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首页> 外文期刊>Human Molecular Genetics >Increased expression of microRNA-15a and microRNA-15b in skeletal muscle from adult offspring of women with diabetes in pregnancy
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Increased expression of microRNA-15a and microRNA-15b in skeletal muscle from adult offspring of women with diabetes in pregnancy

机译：妊娠糖尿病成人后代MicroRNA-15A和MicroRNA-15B表达骨骼肌中的表达

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摘要

Offspring of women with diabetes in pregnancy exhibit skeletal muscle insulin resistance and are at increased risk of developing type 2 diabetes, potentially mediated by epigenetic mechanisms or changes in the expression of small non-coding microRNAs. Members of the miR-15 family can alter the expression or function of important proteins in the insulin signalling pathway, affecting insulin sensitivity and secretion. We hypothesized that exposure to maternal diabetes may cause altered expression of these microRNAs in offspring skeletal muscle, representing a potential underlying mechanism by which exposure to maternal diabetes leads to increased risk of cardiometabolic disease in offspring. We measured microRNA expression in skeletal muscle biopsies of 26- to 35-year-old offspring of women with either gestational diabetes (O-GDM, n = 82) or type 1 diabetes (O-T1DM, n = 67) in pregnancy, compared with a control group of offspring from the background population (O-BP, n = 57) from an observational follow-up study. Expression of both miR-15a and miR-15b was increased in skeletal muscle obtained from O-GDM (both P 0.001) and O-T1DM (P = 0.024, P = 0.005, respectively) compared with O-BP. Maternal 2 h post OGTT glucose levels were positively associated with miR-15a expression (P = 0.041) in O-GDM after adjustment for confounders and mediators. In all groups collectively, miRNA expression was significantly positively associated with fasting plasma glucose, 2 h plasma glucose and HbA1c. We conclude that fetal exposure to maternal diabetes is associated with increased skeletal muscle expression of miR-15a and miR-15b and that this may contribute to development of metabolic disease in these subjects.
机译：妊娠糖尿病患者的后代表现出骨骼肌胰岛素抵抗力，并且正在增加2型糖尿病的风险，可能通过表观遗传机制或表达小非编码微稻草的表达的变化介导。 miR-15家族的成员可以改变胰岛素信号通路中重要蛋白的表达或功能，影响胰岛素敏感性和分泌。我们假设暴露于母体糖尿病可能导致这些微小肌肉中这些微小肌肉肌肉的表达改变，代表潜在的基础机制，通过这种潜在的基础机制，通过这种潜在的潜在机制导致后代心肌斑症疾病的风险增加。我们测量妊娠期糖尿病（O-GDM，N = 82）或1型妊娠期糖尿病（O-GDM，N = 82）或1型糖尿病（O-T1DM，N = 67）的骨骼肌肉活检中的microRNA表达通过从观察到随访研究中，从背景群体（O-BP，N = 57）中的后代对照组。与O-BP相比，MiR-15a和miR-15b的表达在由O-GDM（P <0.001）和O-T1DM（P = 0.024，P = 0.005）获得的骨骼肌中增加。母体2小时后OGTT葡萄糖水平与O-GDM的miR-15a表达（p = 0.041）呈正相关，伴有混合物和介质调整后的O-GDM。在所有组中，与空腹血糖，2小时血浆葡萄糖和HBA1c相应地，miRNA表达显着呈正相关。我们得出结论，胎儿暴露于母体糖尿病与miR-15a和miR-15b的骨骼肌表达增加有关，这可能有助于这些受试者的代谢疾病的发展。

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  • 来源
    《Human Molecular Genetics》 |2018年第10期|共9页
  • 作者

    Houshmand-Oeregaard Azadeh; Schrolkamp Maren; Kelstrup Louise; Hansen Ninna S.; Hjort Line; Thuesen Anne Cathrine B.; Broholm Christa; Mathiesen Elisabeth R.; Clausen Tine D.; Vaag Allan; Damm Peter;

  • 作者单位

    Rigshosp Dept Obstet Ctr Pregnant Women Diabet DK-2100 Copenhagen Denmark;

    Rigshosp Dept Endocrinol Diabet &

    Metab DK-2100 Copenhagen Denmark;

    Rigshosp Dept Obstet Ctr Pregnant Women Diabet DK-2100 Copenhagen Denmark;

    Rigshosp Dept Endocrinol Diabet &

    Metab DK-2100 Copenhagen Denmark;

    Rigshosp Dept Endocrinol Diabet &

    Metab DK-2100 Copenhagen Denmark;

    Rigshosp Dept Endocrinol Diabet &

    Metab DK-2100 Copenhagen Denmark;

    Rigshosp Dept Endocrinol Diabet &

    Metab DK-2100 Copenhagen Denmark;

    Univ Copenhagen Inst Clin Med Fac Hlth &

    Med Sci DK-2200 Copenhagen Denmark;

    Univ Copenhagen Inst Clin Med Fac Hlth &

    Med Sci DK-2200 Copenhagen Denmark;

    Rigshosp Dept Endocrinol Diabet &

    Metab DK-2100 Copenhagen Denmark;

    Rigshosp Dept Obstet Ctr Pregnant Women Diabet DK-2100 Copenhagen Denmark;

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  • 正文语种 eng
  • 中图分类 医学遗传学;
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