Hydrogen sulfide from adipose tissue is a novel insulin resistance regulator
Hydrogen sulfide from adipose tissue is a novel insulin resistance regulator
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来自脂肪组织的硫化氢是一种新型的胰岛素抵抗调节剂。
DOI：
10.1016/j.bbrc.2009.01.059
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发表时间：
2009-02-27
影响因子：
3.1
通讯作者：
Geng, Bin
中科院分区：
文献类型：
--
作者：
Feng, Xuejuan;Chen, Yu;Geng, Bin
最近的研究表明，内源性硫化氢（H2S）参与糖尿病的发病机制。在这里，我们发现半胱硫氨酸γ裂解酶（CSE）在大鼠脂肪组织和内源性H2S中表达。CSE/H2S系统存在于大鼠脂肪细胞和前脂肪细胞中。该系统随着年龄的增长而上调，尽管高水平的葡萄糖以浓度和时间依赖的方式调节该系统。H2S抑制了基础和胰岛素刺激的成熟脂肪细胞的葡萄糖摄取，而CSE抑制剂的使用增强了脂肪细胞的葡萄糖摄取。H2S对葡萄糖摄取的抑制作用与PI3K通路有关，而与K-ATP通路无关。最后，在果糖诱导的大鼠糖尿病中，我们证实了脂肪组织中CSE/H2S系统的上调。这与该组织的葡萄糖摄取呈负相关。我们的研究结果表明H2S可能是一种新的胰岛素抵抗调节剂。(C) 2009爱思唯尔公司版权所有。
Recent data suggested that endogenous hydrogen sulfide (H2S) contributes to the pathogenesis of diabetes. Here, we identified that cystathionine gamma lyase (CSE) was expressed in adipose tissue in rats and endogenously generated H2S. The CSE/H2S system exists in both rat adipocytes and pre-adipocytes. This system was up-regulated with aging, although a high level Of glucose clown-regulated the system in a concentration- and time-dependent manner. H2S inhibited the basal and insulin-stimulated glucose uptake Of Mature adipocytes, whereas administration of CSE inhibitors enhanced the glucose uptake of adipocytes. The PI3K but not K-ATP channel pathway is involved in the inhibitory effect of H2S on glucose uptake. Finally, in fructose-induced diabetes in rats, we confirmed the up-regulated CSE/H2S system in adipose tissue. which was negatively correlated With glucose uptake in this tissue. Our findings suggest that H2S might be a novel insulin resistance regulator. (C) 2009 Elsevier Inc. All rights reserved.