摘要胰岛β细胞衰老导致的胰岛功能衰退在2型糖尿病的发病机制中起重要作用.衰老的胰岛β细胞复制受限.出现形态及功能改变,即细胞体积增大、小规则,胰岛素分泌模式受损.导致B细胞衰老的机制复杂,包括端粒缩短学说、氧化应激敛DNA损伤学说、致癌基因表达上调学说等.新近研究发现,β-半乳糖苷酶活性增加、p16 1NK4a表达上调及衰老相关的异染色质位点(SAHF)等可作为胰岛β细胞衰老的非特异性生物学标记物,可能对早期预测胰岛β细胞功能衰退、预防2型糖尿病起重要作用.

abstractsDysfunction of islets caused by beta cell senescence plays an important role in the patho-genesis of type 2 diabetes. Senescence induces replicative arrest,which is accompanied with morphologic and functional changes, such as the enlargement and irregularity of cells and impaired insulin secretion. The mechanism of β cell senescence is very complicated, including series theories such as telomere shortening, impaired DNA by oxidative stress, upregulation of oncogene and so on. Recent researches have found some nonspecific biological markers of senescent beta cells,for example,the increased activity of beta galactosidase (β-Gal) ,upregulation of pl6 1NK4a and senescence-associated heterochromatic foci(SAHF) phenomenon,they may play important roles in predicting the development of islet β cell dysfunction and type 2 diabetes mellitus.