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论文题目: Maternal Low Protein Isocaloric Diet Suppresses Pancreatic beta-Cell Proliferation in Mouse Offspring via miR-15b
英文论文题目: Maternal Low Protein Isocaloric Diet Suppresses Pancreatic beta-Cell Proliferation in Mouse Offspring via miR-15b
第一作者: Su, YT; Jiang, XL; Li, YL; Li, F; Cheng, YL; Peng, Y; Song, DL; Hong, J; Ning, G; Cao, YA; Wang, WQ
英文第一作者: Su, YT; Jiang, XL; Li, YL; Li, F; Cheng, YL; Peng, Y; Song, DL; Hong, J; Ning, G; Cao, YA; Wang, WQ
联系作者: Cao, YA; Wang, WQ (reprint author), Shanghai Jiao Tong Univ, Rui Jin Hosp, Sch Med, Shanghai Clin Ctr Endocrine & Metab Dis,Shanghai, Shanghai 200025, Peoples R China.
英文联系作者: Cao, YA; Wang, WQ (reprint author), Shanghai Jiao Tong Univ, Rui Jin Hosp, Sch Med, Shanghai Clin Ctr Endocrine & Metab Dis,Shanghai, Shanghai 200025, Peoples R China.
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发表年度: 2016
卷: 157
期: 12
页码: 4782-4793
摘要: 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 cyclinD1and 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.
英文摘要: 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 cyclinD1and 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.
刊物名称: ENDOCRINOLOGY
英文刊物名称: ENDOCRINOLOGY
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学科: Endocrinology & Metabolism
英文学科: Endocrinology & Metabolism
影响因子: 4.286
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论文类别: Article
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