胰腺α细胞功能障碍发病机制的分子途径。
Molecular pathways underlying the pathogenesis of pancreatic alpha-cell dysfunction.
机构信息
Department of Cellular and Molecular Physiology, Joslin Diabetes Center, and Department of Medicine, Harvard Medical School, Boston, MA, USA.
出版信息
Adv Exp Med Biol. 2010;654:421-45. doi: 10.1007/978-90-481-3271-3_18.
Glucagon plays a critical role in glucose homeostasis by counteracting insulin action, especially during hypoglycemia. Glucagon secretion from pancreatic alpha-cells is regulated by various mechanisms including glycemia, neural input, and secretion from neighboring beta-cells. However, glucagon secretion is dysregulated in diabetic states, causing exacerbation of glycemic disorders. Recently, new therapeutic approaches targeting excess glucagon secretion are being explored for use in diabetes treatment. Therefore, understanding the molecular mechanism of how glucagon secretion is regulated is critical for treating the alpha-cell dysfunction observed in diabetes.
胰高血糖素通过拮抗胰岛素作用在葡萄糖稳态中发挥关键作用，尤其在低血糖期间。胰腺α细胞的胰高血糖素分泌受多种机制调节，包括血糖、神经输入和邻近β细胞的分泌。然而，在糖尿病状态下，胰高血糖素分泌失调，导致血糖紊乱加剧。最近，正在探索针对胰高血糖素分泌过多的新治疗方法，用于糖尿病治疗。因此，了解调节胰高血糖素分泌的分子机制对于治疗糖尿病中观察到的α细胞功能障碍至关重要。
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