Research Article Open Access

Adiponectin Regulation in Type 2 Diabetic Rats: Effects of Insulin, Metformin and Dexamethasone

Tamer Ahmed Ismail1, Mohamed Mohamed Soliman2 and Shimaa Ahmed Ismail3
  • 1 Turabah, Taif University, Saudi Arabia
  • 2 Benha University, Egypt
  • 3 Zagazig University, Egypt
American Journal of Pharmacology and Toxicology
Volume 8 No. 4, 2013, 197-208

DOI: https://doi.org/10.3844/ajptsp.2013.197.208

Submitted On: 12 November 2013
Published On: 23 November 2013

How to Cite: Ismail, T. A., Soliman, M. M. & Ismail, S. A. (2013). Adiponectin Regulation in Type 2 Diabetic Rats: Effects of Insulin, Metformin and Dexamethasone. American Journal of Pharmacology and Toxicology, 8(4), 197-208. https://doi.org/10.3844/ajptsp.2013.197.208

Abstract

Adiponectin is a protein synthesized from adipose tissue, increases peripheral glucose utilization in liver and skeletal muscle. Adiponectin expression and secretion are decreased during obesity and insulin resistance. In this study, the effect of insulin, metformin and dexamethasone on serum lipid profiles was examined in Type 2 Diabetic (T2D) rats. T2D was induced by feeding rats a high fat diet for 4 weeks plus medium dose of Streptozotocin (STZ, 35 mk kg-1 BW). Adiponectin, adiponectin receptors (AdipoR-1 and AdipoR-2), leptin, Peroxisome Prolifrator Activated Receptor gamma (PPAR-γ), Hormone Sensitive Lipase (HSL), Pyruvate Kinase (PK), enolase and Glucose Trasporter-2 (GLUT-2) expression in epididymal adipose and liver tissue were examined using RT-PCR. Results showed that metformin improved insulin resistance by normalizing serum lipid profiles in diabetic rats, while dexamethasone did not alter it. Metformin up-regulated adiponectin, AdipoR-1 and AdipoR-2 expression, while insulin and dexamethasone down-regulated them. Leptin expression was decreased while PPARγ, HSL, PK, enolase and GLUT-2 expression was increased by metformin administration. Dexamethasone failed to improve insulin resistance in T2D rats. In conclusion, metformin ameliorates T2D through controlling adiponectin expression and its consequent genes of lipids and glucose metabolism.

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Keywords

  • Adiponectin Regulation
  • Diabetes
  • Metformin
  • Insulin
  • Glucose and Lipid Metabolism