Diabetes ：男性雄性激素含量低或可增糖尿病风险

近日，英国爱丁堡大学研究人员在新一期《糖尿病》（Diabetes）杂志上报告说，雄性激素含量低的男性患糖尿病的风险可能会较高，因为动物实验显示，雄性激素功能受抑制会引发胰岛素耐受，而胰岛素功能是否正常在糖尿病中起着关键作用。

研究者对一些实验鼠进行了处理，使雄性激素难以发挥作用，结果它们很快就表现出了胰岛素耐受症状。胰岛素可以促进身体分解吸收血液中的糖分，胰岛素耐受就是它难以发挥正常功能，是许多人患上糖尿病的原因。

研究人员因此认为，男性体内雄性激素含量低可能是导致糖尿病的风险因素。进行这一研究的克里·麦金尼斯说，人们通常知道肥胖是引起糖尿病的重要原因，但从本次研究结果看，无论体重多少，雄性激素含量低都会导致糖尿病风险上升。

本次研究还发现，在那些因雄性激素功能受抑制而出现胰岛素耐受症状的实验鼠中，一种名为RBP4的蛋白质含量增高，研究人员认为如果能抑制这种蛋白质，也许可以降低糖尿病风险。研究人员接下来就计划对一些人类糖尿病患者进行检查，仔细分析这种蛋白质在上述发病过程中所起的作用。（生物谷Bioon.com）

doi:10.2337/db11-1136
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Deletion of the Androgen Receptor in Adipose Tissue in Male Mice Elevates Retinol Binding Protein 4 and Reveals Independent Effects on Visceral Fat Mass and on Glucose Homeostasis

Kerry J. McInnes1?, Lee B. Smith2, Nicole I. Hunger1, Philippa T.K. Saunders2, Ruth Andrew1 and Brian R. Walker1

Testosterone deficiency is epidemic in obese ageing males with type 2 diabetes, but the direction of causality remains unclear. Testosterone-deficient males and global androgen receptor (AR) knockout mice are insulin resistant with increased fat, but it is unclear whether AR signaling in adipose tissue mediates body fat redistribution and alters glucose homoeostasis. To investigate this, mice with selective knockdown of AR in adipocytes (fARKO) were generated. Male fARKO mice on normal diet had reduced perigonadal fat but were hyperinsulinemic and by age 12 months, were insulin deficient in the absence of obesity. On high-fat diet, fARKO mice had impaired compensatory insulin secretion and hyperglycemia, with increased susceptibility to visceral obesity. Adipokine screening in fARKO mice revealed a selective increase in plasma and intra-adipose retinol binding protein 4 (RBP4) that preceded obesity. AR activation in murine 3T3 adipocytes downregulated RBP4 mRNA. We conclude that AR signaling in adipocytes not only protects against high-fat diet–induced visceral obesity but also regulates insulin action and glucose homeostasis, independently of adiposity. Androgen deficiency in adipocytes in mice resembles human type 2 diabetes, with early insulin resistance and evolving insulin deficiency.