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饮食诱导的肥胖会调节小鼠脂肪组织中的甘丙肽介导的信号级联。

Diet-induced obesity regulates the galanin-mediated signaling cascade in the adipose tissue of mice.

机构信息

Department of Food and Nutrition, Brain Korea 21 Project, Yonsei University, Seoul, South Korea.

出版信息

Mol Nutr Food Res. 2010 Sep;54(9):1361-70. doi: 10.1002/mnfr.200900317.

Abstract

Galanin is a neuropeptide that regulates the food intake, neurogenesis, memory, and gut secretion. This study was conducted to evaluate the high-fat diet (HFD)-induced regulation of the galanin receptors (GalRs) and the associated signaling molecules in the adipose tissues of mice. Twenty C57BL/6J mice were given either an HFD or a normal diet for 12 wk. The results of the semiquantitative RT-PCR analyses indicated that the HFD upregulated the expression of GalR1, GalR2, GalR3, resistance to audiogenic seizures, peroxisome proliferator-activated receptorgamma2, adipocyte protein 2, and protein kinase Cdelta and downregulated the expression of peroxisome proliferative activated receptor gamma coactivator 1alpha and uncoupling protein 1 in the adipose tissues. The immunoblot results showed that the protein levels of peroxisome proliferator-activated receptorgamma2 and adipocyte protein 2, and the phosphorylation of c-Raf and extracellular signal-regulated kinase 1/2 were increased, while the phosphorylation of cyclic adenosine monophosphate-responsive element-binding protein, which regulates peroxisome proliferative activated receptor gamma coactivator 1alpha and uncoupling protein 1, was decreased in the epididymal adipose tissues of the HFD-fed mice. These results suggest the possible association of the galanin-mediated signaling pathways in the manifestation of the HFD-induced activation of adipogenesis along with the suppression of thermogenesis in the adipose tissues of mice.

摘要

甘丙肽是一种神经肽,可调节摄食、神经发生、记忆和肠道分泌。本研究旨在评估高脂肪饮食(HFD)对小鼠脂肪组织中甘丙肽受体(GalRs)及相关信号分子的调节作用。将 20 只 C57BL/6J 小鼠分为 HFD 组和正常饮食组,分别喂养 12 周。半定量 RT-PCR 分析结果显示,HFD 可上调 GalR1、GalR2、GalR3、抗听觉惊厥、过氧化物酶体增殖物激活受体γ2、脂肪细胞蛋白 2 和蛋白激酶 Cδ的表达,下调过氧化物酶体增殖物激活受体γ共激活物 1α和解偶联蛋白 1 的表达。免疫印迹结果显示,HFD 喂养小鼠附睾脂肪组织中过氧化物酶体增殖物激活受体γ2 和脂肪细胞蛋白 2 的蛋白水平增加,c-Raf 和细胞外信号调节激酶 1/2 的磷酸化增加,而调节过氧化物酶体增殖物激活受体γ共激活物 1α和解偶联蛋白 1 的环磷酸腺苷反应元件结合蛋白的磷酸化减少。这些结果提示,甘丙肽介导的信号通路可能与 HFD 诱导的脂肪生成激活以及脂肪组织产热抑制有关。

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