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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >A family of Acrp30/adiponectin structural and functional paralogs.
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A family of Acrp30/adiponectin structural and functional paralogs.

机译：Acrp30 /脂联素家族的结构和功能旁系同源物。

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摘要

Biochemical, genetic, and animal studies in recent years have established a critical role for the adipokine Acrp30/adiponectin in controlling whole-body metabolism, particularly by enhancing insulin sensitivity in muscle and liver, and by increasing fatty acid oxidation in muscle. We describe a widely expressed and highly conserved family of adiponectin paralogs designated as C1q/tumor necrosis factor-alpha-related proteins (CTRPs) 1-7. In the present study, we focus on mCTRP2, the mouse paralog most similar to adiponectin. At nanomolar concentrations, bacterially produced mCTRP2 rapidly induced phosphorylation of AMP-activated protein kinase, acetyl-CoA carboxylase, and mitogen-activated protein kinase in C2C12 myotubes, which resulted in increased glycogen accumulation and fatty acid oxidation. The discovery of a family of adiponectin paralogs has implications for understanding the control of energy homeostasis and could provide new targets for pharmacologic intervention in metabolic diseases such asdiabetes and obesity.
机译：近年来，生化，遗传和动物研究已对脂肪因子Acrp30 /脂联素在控制全身代谢中发挥了关键作用，特别是通过增强肌肉和肝脏中的胰岛素敏感性以及增加肌肉中的脂肪酸氧化作用。我们描述了广泛表达和高度保守的脂联素旁系同源家族，称为C1q /肿瘤坏死因子-α相关蛋白（CTRPs）1-7。在本研究中，我们集中于mCTRP2，这是与脂联素最相似的小鼠旁系同源物。在纳摩尔浓度下，细菌产生的mCTRP2在C2C12肌管中快速诱导AMP激活的蛋白激酶，乙酰辅酶A羧化酶和促分裂原激活的蛋白激酶的磷酸化，从而导致糖原积累和脂肪酸氧化增加。脂联素旁系同源物家族的发现对于理解能量稳态的控制具有启示意义，并且可以为对诸如糖尿病和肥胖症的代谢性疾病进行药物干预提供新的目标。

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