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母体低蛋白等热量饮食通过miR-15b抑制小鼠后代胰腺β细胞增殖。

Maternal Low Protein Isocaloric Diet Suppresses Pancreatic β-Cell Proliferation in Mouse Offspring via miR-15b.

作者信息

Su Yutong, Jiang Xiuli, Li Yanli, Li Feng, Cheng Yulong, Peng Ying, Song Dalong, Hong Jie, Ning Guang, Cao Yanan, Wang Weiqing

机构信息

Shanghai Clinical Center for Endocrine and Metabolic Diseases (Y.S., X.J., Y.L., F.L., Y.P., D.S., J.H., G.N., Y.C., W.W.), Shanghai Key Laboratory for Endocrine Tumors, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, and Laboratory of Endocrinology and Metabolism (Y.C., G.N.), Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

出版信息

Endocrinology. 2016 Dec;157(12):4782-4793. doi: 10.1210/en.2016-1167. Epub 2016 Oct 18.

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.

摘要

母体营养不良的后代患2型糖尿病易感性增加的潜在机制尚不清楚。在此,我们检验了功能性微小RNA(miRNA)介导母体低蛋白(LP)等热量饮食诱导胰腺β细胞损伤的假说。我们对LP饮食和对照饮食母亲的后代胰岛进行了miRNA分析,以探索导致β细胞功能障碍的潜在功能性miRNA。我们发现,LP后代由于β细胞数量和胰岛素分泌减少而出现糖耐量受损。β细胞增殖率和细胞大小的降低导致了β细胞数量的减少。MiR-15b在LP后代的胰岛中上调。上调的MiR-15b通过靶向细胞周期蛋白D1和细胞周期蛋白D2抑制胰腺β细胞增殖。抑制LP胰岛细胞中的MiR-15b可恢复β细胞增殖和胰岛素分泌。我们的研究结果表明,MiR-15b对母体蛋白质限制后代的胰腺β细胞调节至关重要,这可能为源于子宫内生长受限的β细胞耗竭提供进一步的见解。

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