CAJ | 학술논문

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β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,有单成为治疗糖尿病的潜在策略.
K세포작위일충장도내분비세포,령산분포우위장도,종십이지장지직장체감,분비포도당의뢰성촉이도소다태(GIP).통과대STC-1세포계급형광표기K세포적전기인소서적연구,삼대영양물질조공GIP분비적궤제이축보명료.비반상태존재K세포수량급GIP함량적증가,이2형당뇨병칙존재이도β세포적GIP저항.감소K세포증생혹강저GIP분비가능시일충신적감비조시.이용환자자신K세포,중신회복내원성진찬자격적이도소분비,유단성위치료당뇨병적잠재책략.
As a kind of intestinal endocrine cells,K cells scatter in the gastrointestinal tract,decreasing from the duodenum to the rectum,and secreting glucose-dependent insulinotropic polypeptide (GIP).Through the studies of STC-1 cell lines and fluorescently 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.