Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 437, Issue C, Pages 213-223Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2016.08.037
Keywords
MiR-17-92; Pancreatic beta-cells; Proliferation; Adaptation; PTEN
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Funding
- National Natural Science Foundation of China [81572639, 81370969, 81072190]
- Ministry of Education of the People's Republic of China [20130181110066]
- Chengdu Bureau of Science and Technology [2014-HM01-00382-SF]
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MiR-17-92 cluster contributes to the regulation of mammalian development, aging and tumorigenesis. The functional roles of miR-17-92 in pancreatic beta-cells are largely unknown. In this study, we found that conditional deletion of miR-17-92 in mouse pancreatic beta-cells (miR-17-92 beta KO) significantly reduces glucose tolerance and the first phase of insulin secretion, despite normal ad libitum fed and fasting glucose levels. Proliferation is down-regulated in pancreatic beta-cells after deleting miR-17-92. MiR-17-92 beta KO mice show higher phosphatase and tensin homologue (PTEN) and lower phosphorylated AKT in islets. Under high fat diet challenge for 16 weeks, miR-17-92 beta KO mice lose compensation and exhibit higher glucose levels, and lower insulin secretion. Collectively, these data suggest that miR-17-92 is a critical contributor to molecular mechanisms regulating glucose-stimulated insulin secretion and pancreatic beta-cell adaptation under metabolic stress. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
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