| Literature DB >> 27754789 |
Yutong Su1, Xiuli Jiang1, Yanli Li1, Feng Li1, Yulong Cheng1, Ying Peng1, Dalong Song1, Jie Hong1, Guang Ning1, Yanan Cao1, Weiqing Wang1.
Abstract
The mechanism underlying the increased susceptibility of type 2 diabetes in offspring of maternal malnutrition is poorly determined. Here we tested the hypothesis that functional microRNAs (miRNAs) mediated the maternal low-protein (LP) isocaloric diet induced pancreatic β-cell impairment. We performed miRNA profiling in the islets from offspring of LP and control diet mothers to explore the potential functional miRNAs responsible for β-cell dysfunction. We found that LP offspring exhibited impaired glucose tolerance due to decreased β-cell mass and insulin secretion. Reduction in the β-cell proliferation rate and cell size contributed to the decreased β-cell mass. MiR-15b was up-regulated in the islets of LP offspring. The up-regulated miR-15b inhibited pancreatic β-cell proliferation via targeting cyclin D1 and cyclin D2. Inhibition of miR-15b in LP islet cells restored β-cell proliferation and insulin secretion. Our findings demonstrate that miR-15b is critical for the regulation of pancreatic β-cells in offspring of maternal protein restriction, which may provide a further insight for β-cell exhaustion originated from intrauterine growth restriction.Entities:
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Year: 2016 PMID: 27754789 DOI: 10.1210/en.2016-1167
Source DB: PubMed Journal: Endocrinology ISSN: 0013-7227 Impact factor: 4.736