Effect of Gliclazide on Non-Insulin Dependent Diabetes Mellitus
The hyperglycemia of non-insulin dependent diabetes mellitus (NIDDM) has been attributed to both glucose overproduction by the liver and gluclose under-utilization by peripheral tissues caused by deficient insulin secretion and resistance to insulin action. There is recent evidence that the induction of insulin deficiency creates insulin resistance (1). Several mechanisms have been postulated for the chronic “hypoglycemic” effects of sulfonylurea therapy in NIDDM. In relation to gliclazide (GCZ), there are studies indicating an effect on insulin secretion (2,3,4) and an extra- pancreatic action related to potentiation of the bioeffects of insulin (5,6). In the present study we examined the effects of chronic GCZ therapy on basal insulin levels, glucose and non-glucose (arginine) stimulated insulin responses (Study I), hepatic glucose production rate, peripheral tissue sensitivity to insulin and on red blood cells (RBC) insulin binding (Study II).
KeywordsFasting Plasma Glucose Insulin Binding NIDDM Patient Sulfonylurea Therapy Plasma Insulin Response
Unable to display preview. Download preview PDF.
- 2.Chiasson, J-L., Bergman, R.N., Verdy, M., Hamet, P. and De Lean, A., 1987, Study of the effect of gliclazide on secretion and action of insulin in normal and Type II diabetic humans. IDF Bull. 32: 9–11.Google Scholar
- 3.Matthews, D., Hosker, J. and Turner, R., 1987, Effects of gliclazide on insulin secretion indiced by glucose and aminoacids. IDF Bull 32: 12–15.Google Scholar
- 5.Wajchenberg, B.L., Malerbi, D.A., Giurno Filho, A., Giannella, Neto, D., Cherem, J.J., and Lerario, A.C., 1987, Effect of gliclazide treatment on red blood cell insulin receptors, hepatic glucose production and peripheral glucose utilization in non-insulin-dependent diabetes mellitus. IDF Bul 32: 16–21.Google Scholar
- 7.Judzewitsch, O.G., Pfeifer, M.A., Best, J.D., Beard, A.C., Halter, J.B. and Porte, Jr., D., 1982, Chronic chlorpropamide therapy of non-insulin dependent diabetes augments basal and stimulated insulin secretion by increasing islet sensitivity to glucose. J Clin Endocrinol Metab, 55: 321–328.PubMedCrossRefGoogle Scholar