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Function: require_once
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Filename: controllers/Detail.php
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Function: _error_handler
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Filename: controllers/Detail.php
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Function: _error_handler
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Function: insertAPISummary
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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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.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10686419 | PMC |
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0294432 | PLOS |
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Department of Nephrology, Affiliated Hospital of Jiangxi University of Traditional Chinese Medicine, Medicine Formula-Pattern Research Center of Jiangxi University of Traditional Chinese Medicine, Nanchang, China.
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iScience
December 2024
Department of Anesthesiology, Yale School of Medicine, New Haven, CT 06510, USA.
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Faculty of Pharmacy, Universitas Buana Perjuangan Karawang, Karawang, West Java 41361, Indonesia.
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Department of Respiratory Disease, The First Affiliated Hospital, Jinzhou Medical University, Jinzhou, 121000, People's Republic of China.
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