Regulation of glucose and lipid homeostasis by adiponectin: effects on hepatocytes, pancreatic β cells and adipocytes.
Regulation of glucose and lipid homeostasis by adiponectin: effects on hepatocytes, pancreatic β cells and adipocytes.
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DOI：
10.1016/j.beem.2013.11.003
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发表时间：
2014-01
期刊：
影响因子：
--
通讯作者：
Holland WL
中科院分区：
文献类型：
--
作者：
Tao C;Sifuentes A;Holland WL
脂联素因其潜在的抗糖尿病作用而受到广泛关注。脂肪因子通过在肝脏、脂肪和胰腺内的关键作用来控制葡萄糖和脂质稳态。通过刺激脂肪生成、对抗炎症以及影响脂质氧化和脂解速率，脂联素关键地控制脂质溢出到非脂肪组织中。神经酰胺是一种细胞毒性和胰岛素脱敏脂质代谢产物，当外周组织暴露于过量脂质沉积时形成，脂联素有效对抗。通过脂联素受体AdipoR 1和AdipoR 2，脂联素刺激产生神经酰胺的鞘氨醇通过鞘氨醇激酶脱酰转化为1-磷酸鞘氨醇（S1 P）。由此产生的从神经酰胺到S1 P的转化促进功能性β细胞群的存活，允许胰岛素产生以满足胰岛素需求。减轻肝脏的神经酰胺负荷可改善肝脏胰岛素作用。在这里，我们总结了脂联素诱导的这些组织中的变化如何导致葡萄糖代谢的改善，突出了脂联素与每个动作之间的鞘脂信号传导机制。
Adiponectin has received considerable attention for its potential anti-diabetic actions. The adipokine exerts control of glucose and lipid homeostasis via critical effects within the liver, adipose, and pancreas. By stimulating adipogenesis, opposing inflammation, and influencing rates of lipid oxidation and lipolysis, adiponectin critically governs lipid spillover into non-adipose tissues. Ceramide, a cytotoxic and insulin desensitizing lipid metabolite formed when peripheral tissues are exposed to excessive lipid deposition, is potently opposed by adiponectin. Via adiponectin receptors, AdipoR1 and AdipoR2, adiponectin stimulates the deacylation of ceramide- yielding sphingosine for conversion to sphingosine 1-phosphate (S1P) by sphingosine kinase. The resulting conversion from ceramide to S1P promotes survival of functional beta cell mass, allowing for insulin production to meet insulin demands. Alleviation of ceramide burden on the liver allows for improvements in hepatic insulin action. Here, we summarize how adiponectin-induced changes in these tissues lead to improvements in glucose metabolism, highlighting the sphingolipid signaling mechanisms linking adiponectin to each action.
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