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V V Poltorak

Publications and source records attributed to V V Poltorak.

46 records · Page 3Linked to original sources
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[Biosynthesis and secretion of insulin under the effect of an antibiotic of the tetracycline group].

Formation and secretion of insulin during administration of tetracycline hydrochloride in vivo and in vitro were studied in experimental rat Langerhans islets isolated by enzymatic digestion with collagenase. Insulin secretion was determined by radioimmunoassay, insulin biosynthesis was assessed from 3H-leucin incorporation into the de novo formed proteins of the islets with insulin immunoreactivity (proinsulin plus insulin). Injection of the antibiotic in a dose of 25 mg/kg intraperitoneally for 10 days did not change the functional activity of beta-cells--the rate of insulin formation and secretion at low and high glucose concentrations in the incubation medium. Higher doses of the antibiotic applied in vivo (100 mg/kg intraperitoneally for 10 days) and in vitro (100 mumol, 2-hour incubation) inhibited the glucose-stimulated (15 mmol) insulin secretion but exerted no effect on insulin biosynthesis. The possible importance of ionophore properties of the antibiotic, that changes the concentration of intracellular Ca2+ in the mechanism of dissociated action of tetracycline hydrochloride on insulin formation and secretion, as well as the practical significance of the data obtained are discussed.

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PubMedDate not supplied

[Effect of thyroidectomy on the beta-cell function of the pancreatic islet apparatus].

The functional activity of the insular apparatus of the pancreas with varying function of beta-cells and body sensitivity to insulin were studied in vivo and in vitro in an experimental hypothyroidal condition produced by total removal of the thyroid from rabbits and rats. Insulin was detected by radioimmunoassay, whereas insulin biosynthesis was assessed from 3H-leucin incorporation into the de novo formed islet proteins with insulin immunoreactivity (proinsulin plus insulin). The insulin test (0.3 Units/kg mass, intravenously) was made to study glycemia and the level of non-esterified fatty acids in the blood serum. Thirty days after thyroidectomy glucose homeostasis was not disturbed, and the body sensitivity to sugar-reducing and antilypolytic insulin actions did not undergo any changes. The deficiency of thyroid hormones produced an increase in basal and glucose-induced insulinemia (intravenous glucose tolerance test) and a rise in the exogenous insulin break down rate. No changes in the biosynthesis of insulin by the islets were detected. The increase in the secretory response of beta-cells to glucose with undisturbed insulin formation presents a compensatory reaction aimed at making normal glycemia possible. The regulating effect of thyroid hormones on the secretory response of beta-cells and the essential role of the latter in glucose homeostasis under deficiency of thyroid hormones are discussed.

Animals↗
PubMedDate not supplied

[Effect of hyperthyroidization on (pro)insulin biosynthesis and secretion].

Insulin production and secretion in simulated rat hyperthyrosis induced by L-thyroxin, injected intraperitoneally during 8 to 30 days, were studied on isolated Langerhans' islets, using collagenase fermentation. Insulin secretion in vitro was determined by radioimmunoassay, its biosynthesis being evaluated according to 3H-leucine incorporation into de novo formed islet proteins with insulin immunoreactivity. The dissociated effect of thyroxin on the secretory response of beta-cells and their hormone production was revealed. In hyperthyroidized animals a decrease in the islet insulin secretion was seen in the presence of a low glucose content in the incubating medium (5 mM), (pro-)insulin biosynthesis remaining unchanged. (Pro-)insulin concentration increased comparatively to the control following 8-day thyroxin injection under condition of the islet incubation with 15 mM of glucose. Insulin secretion returns to normal after augmentation of hexose content in the incubating medium up to 15 mM (hormone production being not inhibited), indicating the functional character of a decrease in beta-cell secretory response and a significant role in its genesis of the changed beta-cell sensitivity to glucose action, inducing insulin secretion.

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