Determination of insulin resistance, β-cell function and insulin sensitivity using modified homeostatic model assessment in diabetic rats treated with melatonin

Nwaji, Azubuike Raphael; Bisong, Sunday Agba; Antai, Atim Bassey; Amadi, Chibuzor Stella; Igbinedion, Deborah Esohe; Okafor, Chidiebube Sylvia; Inwang, Uduak Anthony; Uchewa, Obinna Onwe

doi:10.22092/ari.2024.366296.3225

Determination of insulin resistance, β-cell function and insulin sensitivity using modified homeostatic model assessment in diabetic rats treated with melatonin

Articles in Press

Document Type : Original Articles

Authors

¹ Department of Physiology, Faculty of Basic Medical Sciences, Alex Ekwueme Federal University Ndufu-Alike Ebonyi State

² Department of Physiology, Faculty of Basic Medical Sciences, University of Calabar, Calabar-Nigeria

³ Department of Health Sciences and Social Work, Western Illinois University, Illinois, US

⁴ Department of Physiology, Faculty of Basic Medical Sciences, Alex Ekwueme Federal University, Ndufu-Alike, Ebonyi State, Nigeria.

⁵ Department of Anatomy, Faculty of Basic Medical Sciences, Alex Ekwueme Federal University, Ndufu-Alike, Ebonyi State, Nigeria.

10.22092/ari.2024.366296.3225

Abstract

The study aimed to determine insulin resistance, beta cell function and insulin sensitivity of diabetic rats treated with melatonin by employing a structural mathematical/computer model (Homeostatic Model Assessment). Alloxan-fructose-induced type 2 diabetic rat model was created by a single-dose of alloxan (150mg/kg, i.p.) given to 14-days fructose solution (20% w/v) pre-treated (in drinking water) rats. Blood glucose level was assessed three days post induction for hyperglycemia, and rats with fasting blood glucose (FBG) levels greater than 200 mg/dL were considered diabetic. Rats were randomly grouped into four (n=6) and treated as control, melatonin, diabetic untreated and diabetic treated groups respectively. Melatonin (10mg/kg, p.o.) was administered daily for 15 days following diabetic induction. Treatment of diabetic rats with melatonin significantly (P< 0.05) reduced the FBG, C-peptide and insulin resistance with increased insulin sensitivity level when compared with diabetic untreated rats. However, no changes were observed in the insulin and HOMA-%B groups. As evidenced from the positive improvements in beta cell function, insulin sensitivity, and decreased insulin resistance; treating type 2 diabetes with a pharmacological dose of melatonin is an important way to boost the body's antioxidant defense system and subsequently improve anti-hyperglycemic conditions by blocking mechanisms that lead to hyperglycemia. These findings suggest that early and intensive treatment of insulin resistance is the best strategy to delay the emergence of long-term complications from type 2 diabetes, slow down the disease's progression, and maybe prevent its onset. The implementation of straightforward and reliable diagnostic techniques, such as the HOMA model, is necessary for the early detection of insulin resistance and beta-cell dysfunction.

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