作者: A Khan , S Narangoda , B Ahren , C Holm , F Sundler
关键词: Leptin 、 Insulin 、 Glucose 6-phosphatase 、 Hormone-sensitive lipase 、 Radioimmunoassay 、 Endocrinology 、 Pancreatic hormone 、 Internal medicine 、 Chemistry 、 Triglyceride 、 Islet
摘要: OBJECTIVE: Previous studies have demonstrated that leptin inhibits glucose-stimulated insulin secretion from isolated islets, although a lack of effect on has also been reported. The long term in vivo treatment has, however, not established. Therefore, the present study, we evaluated glucose-induced ob/ob mice. METHODS: After 7 days' (100 microg daily s.c.), release was measured islets by batch incubation followed radioimmunoassay. Glucose utilization and oxidation were measuring formation (3)H(2)O (14)CO(2) [5-(3)H] [U-(14)C] glucose, respectively. Glucose-6-phosphatase activity conversion (14)C-glucose-6-P to (14)C-glucose. In addition, immunohistochemistry pancreatic specimens undertaken for study expression insulin, GLUT-2 hormone-sensitive lipase (HSL). RESULTS: Leptin significantly improved both at 5.5 mM (by 15%; P<0.05) 16.7 85%; P<0.001) compared vehicle-treated controls. Furthermore, whereas did affect islet or DNA contents, significant decrease triglyceride content glucose-6-phosphatase observed. Moreover, immunocytochemical data revealed an increased immunostaining (HSL) leptin-treated CONCLUSION: results suggest long-term mice improves parallel with reduced activity, HSL decreased levels islets. These perturbations may explain improvement induced leptin. (Less)