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Nwaji, Azubuike, Bisong, Sunday, Antai, Atim, Amadi, Chibuzor, Igbinedion, Deborah, Okafor, Chidiebube, Inwang, Uduak, Uchewa, Obinna. (1404). Determination of insulin resistance, β-cell function and insulin sensitivity using modified homeostatic model assessment in diabetic rats treated with melatonin. سامانه مدیریت نشریات علمی, 80(3), 665-673. doi: 10.32592/ARI.2025.80.3.665
Azubuike Raphael Nwaji; Sunday Agba Bisong; Atim Bassey Antai; Chibuzor Stella Amadi; Deborah Esohe Igbinedion; Chidiebube Sylvia Okafor; Uduak Anthony Inwang; Obinna Onwe Uchewa. "Determination of insulin resistance, β-cell function and insulin sensitivity using modified homeostatic model assessment in diabetic rats treated with melatonin". سامانه مدیریت نشریات علمی, 80, 3, 1404, 665-673. doi: 10.32592/ARI.2025.80.3.665
Nwaji, Azubuike, Bisong, Sunday, Antai, Atim, Amadi, Chibuzor, Igbinedion, Deborah, Okafor, Chidiebube, Inwang, Uduak, Uchewa, Obinna. (1404). 'Determination of insulin resistance, β-cell function and insulin sensitivity using modified homeostatic model assessment in diabetic rats treated with melatonin', سامانه مدیریت نشریات علمی, 80(3), pp. 665-673. doi: 10.32592/ARI.2025.80.3.665
Nwaji, Azubuike, Bisong, Sunday, Antai, Atim, Amadi, Chibuzor, Igbinedion, Deborah, Okafor, Chidiebube, Inwang, Uduak, Uchewa, Obinna. Determination of insulin resistance, β-cell function and insulin sensitivity using modified homeostatic model assessment in diabetic rats treated with melatonin. سامانه مدیریت نشریات علمی, 1404; 80(3): 665-673. doi: 10.32592/ARI.2025.80.3.665

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

Archives of Razi Institute
مقاله 15، دوره 80، شماره 3، مرداد و شهریور 2025، صفحه 665-673    اصل مقاله (606.53 K)
نوع مقاله: Original Articles
شناسه دیجیتال (DOI): 10.32592/ARI.2025.80.3.665
نویسندگان
Azubuike Raphael Nwaji* 1؛ Sunday Agba Bisong2؛ Atim Bassey Antai2؛ Chibuzor Stella Amadi3؛ Deborah Esohe Igbinedion4؛ Chidiebube Sylvia Okafor4؛ Uduak Anthony Inwang4؛ Obinna Onwe Uchewa5
1Department of Physiology, Faculty of Basic Medical Sciences, Alex Ekwueme Federal University Ndufu-Alike Ebonyi State
2Department of Physiology, Faculty of Basic Medical Sciences, University of Calabar, Calabar-Nigeria
3Department of Health Sciences and Social Work, Western Illinois University, Illinois, US
4Department of Physiology, Faculty of Basic Medical Sciences, Alex Ekwueme Federal University, Ndufu-Alike, Ebonyi State, Nigeria.
5Department of Anatomy, Faculty of Basic Medical Sciences, Alex Ekwueme Federal University, Ndufu-Alike, Ebonyi State, Nigeria.
چکیده
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.
کلیدواژه‌ها
Type 2 diabetes؛ insulin resistance and sensitivity؛ β-cell functions؛ HOMA؛ melatonin
مراجع
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