摘要
脂毒性是导致2型糖尿病胰岛β细胞功能衰竭的重要原因之一。脂毒性可通过多种途径、多种因素促进β细胞的功能障碍和凋亡，如神经酰胺途径、内质网应激等。如何防止或延缓胰岛β细胞功能衰竭，延缓2型糖尿病的发生、发展是重要的任务。目前研究发现，过氧化物酶体增殖物活化受体（PPAR）1激活后会逆转胰岛β细胞的脂毒性，从而对胰岛β细胞发挥保护作用。其机制主要是减少β细胞凋亡、调节脂代谢相关基因的表达或直接调控胰岛素分泌相关因子的表达、拮抗游离脂肪酸引起的炎性反应等。
Lipotoxicity is one of the important reasons of β-cell failure in type 2 diabetes. Lipotoxicity contributes to β-cell dysfunction and apoptosis through a variety of ways and factors, such as eeramide, endoplasmic reticulum stress,etc. How to prevent or delay the β-cell failure, decreasing the occumence or devel- opment of type 2 diabetes, is an important task. The present studies show that the activation of peroxisome proliferator-activated receptor （PPAR）γ would reverse the pancreatic β-cell llpotoxicity, and thus play a protective effect of pancreatic islet β-cell. Its mechanism includes reducing β-cell apoptosis,regulating lipid metabolism-related gene expression or directly controlling the expression of insulin-related factors,resisting the inflammatoly response induced by free fatty acid.
出处
《国际内分泌代谢杂志》
2010年第6期391-394,共4页
International Journal of Endocrinology and Metabolism
