Islet β -cell regeneration.docVIP

 PAGE \* MERGEFORMAT 13 Islet β -cell regeneration Keywords: insulin (INS) gene diabetic islet β -cell regeneration Body sugar balance is achieved primarily by the insulin (INS) control of pancreatic β cells can regulate the release of INS postprandial blood glucose, but also through the growth of β -cell to adapt to long-term INS needs, if any one link happened barrier, causing a lack of an absolute or relative INS may lead to diabetes. Related to the biological synthesis and release of INS regulation has carried out extensive research, but for β -cell regeneration studies to side in recent years, attention. Non-INS-dependent diabetes mellitus (NIDDM) pathogenesis is not very clear. But there is evidence that: response to glucose stimulation of INS secretion and β cell growth to reduce this disease 〔 1〕 easy enough, while the elderly persons have a low regenerative capacity of pancreatic islets, may be related to the high prevalence of diabetes. Type Ⅰ diabetes is caused by autoimmune β -cell damage, caused by decompensation, the disease often have INS in primary short-term recovery, indicating defects in pancreatic islet cells in the body trying to meet INS requirements. The regulation of β cell growth will help to understand the pathogenesis of diabetes, the treatment of diabetes will also have an important significance. In this paper, the difficulty of β -cell growth, how growth factors regulate issues such as research with a brief overview. 1 β cell growth ability and diabetes C57BL/6J mice were the most commonly used as a research NIDDM animal model of genetic diabetes, the germ-line in 1988 by the United States Duke University, the successful cultivation of a single genetic disease diabetic mice. The rats under normal feeding is not the disease, in high-fat (33%), high simple sugar (38%), low cellulose ( amp;quot;3%) feed induced, after 4 w (starting from 4 weeks to 8 weeks years) disease. It C57BL/KSJ rat islet regenerative capacity of differ