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dc.contributor.authorAbidov M.
dc.contributor.authorSokolova K.
dc.contributor.authorDanilova I.
dc.contributor.authorBaykenova M.
dc.contributor.authorGette I.
dc.contributor.authorMychlynina E.
dc.contributor.authorOzgur B.A.
dc.date.accessioned2024-02-04T13:30:15Z
dc.date.available2024-02-04T13:30:15Z
dc.date.issued2023
dc.identifier.issn19326203
dc.identifier.urihttps://doi.org/10.1371/journal.pone.0294432
dc.identifier.urihttp://hdl.handle.net/11446/4877
dc.description.abstractInsulin-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. © 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.en_US
dc.language.isoengen_US
dc.publisherPublic Library of Scienceen_US
dc.relation.ispartofPLoS ONEen_US
dc.identifier.doi10.1371/journal.pone.0294432
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectalanine aminotransferaseen_US
dc.subjectalkaline phosphataseen_US
dc.subjectaspartate aminotransferaseen_US
dc.subjecthemoglobin A1cen_US
dc.subjectinsulinen_US
dc.subjectparathyroid hormoneen_US
dc.subjecttranscription factoren_US
dc.subjecthuman insulinen_US
dc.subjectinsulinen_US
dc.subjectaffinity chromatographyen_US
dc.subjectanimal experimenten_US
dc.subjectanimal modelen_US
dc.subjectanimal tissueen_US
dc.subjectArticleen_US
dc.subjectB cell dysfunctionen_US
dc.subjectconfocal microscopyen_US
dc.subjectcontrolled studyen_US
dc.subjectenzyme linked immunosorbent assayen_US
dc.subjectflow cytometryen_US
dc.subjectglucose blood levelen_US
dc.subjectglucose toleranceen_US
dc.subjectglycemic controlen_US
dc.subjecthistologyen_US
dc.subjecthistopathologyen_US
dc.subjecthomeostasis model assessmenten_US
dc.subjecthypoglycemiaen_US
dc.subjectinflammationen_US
dc.subjectinsulin deficiencyen_US
dc.subjectinsulin dependent diabetes mellitusen_US
dc.subjectinsulin resistanceen_US
dc.subjectinsulin synthesisen_US
dc.subjectmaleen_US
dc.subjectmitosis indexen_US
dc.subjectmorphometryen_US
dc.subjectnon insulin dependent diabetes mellitusen_US
dc.subjectnonalcoholic fatty liveren_US
dc.subjectnonhumanen_US
dc.subjectoral glucose tolerance testen_US
dc.subjectorgan injuryen_US
dc.subjectpancreas islet beta cellen_US
dc.subjectraten_US
dc.subjectanimalen_US
dc.subjectcell differentiationen_US
dc.subjectexperimental diabetes mellitusen_US
dc.subjectgeneticsen_US
dc.subjectinsulin dependent diabetes mellitusen_US
dc.subjectliveren_US
dc.subjectmetabolismen_US
dc.subjectnon insulin dependent diabetes mellitusen_US
dc.subjectpancreas islet beta cellen_US
dc.subjectAnimalsen_US
dc.subjectCell Differentiationen_US
dc.subjectDiabetes Mellitus, Experimentalen_US
dc.subjectDiabetes Mellitus, Type 1en_US
dc.subjectDiabetes Mellitus, Type 2en_US
dc.subjectInflammationen_US
dc.subjectInsulinen_US
dc.subjectInsulin, Regular, Humanen_US
dc.subjectInsulin-Secreting Cellsen_US
dc.subjectLiveren_US
dc.subjectRatsen_US
dc.titleHepatic insulin synthesis increases in rat models of diabetes mellitus type 1 and 2 differentlyen_US
dc.typearticleen_US
dc.departmentDBÜen_US
dc.identifier.issue11 Novemberen_US
dc.identifier.volume18en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.department-tempAbidov, M., Institute of Immunopathology and Preventive Medicine, Ljubljana, Slovenia; Sokolova, K., Institute of Immunology and Physiology, Ural Branch, Russian Academy of Sciences, Yekaterinburg, Russian Federation; Danilova, I., Institute of Immunology and Physiology, Ural Branch, Russian Academy of Sciences, Yekaterinburg, Russian Federation; Baykenova, M., Kostanay Oblast Tuberculosis Dispensary, Kostanay, Kazakhstan; Gette, I., Institute of Immunology and Physiology, Ural Branch, Russian Academy of Sciences, Yekaterinburg, Russian Federation; Mychlynina, E., Institute of Immunology and Physiology, Ural Branch, Russian Academy of Sciences, Yekaterinburg, Russian Federation; Ozgur, B.A., 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, A.O., Department of Immunology, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey, Diabetes Application and Research Center, Istanbul University, Istanbul, Turkey; Yilmaz, M.T., International Diabetes Center, Acibadem University, Istanbul, Turkeyen_US
dc.identifier.pmid38019818en_US
dc.identifier.scopus2-s2.0-85178209972en_US
dc.authorscopusid36794468800
dc.authorscopusid57200379414
dc.authorscopusid57220344666
dc.authorscopusid58729835500
dc.authorscopusid55884512200
dc.authorscopusid58731062900
dc.authorscopusid58041491000


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