اخبار و اعلانات

 آمار

تعداد نشریات285
تعداد نشریات سازمان83
تعداد شماره‌ها3,084
تعداد مقالات34,405
تعداد مشاهده مقاله48,441,870
تعداد دریافت فایل اصل مقاله79,092,259
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 (607.49 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
  1. Go H-K, Rahman MM, Kim G-B, Na C-S, Song C-H, Kim J-S, et al. Antidiabetic effects of yam (Dioscorea batatas) and its active constituent, allantoin, in a rat model of streptozotocin-induced diabetes. Nutrients. 2015;7(10):8532-44.
  2. Duarte JM. Metabolic alterations associated to brain dysfunction in diabetes. Aging and disease. 2015;6(5):304.
  3. Yapislar H, Haciosmanoglu E, Sarioglu T, Degirmencioglu S, Sogut I, Poteser M, et al. Anti-inflammatory effects of melatonin in rats with induced type 2 diabetes mellitus. Life. 2022;12(4):574.
  4. Watanabe K, Nakano M, Maruyama Y, Hirayama J, Suzuki N, Hattori A. Nocturnal melatonin increases glucose uptake via insulin-independent action in the goldfish brain. Frontiers in Endocrinology. 2023;14:1173113.
  5. Reiter RJ, Mayo JC, Tan DX, Sainz RM, Alatorre‐Jimenez M, Qin L. Melatonin as an antioxidant: under promises but over delivers. Journal of pineal research. 2016;61(3):253-78.
  6. Antuna-Puente B, Disse E, Rabasa-Lhoret R, Laville M, Capeau J, Bastard J-P. How can we measure insulin sensitivity/resistance? Diabetes & metabolism. 2011;37(3):179-88.
  7. Morris AD, Ueda S, Petrie JR, Connell JM, Elliott HL, Donnelly R. The euglycaemic hyperinsulinaemic clamp: an evaluation of current methodology. Clinical and experimental pharmacology and physiology. 1997;24(7):513-8.
  8. Matthews DR, Hosker JP, Rudenski AS, Naylor B, Treacher DF, Turner R. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man. diabetologia. 1985;28:412-9.
  9. Song YS, Hwang Y-C, Ahn H-Y, Park C-Y. Comparison of the usefulness of the updated homeostasis model assessment (HOMA2) with the original HOMA1 in the prediction of type 2 diabetes mellitus in Koreans. Diabetes & metabolism journal. 2016;40(4):318.
  10. Levy JC, Matthews DR, Hermans MP. Correct homeostasis model assessment (HOMA) evaluation uses the computer program. Diabetes care. 1998;21(12):2191.
  11. Wallace TM, Levy JC, Matthews DR. Use and abuse of HOMA modeling. Diabetes care. 2004;27(6):1487-95.
  12. Saisho Y. Postprandial C-peptide to glucose ratio as a marker of β cell function: implication for the management of type 2 diabetes. International journal of molecular sciences. 2016;17(5):744.
  13. Edebor F, Fasanmade A. Evaluation of the characteristics of diabetes induced by the administration of alloxan to fructose fed Wistar rat. Journal of Chemical Information and Modeling. 2019;10(2):881-9.
  14. Bolen S, Feldman L, Vassy J, Wilson L, Yeh H-C, Marinopoulos S, et al. Systematic review: comparative effectiveness and safety of oral medications for type 2 diabetes mellitus. Annals of internal medicine. 2007;147(6):386-99.
  15. Xuyan Z, Ping YJ, Zhongjing W, Sheng D, Li L, Fan Y, et al. Melatonin reverses type 2 diabetes-induced cognitive deficits via attenuation of oxidative/nitrosative stress and NF-κB-mediated neuroinflammation in rat hippocampus. Tropical journal of pharmaceutical research. 2017;16(12):2865-75.
  16. Lo C-C, Lin S-H, Chang J-S, Chien Y-W. Effects of melatonin on glucose homeostasis, antioxidant ability, and adipokine secretion in ICR mice with NA/STZ-induced hyperglycemia. Nutrients. 2017;9(11):1187.
  17. Abdulwahab DA, El-Missiry MA, Shabana S, Othman AI, Amer ME. Melatonin protects the heart and pancreas by improving glucose homeostasis, oxidative stress, inflammation and apoptosis in T2DM-induced rats. Heliyon. 2021;7(3).
  18. Leighton E, Sainsbury CA, Jones GC. A practical review of C-peptide testing in diabetes. Diabetes therapy. 2017;8:475-87.
  19. Prunet-Marcassus B, Desbazeille M, Bros A, Louche K, Delagrange P, Renard P, et al. Melatonin reduces body weight gain in Sprague Dawley rats with diet-induced obesity. Endocrinology. 2003;144(12):5347-52.
  20. She M, Hou H, Wang Z, Zhang C, Laudon M, Yin W. Melatonin rescues 3T3-L1 adipocytes from FFA-induced insulin resistance by inhibiting phosphorylation of IRS-1 on Ser307. Biochimie. 2014;103:126-30.
  21. Shen S, Liao Q, Wong YK, Chen X, Yang C, Xu C, et al. The role of melatonin in the treatment of type 2 diabetes mellitus and Alzheimer's disease. International journal of biological sciences. 2022;18(3):983.
  22. Amaral FGd, Cipolla-Neto J. A brief review about melatonin, a pineal hormone. Archives of endocrinology and metabolism. 2018;62:472-9.
  23. Mayo JC, Aguado A, Cernuda-Cernuda R, Álvarez-Artime A, Cepas V, Quirós-González I, et al. Melatonin uptake by cells: an answer to its relationship with glucose? Molecules. 2018;23(8):1999.
  24. Peschke E, Frese T, Chankiewitz E, Peschke D, Preiss U, Schneyer U, et al. Diabetic Goto Kakizaki rats as well as type 2 diabetic patients show a decreased diurnal serum melatonin level and an increased pancreatic melatonin‐receptor status. Journal of pineal research. 2006;40(2):135-43.
آمار
تعداد مشاهده مقاله: 338
تعداد دریافت فایل اصل مقاله: 363


counter
سامانه مدیریت نشریات علمی. طراحی و پیاده سازی از سیناوب