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首页> 外文期刊>Cellular Physiology and Biochemistry >GLP-1/GLP-1R Signaling in Regulation of Adipocyte Differentiation and Lipogenesis
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GLP-1/GLP-1R Signaling in Regulation of Adipocyte Differentiation and Lipogenesis

机译：GLP-1 / GLP-1R信号调节脂肪细胞分化和脂肪生成

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>Background/Aims: The aim of this study was to determine the direct role of liraglutide (LG) in adipogenesis and lipid metabolism. Methods: Lipid accumulation was evaluated by oil red O staining, quantitative real-time PCR (qPCR) was performed to determine glucagon-like peptide 1 receptor (GLP-1R), fatty acid synthase (FASN) and adipose triglyceride lipase (ATGL) expression in 3T3-L1 preadipocytes, differentiated adipocytes and in adipose tissues from mice. The effects of LG on 3T3-L1 adipogenesis and lipid metabolism were analyzed with qPCR, Western Blotting, oil red O staining, immunohistochemistry (IHC) and immunofluorescence (IF). All measurements were performed at least three times. Results: LG increased the expression of differentiation marker genes and lipid accumulation during preadipocyte differentiation. In differentiated adipocytes, LG decreased FASN expression, and simultaneously led to CREB phosphorylation and ERK1/2 activation which were abolished by a GLP-1R antagonist, exendin (9-39). LG induced-FASN down-regulation was partially reversed by PKA and ERK1/2 inhibitors. Consistent with above in vitro findings, LG treatment significantly reduced FASN expression in visceral adipose tissues of ob/ob mice, and reduced body weight gain. Conclusion: LG promotes preadipocytes differentiation, and inhibits FASN expression in adipocytes. LG induced down-regulation of FASN is at least partially mediated by PKA and MAPK signaling pathways.
机译：> 背景/目的： 这项研究的目的是确定利拉鲁肽（LG）在脂肪形成和脂质代谢中的直接作用。 方法： 通过油红O染色评估脂质积累，进行实时定量PCR（qPCR）来测定胰高血糖素样肽1受体（GLP-1R），小鼠中3T3-L1脂肪细胞，分化的脂肪细胞和脂肪组织中的脂肪酸合酶（FASN）和脂肪甘油三酸酯脂肪酶（ATGL）的表达。通过qPCR，蛋白质印迹，油红O染色，免疫组化（IHC）和免疫荧光（IF）分析了LG对3T3-L1脂肪形成和脂质代谢的影响。所有测量至少进行了三次。 结果： LG增加了前脂肪细胞分化过程中分化标志物基因的表达和脂质积累。在分化的脂肪细胞中，LG降低FASN表达，并同时导致CREB磷酸化和ERK1 / 2活化，这被GLP-1R拮抗剂exendin消除（9-39）。 LG诱导的FASN下调被PKA和ERK1 / 2抑制剂部分逆转。与上述体外结果一致，LG治疗显着降低了 ob / ob 小鼠内脏脂肪组织中FASN的表达，并降低了体重增加。 结论： LG促进脂肪细胞的分化，并抑制脂肪细胞中FASN的表达。 LG诱导的FASN下调至少部分由PKA和MAPK信号通路介导。

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