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脂肪组织中的硫化氢——生理学、病理学及药物治疗靶点

Hydrogen Sulfide in the Adipose Tissue-Physiology, Pathology and a Target for Pharmacotherapy.

作者信息

Bełtowski Jerzy, Jamroz-Wiśniewska Anna

机构信息

Department of Pathophysiology, Medical University, 20-090 Lublin, Poland.

Department of Neurology, Medical University, 20-090 Lublin, Poland.

出版信息

Molecules. 2016 Dec 31;22(1):63. doi: 10.3390/molecules22010063.

DOI:10.3390/molecules22010063
PMID:28042862
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6155731/
Abstract

Hydrogen sulfide (H₂S) is synthesized in the adipose tissue mainly by cystathionine γ-lyase (CSE). Several studies have demonstrated that H₂S is involved in adipogenesis, that is the differentiation of preadipocytes to adipocytes, most likely by inhibiting phosphodiesterases and increasing cyclic AMP concentration. The effect of H₂S on adipose tissue insulin sensitivity and glucose uptake is controversial. Some studies suggest that H₂S inhibits insulin-induced glucose uptake and that excess of H₂S contributes to adipose tissue insulin resistance in metabolic syndrome. In contrast, other studies have demonstrated that H₂S stimulates glucose uptake and its deficiency contributes to insulin resistance. Similarly, the effect of H₂S on adipose tissue lipolysis is controversial. H₂S produced by perivascular adipose tissue decreases vascular tone by activating ATP-sensitive and/or voltage-gated potassium channels in smooth muscle cells. Experimental obesity induced by high calorie diet has a time dependent effect on H₂S in perivascular adipose tissue; short and long-term obesity increase and decrease H₂S production, respectively. Hyperglycemia has been consistently demonstrated to suppress CSE-H₂S pathway in various adipose tissue depots. Finally, H₂S deficiency may contribute to adipose tissue inflammation associated with obesity/metabolic syndrome.

摘要

硫化氢(H₂S)主要由胱硫醚γ-裂解酶(CSE)在脂肪组织中合成。多项研究表明,H₂S参与脂肪生成,即前脂肪细胞向脂肪细胞的分化,最有可能是通过抑制磷酸二酯酶并增加环磷酸腺苷(cAMP)浓度来实现的。H₂S对脂肪组织胰岛素敏感性和葡萄糖摄取的影响存在争议。一些研究表明,H₂S抑制胰岛素诱导的葡萄糖摄取,且H₂S过量会导致代谢综合征中脂肪组织的胰岛素抵抗。相反,其他研究表明,H₂S刺激葡萄糖摄取,其缺乏会导致胰岛素抵抗。同样,H₂S对脂肪组织脂肪分解的影响也存在争议。血管周围脂肪组织产生的H₂S通过激活平滑肌细胞中的ATP敏感性和/或电压门控钾通道来降低血管张力。高热量饮食诱导的实验性肥胖对血管周围脂肪组织中的H₂S有时间依赖性影响;短期和长期肥胖分别增加和减少H₂S的产生。高血糖已被证实会抑制各种脂肪组织库中的CSE-H₂S途径。最后,H₂S缺乏可能导致与肥胖/代谢综合征相关的脂肪组织炎症。

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