The effect of oxytocin on Langerhans beta-islet cell function and on carbohydrate metabolic indices in intact rats and in rats with diabetes

• Published in: Fiziolohichnyi zhurnal (Kiev, Ukraine : 1994) Vol. 46; no. 1; pp. 37 - 43
• Main Authors: Kolesnyk, Iu M, Trzhetsyns'kyĭ, S D, Abramov, A V
• Format: Journal Article
• Language: Ukrainian
• Published: Ukraine 2000
• Subjects: Animals; Blood Glucose - drug effects; Blood Glucose - metabolism; Carbohydrate Metabolism; Diabetes Mellitus, Experimental - drug therapy; Diabetes Mellitus, Experimental - metabolism; Drug Evaluation, Preclinical; Injections, Intraperitoneal; Injections, Intraventricular; Insulin - metabolism; Islets of Langerhans - drug effects; Islets of Langerhans - metabolism; Male; Oxytocin - administration & dosage; Oxytocin - pharmacology; Rats; Rats, Wistar; Time Factors
• ISSN: 2522-9028

The experiments were carried out on male Wistar rats. Synthetic oxytocin was administrated to intact and streptozotocin-diabetic animals during 10 days by intracerebroventricular and intraperitoneal injections. The state of pancreatic b-cells was studied by a method of indirect immunofluorescence with the following results computing on VIDAS-386 image analyzing system. The measurement of the area of immunofluorescence and Langerhans islets and determination of insulin concentration and its contents in islets was provided automatically. Insulin and glucose concentration in blood was determined with standard techniques. Oxytocin central injections to intact animals stimulated insulin synthesis and secretion without changing of islets area. Peptide administration to diabetic animals resulted in braking of islets destruction, increasing of its area and contents of insulin. These changes were accompanied with the reducing of glycemia level. Thus, oxytocin administration stimulates insulin synthesis and secretion in intact and diabetic animals and this effect is more expressed with central injections. Besides it is necessary to note the oxytocin braking effect on beta-cells destruction in diabetic animals.