Mechanistic insights into pancreatic beta-cell mass regulation by glucose and free fatty acids

被引:36
作者
Oh, Yoon Sin [1 ,2 ]
机构
[1] Gachon Univ, Lee Gil Ya Canc & Diabet Inst, 191 Hambangmoe Ro, Incheon 406799, South Korea
[2] Gil Hosp, Gachon Med Res Inst, Incheon, South Korea
基金
新加坡国家研究基金会;
关键词
Glucose; Free fatty acids; Beta-cell mass regulation; Proliferation; Apoptosis;
D O I
10.5115/acb.2015.48.1.16
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 ;
摘要
Pancreatic islets are responsible for blood glucose homeostasis. Reduced numbers of functional (insulin-secreting) beta-cells in pancreatic islets underlies diabetes. Restoration of the secretion of the proper amount of insulin is a goal. Beta-cell mass is increased by neogenesis, proliferation and cell hypertrophy, and is decreased by beta-cell death primarily through apoptosis. Many hormones and nutrients affect beta-cell mass, and glucose and free fatty acid are thought to be the most important determinants of beta-cell equilibrium. A number of molecular pathways have been implicated in beta-cell mass regulation and have been studied. This review will focus on the role of the principle metabolites, glucose and free fatty acid, and the downstream signaling pathways regulating beta-cell mass by these metabolites.
引用
收藏
页码:16 / 24
页数:9
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