Xu Weiwei, Morford Jamie, Mauvais-Jarvis Franck
W Xu, Division of Endocrinology and Metabolism, Tulane University, New Orleans, United States.
J Morford, Division of Endocrinology and Metabolism, Tulane University, New Orleans, United States.
J Endocrinol. 2019 Jan 1. doi: 10.1530/JOE-18-0573.
One of the most sexually dimorphic aspects of metabolic regulation is the bidirectional modulation of glucose homeostasis by testosterone in male and females. Severe testosterone deficiency predisposes men to type 2 diabetes (T2D), while in contrast, androgen excess predisposes women to hyperglycemia. The role of androgen deficiency and excess in promoting visceral obesity and insulin resistance in men and women respectively is well established. However, although it is established that hyperglycemia requires β cell dysfunction to develop, the role of testosterone in β cell function is less understood. This review discusses recent evidence that the androgen receptor (AR) is present in male and female β cells. In males, testosterone action on AR in β cells enhances glucose-stimulated insulin secretion by potentiating the insulinotropic action of glucagon-like peptide-1. In females, excess testosterone action via AR in β cells promotes insulin hypersecretion leading to oxidative injury, which in turn predisposes to T2D.
代谢调节中最具性别差异的方面之一是睾酮对男性和女性葡萄糖稳态的双向调节。严重的睾酮缺乏使男性易患2型糖尿病（T2D），而相反，雄激素过多使女性易患高血糖症。雄激素缺乏和过多分别在促进男性和女性内脏肥胖和胰岛素抵抗方面的作用已得到充分证实。然而，尽管已确定高血糖症的发生需要β细胞功能障碍，但睾酮在β细胞功能中的作用却鲜为人知。本综述讨论了近期的证据，即雄激素受体（AR）存在于男性和女性的β细胞中。在男性中，睾酮作用于β细胞中的AR，通过增强胰高血糖素样肽-1的促胰岛素作用来增强葡萄糖刺激的胰岛素分泌。在女性中，通过β细胞中的AR产生的过量睾酮作用会促进胰岛素分泌过多，导致氧化损伤，进而易患T2D。
