Fundamental Toxicological Sciences

Paper Details

Fundamental Toxicological Sciences
Vol. 3 No. 6 December 24, 2016 p.291-296
Original Article
Streptozotocin-induced diabetic state triggers glucose-dependent insulinotropic polypeptide (GIP) expression in the rat liver
  • Yuka Kohda (Laboratory of Pharmacotherapy, Osaka University of Pharmaceutical Sciences /
Yuka Kohda , Chiaki Minamigawa , Mikako Matsuo , Hitoshi Matsumura
Laboratory of Pharmacotherapy, Osaka University of Pharmaceutical Sciences
Keywords: Streptozotocin, Pancreatic β cell toxicity, Hepatic GIP protein, Hypoglycemic action, Diabetes

Streptozotocin (STZ), a toxic glucose analogue for pancreatic β cells, has been demonstrated as a treatment option for insulinoma. Glucose-dependent insulinotropic polypeptide (GIP), an incretin hormone, is secreted by K cells in the duodenum in response to food intake and acts on pancreatic β cells, leading to increased secretion of insulin. We previously reported that GIP gene expression in the liver is modified in a diabetic setting. However, the role of GIP in the liver has not been fully elucidated; we aimed to discover its effects on type 1 diabetes by focusing on GIP protein expression in a type 1 diabetes rat model following STZ administration. In this study, we assessed whether glucose and lipid metabolism affected GIP expression in the liver following STZ-induced diabetes. Diabetes was induced by intraperitoneal injection with 70 mg/kg STZ. We expected that blood glucose levels would be higher because of STZ treatment as a result of reduced insulin secretion in pancreatic β cells. Interestingly, GIP was expressed only in the liver of STZ-treated rats; however, blood glucose levels were not elevated. On the other hand, blood triglyceride and cholesterol levels were higher in STZ-treated rats with hepatic GIP protein expression than in control rats. These findings indicated that GIP protein expression in the liver possibly has hypoglycemic action, which may ameliorate the damage of pancreatic β cells induced by STZ treatment, rather than affect glycolipid metabolism.