Hepatic insulin synthesis increases in rat models of diabetes mellitus type 1 and 2 differently.

Autor: Abidov M; Institute of Immunopathology and Preventive Medicine, Ljubljana, Slovenia., Sokolova K; Institute of Immunology and Physiology, Ural Branch of the Russian Academy of Sciences, Yekaterinburg, Russian Federation., Danilova I; Institute of Immunology and Physiology, Ural Branch of the Russian Academy of Sciences, Yekaterinburg, Russian Federation., Baykenova M; Kostanay Oblast Tuberculosis Dispensary, Kostanay, Republic of Kazakhstan., Gette I; Institute of Immunology and Physiology, Ural Branch of the Russian Academy of Sciences, Yekaterinburg, Russian Federation., Mychlynina E; Institute of Immunology and Physiology, Ural Branch of the Russian Academy of Sciences, Yekaterinburg, Russian Federation., Aydin Ozgur B; Department of Medical Biology and Genetics, Faculty of Medicine, Demiroglu Bilim University, Istanbul, Turkey.; Diabetes Application and Research Center, Demiroglu Bilim University, Istanbul, Turkey., Gurol AO; Department of Immunology, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey.; Diabetes Application and Research Center, Istanbul University, Istanbul, Turkey., Yilmaz MT; International Diabetes Center, Acibadem University, Istanbul, Turkey.
Jazyk: angličtina
Zdroj: PloS one [PLoS One] 2023 Nov 29; Vol. 18 (11), pp. e0294432. Date of Electronic Publication: 2023 Nov 29 (Print Publication: 2023).
DOI: 10.1371/journal.pone.0294432
Abstrakt: Insulin-positive (+) cells (IPCs), detected in multiple organs, are of great interest as a probable alternative to ameliorate pancreatic beta-cells dysfunction and insulin deficiency in diabetes. Liver is a potential source of IPCs due to it common embryological origin with pancreas. We previously demonstrated the presence of IPCs in the liver of healthy and diabetic rats, but detailed description and analysis of the factors, which potentially can induced ectopic hepatic expression of insulin in type 1 (T1D) and type 2 diabetes (T2D), were not performed. In present study we evaluate mass of hepatic IPCs in the rat models of T1D and T2D and discuss factors, which may stimulate it generation: glycaemia, organ injury, involving of hepatic stem/progenitor cell compartment, expression of transcription factors and inflammation. Quantity of IPCs in the liver was up by 1.7-fold in rats with T1D and 10-fold in T2D compared to non-diabetic (ND) rats. We concluded that ectopic hepatic expression of insulin gene is activated by combined action of a number of factors, with inflammation playing a decision role.
Competing Interests: The authors have declared that no competing interests exist.
(Copyright: © 2023 Abidov et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
Databáze: MEDLINE
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