棕榈酸诱导胰岛β细胞功能障碍的分子机制研究进展

Research progress of molecular mechanism of palmitic acid-induced pancreatic β-cell dysfunction

摘要:

2型糖尿病（type 2 diabetes mellitus，T2DM）在临床上是以存在绝对或相对的胰岛素缺乏为特点的一种常见的代谢性疾病。胰岛β细胞是胰岛素分泌和血糖控制的核心。近年来研究发现，棕榈酸可直接或间接诱导胰岛β细胞功能障碍，这与T2DM的发生发展关系密切。但具体机制复杂，仍未充分阐明。因此，探究棕榈酸诱导胰岛β细胞功能障碍的分子机制一直是临床的迫切需要。本文综述了棕榈酸与胰岛β细胞内氧化应激、内质网应激、炎症反应、自噬、增殖、去分化和线粒体相关内质网膜相关分子机制的研究进展，并讨论临床改善胰岛β细胞功能的新靶点和新思路，以期为进一步有关T2DM的机制研究和临床治疗提供参考。

Abstract:

Type 2 diabetes mellitus（T2DM） is a common metabolic disease characterized by absolute or relative insulin deficiency clinically. Pancreatic β-cells are the core of insulin secretion and blood glucose control. In recent years，researches have found that palmitic acid can directly or indirectly induce pancreatic β-cell dysfunction，which is closely related to the occurrence and development of T2DM. However，the specific mechanisms are complex and have not been fully elucidated. Therefore，exploring the molecular mechanism of pancreatic β-cell dysfunction induced by palmitic acid has always been an urgent need in clinical research. This article reviews the research progress of the relationship between palmitic acid and pancreatic β-cells on molecular mechanisms related to oxidative stress，endoplasmic reticulum stress，inflammatory response，autophagy，proliferation，dedifferentiation，and mitochondria-associated endoplasmic reticulum membranes，and discusses new targets and ideas for improving pancreatic β-cell function clinically，in order to provide references for further researches on the mechanism and clinical treatment of T2DM.