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前列腺素作为脂肪生成中的 PPARγ 调节剂。

Prostaglandins as PPARγ Modulators in Adipogenesis.

机构信息

Laboratory of Biodefense and Regulation, Osaka University of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki, Osaka 569-1094, Japan.

出版信息

PPAR Res. 2012;2012:527607. doi: 10.1155/2012/527607. Epub 2012 Dec 25.

DOI:10.1155/2012/527607
PMID:23319937
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3540890/
Abstract

Adipocytes and fat cells play critical roles in the regulation of energy homeostasis. Adipogenesis (adipocyte differentiation) is regulated via a complex process including coordinated changes in hormone sensitivity and gene expression. PPARγ is a ligand-dependent transcription factor and important in adipogenesis, as it enhances the expression of numerous adipogenic and lipogenic genes in adipocytes. Prostaglandins (PGs), which are lipid mediators, are associated with the regulation of PPARγ function in adipocytes. Prostacyclin promotes the differentiation of adipocyte-precursor cells to adipose cells via activation of the expression of C/EBPβ and δ. These proteins are important transcription factors in the activation of the early phase of adipogenesis, and they activate the expression of PPARγ, which event precedes the maturation of adipocytes. PGE(2) and PGF(2α) strongly suppress the early phase of adipocyte differentiation by enhancing their own production via receptor-mediated elevation of the expression of cycloxygenase-2, and they also suppress the function of PPARγ. In contrast, PGD(2) and its non-enzymatic metabolite, Δ(12)-PGJ(2), activate the middle-late phase of adipocyte differentiation through both DP2 receptors and PPARγ. This paper focuses on potential roles of PGs as PPARγ modulators in adipogenesis and regulators of obesity.

摘要

脂肪细胞在能量稳态的调节中起着关键作用。脂肪生成(脂肪细胞分化)受一个复杂的过程调控,包括激素敏感性和基因表达的协调变化。PPARγ 是一个配体依赖性转录因子,在脂肪生成中很重要,因为它增强了脂肪细胞中许多脂肪生成和脂肪形成基因的表达。前列腺素(PGs)是脂质介质,与脂肪细胞中 PPARγ 功能的调节有关。前列环素通过激活 C/EBPβ 和 δ 的表达来促进脂肪前体细胞向脂肪细胞的分化。这些蛋白质是脂肪生成早期阶段激活的重要转录因子,它们激活 PPARγ 的表达,这一事件先于脂肪细胞的成熟。PGE(2)和 PGF(2α)通过受体介导的环氧化酶-2 表达升高来增强自身的产生,强烈抑制脂肪细胞分化的早期阶段,它们还抑制 PPARγ 的功能。相比之下,PGD(2)及其非酶代谢物 Δ(12)-PGJ(2)通过 DP2 受体和 PPARγ 激活脂肪细胞分化的中晚期阶段。本文重点介绍 PG 作为 PPARγ 调节剂在脂肪生成中的潜在作用,以及肥胖的调节剂。

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Depressed levels of prostaglandin F2α in mice lacking Akr1b7 increase basal adiposity and predispose to diet-induced obesity.缺乏 Akr1b7 的小鼠中前列腺素 F2α 水平降低会增加基础肥胖,并易患饮食诱导的肥胖。
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Prostaglandin F2α Affects the Cycle of Clock Gene Expression and Mouse Behavior.前列腺素 F2α 影响生物钟基因表达和小鼠行为的周期。
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Very long-chain-fatty acids enhance adipogenesis through coregulation of Elovl3 and PPARγ in 3T3-L1 cells.超长链脂肪酸通过调控 3T3-L1 细胞中 Elovl3 和 PPARγ 共同促进脂肪生成。
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