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V V Poltorak

Publications and source records attributed to V V Poltorak.

At least 37 records · Page 2Linked to original sources
PubMedDate not supplied

[Expression of the db (diabetes) gene in mice with hereditary load by generalized autoimmune pathology].

A model of genetically determinate diabetes mellitus in hybrid db/db mice with hereditary load by generalized autoimmune pathology has been described. The data on the character of hormonal-metabolic disturbances permit a conclusion on more serious course of diabetes mellitus in mice (C57Bl/Ks x NZB)F2 db/db as against (C57BL/Ks x NZW)F2 db/db, that is correlated with expression of autoimmune pathology in parent lines of New Zealand mice NZB and NZW. It is stated that diabetic syndrome in males proceeds in more serious form than in females.

Animals↗
PubMedDate not supplied

[Study of diabetogenic and lympholytic effects during single and fractional administration of streptozotocin to mice of the mutant strain C57BL/KsIY-db/m].

Single administration of streptozotocin at a dose of 200 mg/kg into mice males of the C57BL/KsJY db/m strain induced severe form of insulin-dependent diabetes within the earlier periods as compared with fractional injection of the drug (40 mg/kg daily within 5 days). Streptozotocin-induced diabetes, developed after single administration of the drug, caused pronounced destructions in lymphoid tissue, primarily in thymus as content of DNA was drastically decreased in the tissue and level of DNA breakdown products was increased. The lympholytic effect of streptozotocin was less distinct after fractional administration.

Animals↗
PubMedDate not supplied

[The effect of glibenclamide on the spontaneous evolution of genetically determined diabetes mellitus in C57BL/KsJY db+/+db mice].

The study was carried out on 25 mice of the mutant C57BL/KsJY line carrying the autosomal-recessive gene db (diabetes) in the homozygous state with basal normo- and hyperglycemia by the beginning of the treatment with glybenclamide (the latent and manifest stages of insulin-independent diabetes mellitus). It was found that long-term oral administration of the drug in the therapeutic dose (20 micrograms per mice a day for 3-3.5 months) enhanced the genetically determined disturbances of glucose homeostasis and the insulin-producing apparatus of the pancreas irrespective of the stage of spontaneous diabetes genesis. The development of the organ-specific autoimmune reactions directed to antigens of the pancreatic islands was found.

Animals↗
PubMedDate not supplied

[The effect of irradiation on the development of streptozotocin diabetes in C57BL/KsJY mice heterozygous and homozygous for gene db (diabetes)].

In experiments with C57BL/KsJY mice carrying a mutant db gene at the heterozygous and homozygous states it has been found that db+/+db mice are much more sensitive to gamma radiation with respect to the survival rate. In homozygotes, in contrast to heterozygotes, irradiation with a dose of 6 Gy does not reduce the severity of the diabetogenic effect of low doses of streptozotocin.

Animals↗
PubMedDate not supplied

[The effect of long-term glibenclamide administration on pancreatic beta cells and on autoimmunity indices].

It was found that administration of glybenclamide in the therapeutic dose to rats exerts the damaging effect on insulin-producing apparatus of the pancreas (inhibition of the secretory reaction of beta-cells, disturbance of their morphological structure, decrease of glucose tolerance test), initiates the development of lymphocellular infiltration of islands (autoimmune insulitis), increases the level of antibodies to blood serum DNA. The inverse temporal dependence between the appearance and degree of diabetogenic effects of chronic sulfanylamide therapy and changes in autoimmunity (the latters are characteristic of earlier treatment with the drug) can be traced.

Acute Disease↗
PubMedDate not supplied

[Importance of db gene for the development of low dose streptozotocin diabetes in C57BL/KsJ mice].

The paper is concerned with some data on the effect of the diabetic gene (db) on mouse sensitivity to streptozotocin (SC). Male mice aged 2-3 mos. of mutant C57BL/KsJ strain (genotypes: m+/+m, db+/+m, db+/+db) were used for investigation. Insulin-dependent diabetes mellitus was induced by intraperitoneal injections of streptozotocin at a daily dose of 40 mg/kg for 5 days. The structure and function of the insular apparatus were histologically assessed as well as by the blood level of insulin and glucose within 15 days after the start of the experiment. The earliest hyperglycemic reaction to SC was typical of mice, homozygous by the diabetic gene; they had normoglycemia at the time of treatment. In mice, heterozygous by the diabetic gene, a hyperglycemic reaction developed later after treatment. However by the end of the investigation it reached values which were typical of mice, homozygous by the diabetic gene, with basal normoglycemia. Mice, not carrying the diabetic gene, as well as homozygotes by this gene with basal hyperglycemia, possessed lesser sensitivity to SC. The expression of hyperglycemic reactions showed correlation with a degree of dystrophic changes and the development of lymphocellular infiltration in the pancreatic islets of mice with basal normoglycemia in low dose streptozotocin diabetes. The development of spontaneous hyperglycemia in homozygotes by the diabetic gene lowered their sensitivity to SC diabetogenic effects.

Animals↗
PubMedDate not supplied

[Role of the time factor in the pancreatic and extrapancreatic mechanisms of action of glibenclamide].

A study was made of the effect of short- and long-term administration of one of the sulfanilurea derivatives of the 2nd generation--glibenclamide on pancreatic beta-cell function and the sensitivity of peripheral tissues to insulin under clinical and experimental conditions. The authors established time correlation of the mechanisms of glibenclamide hypoglycemic action: beta-cytotropic action in acute administration of the drug and extrapancreatic influence in chronic administration. An idea of predominant significance of the postreceptor level in the realization of the extrapancreatic effect of long-term administration of glibenclamide was substantiated.

Adult↗