Role of Incretin Levels in Controlling Diabetic Patients

Journal of Chemical Health Risks

دوره 11، Special Issue: Bioactive Compounds: Their Role in the Prevention and Treatment of Diseases، دی 2021، صفحه 173-178   

نوع مقاله: Original Article

شناسه دیجیتال (DOI): 10.22034/jchr.2021.685648

نویسنده

Rasool Muayad Shukur Al-Obaidi^*

Department of Medical Laboratory Techniques, Faculty Medical and Health Technologies, Ahlulbyt University, Karbala, Iraq

چکیده

Within extremely precise limitations, the management of blood glucose levels in healthy individuals can be achieved and maintained. The glucose level rises immediately after a meal is consumed. Incretin hormones, which are appeared in the digestive system, play an essential function in the order of glucose, the maintenance of energy balance, and the protection of Langerhans islets cells. They are involved in the regulation of glucose levels in the body, and if their secretion is hindered, they can be used to anticipate the development of diabetes as soon as possible.The overarching goal of the research "is to identify the relationship between the production of GLP-1 and the development of insulin resistance", which ultimately results in type 2 diabetes.The case-control portion of current investigationdepends"on a revision of medical records from patients at the Clinic for Endocrinology", Diabetes, and Metabolic Diseases at the Clinical Center of Serbia, and computing the relevant parameters and doing statistical analysis.In terms of glucose profile, there was a substantial statistical divergence between the two groups that was found in the study. The relationship between Glucagon-like peptide 2 (GLP-2) and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) was found to be negative and statistically considerable (p=0.045). There was a statistically considerable positive association between DPP-IV and HOMA-IR (p=0.05).Our finding displays that insulin resistance can result in the suppression of glucagon-like peptide 1 production in persons with diabetes. According to the information presented here, reduction of GLP-1 secretion "is detached and will not occur in all people with poor glucose metabolism". This is due to a condition known as prediabetes, which will be discussed further in this section.

کلیدواژه‌ها

Blood glucose؛ Incretins؛ Type 2 diabetes؛ Insulin resistance؛ HOMA IR

مراجع

1. Bano A, Pera A, Almoukayed A, Clarke TH, Kirmani S, Davies KA, Kern F. CD28 null CD4 T-cell expansions in autoimmune disease suggest a link with cytomegalovirus infection. F1000Research. 2019;p1-8. last page?
2. Boer, G.A. and Holst, J.J., 2020. Incretin Hormones and Type 2 Diabetes—Mechanistic Insights and Therapeutic Approaches. Biology. 9(12), 473. last page?
3. English A., Irwin N., 2019. Nonclassical islet peptides: pancreatic and extrapancreatic actions. Clinical Medicine Insights: Endocrinology and Diabetes. 12, 1179551419888871.
4. Lafferty R., O'Harte F.P., Irwin N., Gault V.A., Flatt P., 2021. Proglucagon-derived peptides as therapeutics. Frontiers in Endocrinology. 12, 585.
5. Grüneis V., Schweiger K., Galassi C., Karl C.M., Treml J., Ley J.P., König J., Krammer G.E., Somoza V., Lieder B., 2021. Sweetness Perception is not Involved in the Regulation of Blood Glucose after Oral Application of Sucrose and Glucose Solutions in Healthy Male Subjects. Molecular Nutrition & Food Research. 65(2), 2000472.
6. Gonzalez-Campoy J.M., 2019. Hormonal regulation of energy balance and energy stores. Bariatric Endocrinology.Springer.37-57:
7. Toft-Nielsen M.B., Damholt M.B., Madsbad S., Hilsted L.M., Hughes T.E., Michelsen B.K., Holst J.J., 2001. Determinants of the impaired secretion of glucagon-like peptide-1 in type 2 diabetic patients. The Journal of Clinical Endocrinology & Metabolism. 86(8), 3717-3723.
8. Ji B., Qu H., Wang H., Wei H., Deng H., 2017. Association between the visceral adiposity index and homeostatic model assessment of insulin resistance in participants with normal waist circumference. Angiology. 68(8), 716-721.
9. Weng, J., Ji, L., Jia, W., Lu, J., Zhou, Z., Zou, D., Zhu, D., Chen, L., Chen, L., Guo, L. and Guo, X., 2016. Standards of care for type 2 diabetes in China. Diabetes/metabolism Research and Reviews. 32(5), 442.last page?
10. Nauck M.A., Heimesaat M.M., Orskov C., Holst J.J., Ebert R., Creutzfeldt W., 1993. Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus. The Journal of Clinical Investigation. 91(1), 301-307.
11. Elahi D., McAloon-Dyke M., Fukagawa N.K., Meneilly G.S., Sclater A.L., Minaker K.L., Habener J.F., Andersen D.K., 1994. The insulinotropic actions of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7–37) in normal and diabetic subjects. Regulatory Peptides. 51(1), 63-74.
12. Bagger J.I., Knop F.K., Lund A., Vestergaard H., Holst J.J., Vilsbøll T., 2011. Impaired regulation of the incretin effect in patients with type 2 diabetes. The Journal of Clinical Endocrinology & Metabolism. 96(3), 737-745.
13. Vilsbøll T., Krarup T., Madsbad S., Holst J., 2002. Defective amplification of the late phase insulin response to glucose by GIP in obese Type II diabetic patients. Diabetologia. 45(8), 1111-1119.
14. Kjems L.L., Holst J.J., Vølund A., Madsbad S., 2003. The influence of GLP-1 on glucose-stimulated insulin secretion: effects on β-cell sensitivity in type 2 and nondiabetic subjects. Diabetes., 52(2), 380-386.
15. Radojin D., Polovina S.P., 2018. Role of incretins in the pathogenesis of type 2 diabetes. Medical Gazette of the Special Hospital for Thyroid and Metabolism Zlatibor. 23(70), 53-65.
16. Johnston L. W., Harris S.B., Retnakaran R., Giacca A., Liu Z., Bazinet R.P., Hanley A. J., 2018. Association of NEFA composition with insulin sensitivity and beta cell function in the Prospective Metabolism and Islet Cell Evaluation (PROMISE) cohort. Diabetologia. 61(4), 821-830.

17.de Araújo, Ana Francisca Lopes Correia., 2017. Glucagon-like peptide-1 and glucagon-like peptide-1 analogs nanotechnology-based systems for prevention and therapy of diabetes.Thesis.