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article · Suez Canal Veterinary Medicine Journal SCVMJ

Biochemical Evaluation the Efficacy of Metformin and GLP1 Receptor Agonist Therapy on Glucose Homeostasis in Male Rats Induced Type 2 Diabetes

Abstract

Background: Type 2 diabetes mellitus (T2DM) is a chronic global disease characterized by serious complications. T2DM is associated with disrupted glucose and lipid homeostasis with abnormal insulin sensitivity and/or secretion. Metformin is a first-line treatment for T2DM whose main actions are the suppression of gluconeogenesis and the improvement of glucose uptake and insulin sensitivity. Glucagon-like peptide 1 (GLP1) receptor agonists are promising therapeutic agents in the treatment of diabetes mellitus. Therefore, the current study aimed to assess the effects of metformin and GLP1 against diabetic in rats. Materials and Methods: 35 healthy male rats were used in the study, and type 2 diabetes mellitus were induced by STZ. Diabetic rats were divided randomly into 3 groups, the control diabetic group and 2 treated groups were treated with metformin and dulaglutide. At the end of the experiment, the weight of rats was estimated. After overnight fasting, the serum levels of blood glucose, insulin, lipid profile, and kidney function were measured. Results: Diabetic rats showed a significant increase in body weight, serum blood glucose, insulin, lipid profile, and impaired kidney function. Dulaglutide was superior to metformin and significant in decrease blood glucose level, serum lipid profile, and improved kidney functions. Conclusion: we explored the effect of Metformin and Dulaglutide, glucagon-like peptide-1 (GLP-1) agonist on T2DM. We found that Dulaglutide ameliorate body weight, serum blood glucose, lipid profile. The present study provides a potential mechanism for the protective renal and hepatic effects of a GLP-1 in a rat model of diabetes.

Research topics

  • Diabetes Treatment and Management
  • Apelin-related biomedical research
  • Natural Antidiabetic Agents Studies

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DOI: 10.21608/scvmj.2024.305936.1175

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