Insulin Secretory Dysfunction as the Underlying Mechanism of Diabetogenesis in Neonatal Streptozotocin-Induced Type 2 Diabetes Model Rats

Indian Journal of Pharmaceutical Education and Research

  • Ramendu Parial1Department of Biochemistry and Molecular Biology, University of Chittagong, Chattogram, BANGLADESH.
  • Manisha Das2EuGEF Research Foundation, Chattogram, BANGLADESH.
  • Masfida Akhter3Hamdard Institute of Traditional Medicine and Natural Product Research, Hamdard University Bangladesh, Munshiganj, BANGLADESH.
  • JMA Hannan4Department of Pharmacy, Independent University, Bangladesh (IUB), Dhaka, BANGLADESH.
  • Dwaipayan Sikdar1Department of Biochemistry and Molecular Biology, University of Chittagong, Chattogram, BANGLADESH.
  • Liaquat Ali5Pothikrit Institute of Health Studies (PIHS), Dhaka, BANGLADESH.

Volume 60 Issue 1s Pages s274-s279

DOI: 10.5530/ijper.20266401

Abstract

Background: Neonatal Streptozotocin (n-STZ) rats are widely used as models for type 2 diabetes mellitus, but the basic defects of diabetes (insulin secretion and resistance) have not yet been adequately characterized in all species of such rats. Materials and Methods: In this study, the basic defects were studied in a group of neonatal streptozotocin-induced type-2 (n-2 STZ) diabetic models of Long Evans rats. The model rats were produced with a single intraperitoneal injection of streptozotocin to 48 hr old pups. Glucose and lipid levels were measured using the standard method. Insulin was measured by ELISA. The intestinal perfusion method was followed to check for the intestinal absorption of glucose. Insulin secretory capacity and resistance were measured using the Homeostasis Model Assessment (HOMA) and Insulin Sensitivity Index (ISI) methods. Results: Type 2 diabetic rats showed significantly higher blood glucose levels at fasting (p<0.001) and at 90 min (p<0.001). Significantly high levels of total cholesterol (p=0.002), triglycerides (p=0.04), and low levels of HDL cholesterol (p=0.04) were observed in diabetic rats compared to control. Glucose absorption in the intestine was found to be significantly higher in almost all the perfusate samples. The diabetic rats had significantly lower serum insulin levels as compared to the control at fasting and at the 90 min period (p<0.001) after oral glucose load. In diabetic rats, insulin secretory capacity (HOMA%B) and ISI composite were notably lower (p<0.001) and insulin sensitivity (HOMA%S) was significantly higher (p<0.001) compared to control. Conclusion: n-2 STZ Long Evans rats showed glycemic and lipidemic abnormalities due to insulin secretory dysfunction which could not be balanced by inadequate compensatory decrease in insulin resistance. Experimental scientists are required to be aware of this basic defect when interpreting their data on such animals.

Keywords

  • Long Evans rats
  • Streptozotocin
  • Insulin secretory dysfunction
  • Insulin resistance
  • Lipids.
IJOPP

Loading…