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Fatty acid metabolism

About: Fatty acid metabolism is a research topic. Over the lifetime, 4481 publications have been published within this topic receiving 189094 citations. The topic is also known as: GO:0006631 & fatty acid metabolism.


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Journal ArticleDOI
TL;DR: A current understanding of the effects of PPARs, their molecular mechanisms and the role of these receptors in nutrition and therapeutic treatment are delineated in this paper.
Abstract: Peroxisome proliferator-activated receptors are expressed in many tissues, including adipocytes, hepatocytes, muscles and endothelial cells; however, the affinity depends on the isoform of PPAR, and different distribution and expression profiles, which ultimately lead to different clinical outcomes. Because they play an important role in lipid and glucose homeostasis, they are called lipid and insulin sensors. Their actions are limited to specific tissue types and thus, reveal a characteristic influence on target cells. PPARα mainly influences fatty acid metabolism and its activation lowers lipid levels, while PPARγ is mostly involved in the regulation of the adipogenesis, energy balance, and lipid biosynthesis. PPARβ/δ participates in fatty acid oxidation, mostly in skeletal and cardiac muscles, but it also regulates blood glucose and cholesterol levels. Many natural and synthetic ligands influence the expression of these receptors. Synthetic ligands are widely used in the treatment of dyslipidemia (e.g. fibrates - PPARα activators) or in diabetes mellitus (e.g. thiazolidinediones - PPARγ agonists). New generation drugs - PPARα/γ dual agonists - reveal hypolipemic, hypotensive, antiatherogenic, anti-inflammatory and anticoagulant action while the overexpression of PPARβ/δ prevents the development of obesity and reduces lipid accumulation in cardiac cells, even during a high-fat diet. Precise data on the expression and function of natural PPAR agonists on glucose and lipid metabolism are still missing, mostly because the same ligand influences several receptors and a number of reports have provided conflicting results. To date, we know that PPARs have the capability to accommodate and bind a variety of natural and synthetic lipophilic acids, such as essential fatty acids, eicosanoids, phytanic acid and palmitoylethanolamide. A current understanding of the effects of PPARs, their molecular mechanisms and the role of these receptors in nutrition and therapeutic treatment are delineated in this paper.

854 citations

Journal ArticleDOI
TL;DR: PPAR gamma is present at low levels in 3T3-L1 preadipocytes and is induced dramatically during adipocyte conversion using either normal differentiating conditions or the PPAR activator, WY-14,643.
Abstract: Activators of peroxisome proliferator activated receptor (PPAR) regulate fatty acid metabolism and can induce adipocyte differentiation. We show here that the gamma subtype of PPAR is expressed at high levels in adipose tissue in contrast to a variety of other tissues, where little gene expression was noted. In addition, PPAR gamma is present at low levels in 3T3-L1 preadipocytes and is induced dramatically during adipocyte conversion using either normal differentiating conditions (fetal calf serum, dexamethasone, isobutyl-methylxanthine, and insulin) or the PPAR activator, WY-14,643. Thus PPAR gamma may be important for adipose cell development and function.

846 citations

Journal ArticleDOI
TL;DR: PPARα modulates constitutive expression of genes encoding several mitochondrial fatty acid-catabolizing enzymes in addition to mediating inducible mitochondrial and peroxisomal fatty acid β-oxidation, thus establishing a role for the receptor in fatty acid homeostasis.

838 citations

Journal ArticleDOI
TL;DR: Evidence for a functional role for CD36 in lipoprotein/fatty acid metabolism that was previously underappreciated is provided.

774 citations

Journal ArticleDOI
TL;DR: It is concluded that Cd36 deficiency underlies insulin resistance, defective fatty acid metabolism and hypertriglyceridaemia in SHR and may be important in the pathogenesis of human insulin-resistance syndromes.
Abstract: The human insulin-resistance syndromes, type 2 diabetes, obesity, combined hyperlipidaemia and essential hypertension, are complex disorders whose genetic basis is unknown. The spontaneously hypertensive rat (SHR) is insulin resistant and a model of these human syndromes. Quantitative trait loci (QTLs) for SHR defects in glucose and fatty acid metabolism, hypertriglyceridaemia and hypertension map to a single locus on rat chromosome 4. Here we combine use of cDNA microarrays, congenic mapping and radiation hybrid (RH) mapping to identify a defective SHR gene, Cd36 (also known as Fat, as it encodes fatty acid translocase), at the peak of linkage to these QTLs. SHR Cd36 cDNA contains multiple sequence variants, caused by unequal genomic recombination of a duplicated ancestral gene. The encoded protein product is undetectable in SHR adipocyte plasma membrane. Transgenic mice overexpressing Cd36 have reduced blood lipids. We conclude that Cd36 deficiency underlies insulin resistance, defective fatty acid metabolism and hypertriglyceridaemia in SHR and may be important in the pathogenesis of human insulin-resistance syndromes.

750 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023114
2022186
2021238
2020230
2019209
2018179