ObjectiveTo explore the effect of endotoxin on insulin secretion from islet βcell of rat pancreas.MethodsAfter the model of endotoxemia was established in rats with intraperitoneal injection of LPS (2 mg/kg),the changes of insulin level in the serum and pancreas were dynamically determined, the expression of inducible nitric oxide synthase (iNOS) by situ hybridization and DNA damage in islet cells were also observed, the effect of sodium nitroprusside (exogenous NO) on synthesis and secretion of insulin from isolated islet βcell of normal rat pancreas under high glucose stimulation was also evaluated.ResultsThe level of glucose and insulin in plasma were significantly increased at 12th and 6th h, respectively and kept on 3 d after injection of LPS,but the insulin level in pancreas was not remarkably altered.The expression of iNOS and DNA damaged significantly enhanced at 6 d after endotoxemia. The high glucosestimulated insulin synthesis and secretion were bly inhibited by exogenous NO.ConclusionThese findings suggest that LPS be stimulate the expression of iNOS and NO product,which inhibites synthesis and secretion of insulin in islet βcells,but it stimulates insulin secretion by another mechanism,and results in dysfunction and destruction of the rat pancreas.
目的 探讨血尿酸与胰岛素分泌和敏感性的关系。 方法 对成都市龙泉驿区2007年6月－7月间20～75岁常住自然人群565人进行人口学、腰围、臀围、血压、75 g葡萄糖耐量及胰岛素测定（0、30、120 min），血脂、血肌酐及血尿酸检测。以早期胰岛素分泌功能指数（△I30/△G30）和葡萄糖处置指数（DIo）代表胰岛素分泌功能，以Matsuda 指数代表胰岛素敏感性，分别与血尿酸进行相关性研究。 结果 男性的血尿酸与年龄呈负相关，与舒张压、葡萄糖负荷后120 min胰岛素和甘油三酯呈正相关。女性的血尿酸与甘油三酯、低密度脂蛋白、血肌酐呈正相关，与高密度脂蛋白、Matsuda指数呈负相关。无论男性和女性，均未发现血尿酸与△I30/△G30、DIo相关。 结论 女性的胰岛素敏感性下降与血尿酸升高有关。未发现血尿酸与胰岛素分泌有相关关系。
Objective To summarize the relationship of diabetes and its complications with microRNA. Methods Domestic and international researches were collected by searching to summarize the role of microRNA in diabetes and its complications. Results MicroRNA could affect the secretion of insulin and interfer metabolism of gulcose in fat cells， muscle cells， and liver cells， which resulting in insulin resistance. At the same time， the microRNA also played an role in damage of vascular endothelial cells and myocardial cell in diabetes. Conclusion MicroRNA acts an important role in the process of diabetes and its complications.
ObjectiveTo investigate the effects and mechanisms of differentiation of bone marrow mesenchymal stem cells (BMSCs) into insulin producing cells (IPCs) induced by injured pancreatic tissue extract of rat. MethodsEighty 6-week-old Sprague Dawley rats were selected. Forty rats underwent removal of 60% pancreas and the injured pancreas tissue was obtained after 48 hours to prepare the injured pancreatic tissue extract; and normal pancreatic tissue extract was prepared from the other 40 rats. The BMSCs were isolated from the tibia and femur of 4-week-old Sprague Dawley rats. BMSCs at passage 3 were co-cultured with rat injured pancreatic tissue extract as experimental group, with rat normal pancreatic tissue extract as normal control group, and with cell culture medium as blank control group for 14 days. The expressions of pancreas development related genes and proteins were detected, and cell morphological changes were observed. Then the C peptide positive cell rate was detected by flow cytometry analysis and insulin secretion levels were detected by glucose stimulation experiment at 14 days. ResultsInjured pancreatic tissue extract can induced BMSCs differentiating into IPCs. The pancreatic development related genes of pancreatic duodenal homeobox 1 (PDX-1), islet 1, Nkx6.1, glucose transporter type 2, proprotein convertase 2, neurogenin 3, and somatostatin were expressed sequentially in the differentiation process of experimental group; mature pancreatic proteins of PDX-1, insulin, C peptide, Nkx6.1 also were expressed. But there was no morphological changes and expression of pancreatic development related genes and proteins in normal control and blank control groups. The C peptide positive cell rate of experimental group (13.8%±1.8%) were significantly higher than those of normal control and blank control groups (1.6%±0.4%) (P<0.05). The insulin secretion of experimental group was significantly higher than that of normal control and blank control groups (P<0.05), but it was 1/40 and 1/47 of natural islet cells (P<0.05). ConclusionAfter pancreatic injury, injured pancreas would secrete transcription proteins related to development, differentiation, and repair of pancreas, which can promote the differentiation of BMSCs into IPCs.