摘要
K细胞作为一种肠道内分泌细胞，零散分布于胃肠道，从十二指肠至直肠递减，分泌葡萄糖依赖性促胰岛素多肽（GIP）。通过对STC-1细胞系及荧光标记K细胞的转基因小鼠的研究，三大营养物质调控GIP分泌的机制已逐步明了。肥胖状态存在K细胞数量及GIP含量的增加，而2型糖尿病则存在胰岛B细胞的GIP抵抗。减少K细胞增生或降低GIP分泌可能是一种新的减肥措施。利用患者自身K细胞，重新恢复内源性进餐刺激的胰岛素分泌，有望成为治疗糖尿病的潜在策略。
As a kind of intestinal endocrine cells, K cells scatter in the gastrointestinal tract, decrea-sing from the duodenum to the rectum, and secreting glucose-dependent insulinotropic polypeptide （ GIP ）. Through the studies of STC-1 cell lines and fluoreseently labeled K cells of transgenic mice, the mechanism of the three major nutrients in the regulation of GIP secretion has gradually been revealed. The density of K cells and GIP content increase under obesity, and GIP resistance in islet β cell exists in type 2 diabetes. Preventing K cells hyperplasia or reducing GIP production may be a new therapeutic option to treat obesity. Utilizing a patient＇s own K cells to reestablish endogenous meal-regulated insulin secretion represents a potential strategy to treat diabetes.
出处
《国际内分泌代谢杂志》
北大核心
2012年第4期251-254,共4页
International Journal of Endocrinology and Metabolism
基金
国家自然科学基金资助项目（81070621/H0704）
江苏省医学重点人才项目（RC2011068）
关键词
K细胞
葡萄糖依赖性促胰岛素多肽
肥胖
糖尿病
K cells
Glucose-dependent insulinotropic polypeptide
Obesity
Diabetes mellitus
