Influence of macrophage modulation on the state of extra islet insulin-producing system in hypergycemia

 
PIIS102872210002424-1-1
DOI10.31857/S102872210002424-1
Publication type Article
Status Published
Authors
Affiliation:
Institute of Immunology and Physiology of the Ural Branch of the Russian Academy of Sciences
Ural Federal University named after the first President of Russia B.N. Yeltsin
Affiliation: Institute of Immunology and Physiology of the Ural Branch of the Russian Academy of Sciences
Affiliation:
Institute of Immunology and Physiology of the Ural Branch of the Russian Academy of Sciences
Ural Federal University named after the first President of Russia B.N. Yeltsin
Affiliation:
Institute of Immunology and Physiology of the Ural Branch of the Russian Academy of Sciences
Ural Federal University named after the first President of Russia B.N. Yeltsin
Affiliation: Ural Federal University named after the first President of Russia B.N. Yeltsin
Journal nameRossiiskii immunologicheskii zhurnal
EditionVolume 12 Issue 3
Pages439-443
Abstract

Restoring of insulin-synthesizing cell pool by means of macrophage activity modulation can be a promising direction in the treatment of diabetes mellitus. Modeling of type 2 diabetes mellitus in rats (110 mg / kg of nicotinamide and 65 mg / kg of streptozotocin) caused a spontaneous compensatory increase in the number of extra islet insulin-producing cells up to 30 days, followed by a decrease in the number of these cells by 60 days without enhancing their functional activity. Modulation of macrophage activity with the administration of aminophthalhydrazide (2 mg / kg, 20 injections) to diabetic rats was accompanied by an increase in the number of the extra islet insulin-producing cells, the accumulation of insulin in all the studied groups of these cells, and a reduction in hyperglycemia.

Keywordsmacrophages, streptozotocin diabetes, extra islet insulin-producing cells
AcknowledgmentThe work was performed in the framework of the state. tasks IIII UB RAS. No. of state. registration of the topic AAAA-A18–118020590107–0.
Received12.01.2019
Publication date12.01.2019
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