作者: Shalea Piteau , Amy Olver , Su-Jin Kim , Kyle Winter , John Andrew Pospisilik
DOI: 10.1016/J.BBRC.2007.08.115
关键词:
摘要: In type 2 diabetes (T2DM) beta-cell responsiveness to glucose-dependent insulinotropic polypeptide (GIP) is reduced. a model of T2DM, the VDF Zucker rat, GIP receptor mRNA and protein levels were shown be down-regulated. Possible restoration in rats by reducing hyperglycemia has been examined. ZDF with extreme demonstrated greater islet down-regulation (94.3+/-3.8%) than ZF (48.8+/-22.8%). returned 83.0+/-17.9% lean following normalization phlorizin treatment pancreas perfusions markedly improved responsiveness. Treatment DP IV inhibitor (P32/98) resulted glucose tolerance restored sensitivity isolated pancreata. These findings support proposal that rodent T2DM secondary chronic glycemia can restore sensitivity.