatory region of target genes. Many PPAR-regulated genes encode proteins that regulate fatty acid oxidation and storage. Elucidation of the biological functions of PPARs has been aided by the development of PPAR-null mice and the identification of humans bearing PPAR mutations, together with the discovery of synthetic small-molecule ligands that selectively activate individual PPAR subtypes. Using these genetic and pharmacological approaches, it has been shown that PPARα predominantly regulates pathways of fatty acid oxidation, whereas PPARγ modifies fatty acid synthesis and storage in adipose tissues. By reducing systemic fatty acid availability, thiazolidinedione PPARγ activators regulate glucose metabolism and are now used clinically in the treatment of Type II diabetes. In summary, PPARs play a central role in the mechanisms that balance fatty acid oxidation and storage in the face of fluctuations of dietary fat intake and energy expenditure.
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Stapaj, P. V., N. P. Stakhiv, V. V. Havryliak, O. O. Smolianinova, and O. S. Tyutyunnyk. "Lipid nutrition of sheep." Animal Biology 22, no. 2 (July 2020): 3–8. http://dx.doi.org/10.15407/animbiol22.02.003.
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The analysis of literature and personal research data on the role of lipids and their individual fatty acids in the nutrition of sheep has been presented. Experimental data indicate a positive effect of lipids on the body of sheep. However, the question of lipid nutrition is poorly studied, which explains the lack of scientifically based standards for the content of raw fat in sheep diets in general and of individual saturated and unsaturated fatty acids, in particular, which leads to an overrun of the most expensive and deficient component of the diet — protein, as well as negatively affects the productivity of animals and the quality of wool, meat and dairy products. A significant amount of data is devoted to the characterization of lipids and their individual fatty acids in various feeds. In particular, it has been shown that plant seeds (wheat, barley, oats, peas) mostly contain structural lipids (phospholipids, glycolipids) in which linoleic (C18:2) acid, which is the parent of acid family ω-6, predominates quantitatively (from 45 to 61%). The amount of linoleic (C18:2) acid does not exceed 7%, and it is a representative of acid family ω-3. This acid and ω-9 are precursors of various biologically active substances, in particular prostaglandins, leukotrienes, platelets and others. It is emphasized that with the increase in the ω-3 fatty acids in the diets of animals, the spectrum of fatty acids of lipids in tissues and organs changes in the direction of increasing their unsaturation, and therefore, the ratio of ω-6/ω-3 acids in the diets should be taken into account for the normal provision of the body with polyunsaturated fatty acids. It is known that the body of sheep is characterized by high requirements for mineral nutrition, which is associated with their products, in particular wool, and among the whole spectrum of mineral elements a special role belongs to Sulfur, whose content in wool is 3–5%. Therefore, the synthesis of keratin is inextricably linked to the intensive use of sulfur-containing compounds, mainly cystine. Our studies have shown that the increase in productivity under the influence of feeding sheep with sulfo-containing compounds is closely related to lipid metabolism, in particular phospholipids, since in sulfate sulfur experiments in vitro particularly the sulfolipid fraction is intensively incorporated into polar skin-lipids. Sulfur-containing compounds stimulate the synthesis of lipids and fatty acids in the body and this is due to the fact that Sulfur is a part of proteins, lipids, vitamins and other biologically active substances.
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Schmutzler, Sandra, Lisa Bachmann, Herbert Fuhrmann, and Julia Schumann. "PUFA-dependent alteration of oxidative parameters of a canine mastocytoma cell line." Acta Veterinaria Hungarica 58, no. 4 (December 1, 2010): 453–64. http://dx.doi.org/10.1556/avet.58.2010.4.6.
Full textAbstract:
Mast cells play a key role in the immune response. Thereby, the balance of oxidative metabolism is of importance in mast cell mediator synthesis and release. Fatty acids may modify mast cell function in several ways. In this study, we investigated the influence of polyunsaturated fatty acids (PUFAs) on oxidative parameters of a canine mastocytoma cell line. C2 cells were cultured in media supplemented with linoleic acid, arachidonic acid, alpha-linolenic acid and eicosapentaenoic acid, respectively. Production of reactive oxygen species (ROS) as well as lipid peroxides was tested. Furthermore, stressor-induced DNA damage was measured. Exposure of the cells to PUFAs resulted in a significant increase in the synthesis of both ROS and lipid peroxides. Distinct differences between the PUFAs tested underline the impact of the unsaturation degree of fatty acids as well as the position of double bonds on mast cells.
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Clandinin, M. T. "Fatty Acids: Evolution in Relation to Neurobiology." Canadian Journal of Physiology and Pharmacology 71, no. 9 (September 1, 1993): 683. http://dx.doi.org/10.1139/y93-101.
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Metabolism of long-chain polyunsaturated fatty acids derived from 18:2ω−6 and 18:3ω−3 by chain elongation – desaturation is essential for synthesis of complex structural lipids, leukotrienes, thromboxanes, and prostaglandins. These essential fatty acids are required for normal function in developing tissues and appropriate maturation of a wide variety of physiological processes. During development, fetal accretion of long-chain metabolites of ω−6 and ω−3 fatty acids may result from maternal or placental synthesis and transfer or, alternatively, from the metabolism of 18:2ω−6 and 18:3ω−3 to longer chain homologues by the fetus. After birth the infant must synthesize or be fed the very long chain polyunsaturated fatty acids of C20 and C22 type derived from 18:2ω−6 and 18:3ω−3.Metabolism of ω−6 and ω−3 fatty acids utilizes the same enzyme system and is competitive. When levels of dietary ω−3 and ω−6 C18 fatty acids are altered, the levels of metabolites of these precursor fatty acids change in specific brain membranes, influencing membrane lipid dependent functions. For example, a diet unbalanced in very long chain ω−3 and ω−6 fatty acids may increase brain membrane ω−3 fatty acid content when 20:5ω−3 is fed, while decreasing membrane fatty acid content of the ω−6 series of competing fatty acids. As 20:4ω−6 is quantitatively and qualitatively important to brain phospholipid, significant reduction in brain levels of 20:4ω−6 may be less than optimal. The impact of these compositional changes on brain function is not yet clear.The authors in this symposium address how this general area of essential fatty acid metabolism is relevant to the evolution of man, growth and development of fish, function of the retina and neural tissue, cognitive development of infants, and infant nutrition.
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Oliveros, Liliana B., María A. Domeniconi, Verónica A. Vega, Laura V. Gatica, Ana M. Brigada, and María S. Gimenez. "Vitamin A deficiency modifies lipid metabolism in rat liver." British Journal of Nutrition 97, no. 2 (February 2007): 263–72. http://dx.doi.org/10.1017/s0007114507182659.
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Liver fatty acid metabolism of male rats fed on a vitamin A-deficient diet for 3 months from 21 d of age was evaluated. Vitamin A restriction produced subclinical plasma and negligible liver retinol concentrations, compared with the control group receiving the same diet with 4000 IU vitamin A (8 mg retinol as retinyl palmitate)/kg diet. Vitamin A deficiency induced a hypolipidaemic effect by decreasing serum triacylglycerol, cholesterol and HDL-cholesterol levels. The decrease of liver total phospholipid was associated with low phosphatidylcholine synthesis observed by lower [14C]choline incorporation into phosphatidylcholine, compared with control. Also, liver fatty acid synthesis decreased, as was indicated by activity and mRNA expression of acetyl-CoA carboxylase (ACC), and incorporation of [14C]acetate into saponified lipids. A decrease of the PPARα mRNA expression was observed. Liver mitochondria of vitamin A-deficient rats showed a lower total phospholipid concentration coinciding with a decrease of the cardiolipin proportion, without changes in the other phospholipid fractions determined. The mitochondria fatty acid oxidation increased by 30 % of the control value and it was attributed to a high activity and mRNA expression of carnitine palmitoyltransferase-I (CPT-I). An increase in serum β-hydroxybutyrate levels was observed in vitamin A-deficient rats. Vitamin A deficiency alters the mitochondria lipid composition and also enhances fatty acid oxidation by modifiying the production of malonyl-CoA, the endogenous inhibitor of CPT-I, due to decreased activity of liver ACC. The incorporation of vitamin A into the diet of vitamin A-deficient rats reverted all the changes observed.
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ROTSTEIN, N. P., G. L. PENNACCHIOTTI, H. SPRECHER, and M. I. AVELDAÑO. "Active synthesis of C24:5, n-3 fatty acid in retina." Biochemical Journal 316, no. 3 (June 15, 1996): 859–64. http://dx.doi.org/10.1042/bj3160859.
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The formation of 14C-labelled long-chain and very-long-chain (n-3) pentaenoic and hexaenoic fatty acids was studied in bovine retina by following the metabolism of [14C]docosapentaenoate [C22:5, n-3 fatty acid (22:5 n-3)], [14C]docosahexaenoate (22:6 n-3), and [14C]acetate. With similar amounts of 22:5 n-3 and 22:6 n-3 as substrates, the former was actively transformed into 24:5 n-3, whereas the latter was virtually unmodified. Labelled 24:5, 26:5, 24:6 and 22:6 were formed from [1-14C]22:5 n-3, showing that pentaenoic fatty acids including 24:5 n-3 can be elongated and desaturated within the retina. When retinal microsomes were incubated with [1-14C]22:5 n-3, 24:5 n-3 was the only fatty acid formed. In retinas incubated with [14C]acetate, 24:5 n-3 was the most highly labelled fatty acid among the polyenes synthesized, 24:6 n-3 being a minor product. Such selectivity in the elongation of two fatty acids identical in length, 22:5 n-3 and 22:6 n-3, despite the fact that 22:5 is a minor and 22:6 a major fatty acid constituent of retina, suggests that the active formation of 24:5 n-3 plays a key role in n-3 polyunsaturated fatty acid (PUFA) metabolism. This compound might give rise to even longer pentaenes via elongation, and to the major PUFAs of retina, 22:6 n-3, by 6-desaturation and chain shortening. Of all retinal lipids, a minor component, triacylglycerol (TG), incorporated the largest amounts of [14C]22:5 and 22:6. TG also concentrated most of the [14C]24:5 formed in retina, whether from [14C]22:5 n-3 or from [14C]acetate, suggesting an important role for this lipid in supporting PUFA metabolism and the synthesis of 22:6 n-3.
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Belviso, Simona, Laura Bardi, Alessandra Biondi Bartolini, and Mario Marzona. "Lipid nutrition of Saccharomyces cerevisiae in winemaking." Canadian Journal of Microbiology 50, no. 9 (September 1, 2004): 669–74. http://dx.doi.org/10.1139/w04-051.
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Biosynthesis of cell membrane lipids is a crucial metabolic pathway for the growth and viability of eucaryotic microorganisms. In Saccharomyces cerevisiae, unsaturated fatty acids and ergosterol synthesis needs molecular oxygen. Stuck and sluggish fermentations are related to this aspect of metabolism and constitute a major problem in the wine industry. Anaerobiosis, when lipids are not available in the growth medium, highly stresses cells. They release lipid biosynthesis metabolites and soon cease to multiply. This paper describes an investigation of the nutritional role of exogenous lipids from inactivated yeast cells (IYCs). Fermentations were carried out in a nitrogen-rich synthetic medium similar to grape juice with glucose and fructose as carbon sources, without lipid sources, and in anaerobiosis. The effect of the addition of IYC was assessed. Cell growth, cell lipid composition, glucose and fructose consumption, and acetic acid production were measured during fermentation. Addition of IYC boosted cell growth and sugar consumption, whereas acetic acid production decreased. Biomass yield was influenced by ergosterol availability and increased when IYCs were added. Fatty acid composition of yeast cells was changed by IYC addition.Key words: fermentation, lipids, nutrition, Saccharomyces cerevisiae, wine.
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Jensen, Kristian K., Stephen F. Previs, Lei Zhu, Kithsiri Herath, Sheng-Ping Wang, Gowri Bhat, Guanghui Hu, et al. "Demonstration of diet-induced decoupling of fatty acid and cholesterol synthesis by combining gene expression array and 2H2O quantification." American Journal of Physiology-Endocrinology and Metabolism 302, no. 2 (January 15, 2012): E209—E217. http://dx.doi.org/10.1152/ajpendo.00436.2011.
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The liver is a crossroad for metabolism of lipid and carbohydrates, with acetyl-CoA serving as an important metabolic intermediate and a precursor for fatty acid and cholesterol biosynthesis pathways. A better understanding of the regulation of these pathways requires an experimental approach that provides both quantitative metabolic flux measurements and mechanistic insight. Under conditions of high carbohydrate availability, excess carbon is converted into free fatty acids and triglyceride for storage, but it is not clear how excessive carbohydrate availability affects cholesterol biosynthesis. To address this, C57BL/6J mice were fed either a low-fat, high-carbohydrate diet or a high-fat, carbohydrate-free diet. At the end of the dietary intervention, the two groups received 2H2O to trace de novo fatty acid and cholesterol synthesis, and livers were collected for gene expression analysis. Expression of lipid and glucose metabolism genes was determined using a custom-designed pathway focused PCR-based gene expression array. The expression analysis showed downregulation of cholesterol biosynthesis genes and upregulation of fatty acid synthesis genes in mice receiving the high-carbohydrate diet compared with the carbohydrate-free diet. In support of these findings, 2H2O tracer data showed that fatty acid synthesis was increased 10-fold and cholesterol synthesis was reduced by 1.6-fold in mice fed the respective diets. In conclusion, by applying gene expression analysis and tracer methodology, we show that fatty acid and cholesterol synthesis are differentially regulated when the carbohydrate intake in mice is altered.
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Zhao, Mei, Maria A. Ralat, Vanessa da Silva, Timothy J. Garrett, Stephan Melnyk, S. Jill James, and Jesse F. Gregory. "Vitamin B-6 restriction impairs fatty acid synthesis in cultured human hepatoma (HepG2) cells." American Journal of Physiology-Endocrinology and Metabolism 304, no. 4 (February 15, 2013): E342—E351. http://dx.doi.org/10.1152/ajpendo.00359.2012.
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Vitamin B-6 deficiency has been reported to alter n-6 and n-3 fatty acid profiles in plasma and tissue lipids; however, the mechanisms underlying such metabolic changes remain unclear. The objective of this study was to determine the effects of vitamin B-6 restriction on fatty acid profiles and fatty acid synthesis in HepG2 cells. Cells were cultured for 6 wk in media with four different vitamin B-6 concentrations (10, 20, 50, and 2,000 nM added pyridoxal, representing deficient, marginal, adequate, and supraphysiological conditions) that induced a range of steady-state cellular concentrations of pyridoxal phosphate. Total cellular lipid content was greatest in the deficient (10 nM pyridoxal) medium. The percentage of arachidonic acid and the ratio of arachidonic acid to linoleic acid in the total lipid fraction were ∼15% lower in vitamin B-6-restricted cells, which suggests that vitamin B-6 restriction affects n-6 fatty acid interconversions. Metabolic flux studies indicated significantly lower fractional synthesis rate of oleic acid and arachidonic acid at 10, 20, and 50 nM pyridoxal, whereas that of eicosapentaenoic acid was lower in the cells cultured in 10 nM pyridoxal. Additionally, relative mRNA expressions of Δ5 and Δ6 desaturases were 40–50% lower in vitamin B-6-restricted cells. Overall, these findings suggest that vitamin B-6 restriction alters unsaturated fatty acid synthesis, particularly n-6 and n-3 polyunsaturated fatty acid synthesis. These results and observations of changes in human plasma fatty acid profiles caused by vitamin B-6 restriction suggest a mechanism by which vitamin B-6 inadequacy influences the cardiovascular risk.
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Garg, M. L., M. Keelan, A. B. R. Thomson, and M. T. Clandinin. "Intestinal microsomes: polyunsaturated fatty acid metabolism and regulation of enterocyte transport properties." Canadian Journal of Physiology and Pharmacology 68, no. 5 (May 1, 1990): 636–41. http://dx.doi.org/10.1139/y90-093.
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Recent evidence has suggested that transport of nutrients from the lumen to the interior of the gastrointestinal epithelium and exit of nutrients from the enterocyte to the circulation is governed by physicochemical properties of brush border and basolateral membranes, respectively. The main determinants of membrane properties are phospholipid, cholesterol, and fatty acyl chain composition (chain length and degree of unsaturation). Lipid synthesis occurs in enterocyte microsomes and the fine tuning of lipid composition is done at other subcellular sites by deacylation–reacylation or by changing the polar head group (e.g., by phosphatidylethanolamine methyltransferase). The present paper will focus on the mechanisms by which enterocyte membranes adapt functional properties in response to external stimuli. It is proposed that under the influence of internal or external stress, the enzymes of lipid metabolism in microsomes are modulated. These changes in lipid synthesis are reflected in other subcellular membranes, changing their physicochemical status and thus transport phenomena. One of the initial events appears to be alteration in desaturase enzyme activity. Our results suggest that desaturase activity and the fatty acyl profiles of the intestinal mucosal phospholipid rapidly respond to physiological conditions such as fasting and dietary fat treatment.Key words: polyunsaturated fatty acids, desaturases, enterocyte, intestinal microsomes, adaptation.