| First Author | Su Y | Year | 2016 |
| Journal | Endocrinology | Volume | 157 |
| Issue | 12 | Pages | 4782-4793 |
| PubMed ID | 27754789 | Mgi Jnum | J:240759 |
| Mgi Id | MGI:5892184 | Doi | 10.1210/en.2016-1167 |
| Citation | Su Y, et al. (2016) Maternal Low Protein Isocaloric Diet Suppresses Pancreatic beta-Cell Proliferation in Mouse Offspring via miR-15b. Endocrinology 157(12):4782-4793 |
| abstractText | 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 beta-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 beta-cell dysfunction. We found that LP offspring exhibited impaired glucose tolerance due to decreased beta-cell mass and insulin secretion. Reduction in the beta-cell proliferation rate and cell size contributed to the decreased beta-cell mass. MiR-15b was up-regulated in the islets of LP offspring. The up-regulated miR-15b inhibited pancreatic beta-cell proliferation via targeting cyclin D1 and cyclin D2. Inhibition of miR-15b in LP islet cells restored beta-cell proliferation and insulin secretion. Our findings demonstrate that miR-15b is critical for the regulation of pancreatic beta-cells in offspring of maternal protein restriction, which may provide a further insight for beta-cell exhaustion originated from intrauterine growth restriction. |
