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Arginine-vasopressin directly promotes a thermogenic and pro-inflammatory adipokine expression profile in brown adipocytes

机译:精氨酸加压素直接促进棕色脂肪细胞中的产热和促炎性脂肪因子表达谱

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摘要

Arginine-vasopressin (AVP) - via activation of the hypothalamic-pituitary-adrenal (HPA) - axis may play a role in the regulation of energy homeostasis and related cardiovascular complications. Brown adipose tissue (BAT) - via dissipation of energy in the form of heat - contributes to whole body energy balance. BAT expresses vasopressin receptors. We investigated direct effects of AVP on brown adipose endocrine and metabolic functions. UCP-1 protein expression in differentiated brown adipocytes was induced after acute exposure of adipocytes to AVP. This effect was time-dependent with a maximum increase after 8 h. AVP also induced a time-and dose-dependent increase in p38 MAP kinase phosphorylation. Pharmacological inhibition of p38 MAP kinase with SB 202190 abolished the induction of UCP-1 protein expression. Furthermore, while acute AVP treatment enhanced mRNA expression of MCP-1 and IL-6, adiponectin mRNA expression was reduced. Yet, on the level of intracellular glucose uptake, there was no AVP-induced change of adipose insulin-induced glucose uptake. Finally, there was no difference in lipid accumulation between control and AVP-treated cells.
机译:精氨酸加压素(AVP)-通过激活下丘脑-垂体-肾上腺(HPA)-轴可能在调节能量稳态和相关的心血管并发症中起作用。褐色脂肪组织(BAT)-通过以热能的形式耗散能量-有助于全身能量平衡。 BAT表达血管加压素受体。我们调查了AVP对棕色脂肪内分泌和代谢功能的直接影响。将脂肪细胞急性暴露于AVP后,诱导分化的棕色脂肪细胞中的UCP-1蛋白表达。这种作用是时间依赖性的,在8小时后最大增加。 AVP还引起p38 MAP激酶磷酸化的时间和剂量依赖性增加。用SB 202190抑制p38 MAP激酶的药理作用消除了对UCP-1蛋白表达的诱导。此外,尽管急性AVP处理可增强MCP-1和IL-6的mRNA表达,但脂联素mRNA的表达却降低。然而,就细胞内葡萄糖摄取的水平而言,没有AVP诱导的脂肪胰岛素诱导的葡萄糖摄取变化。最后,对照组和经AVP处理的细胞之间的脂质蓄积没有差异。

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