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Effects of antecedent hypoglycemia, antecedent hyperinsulinemia, and antecedent corticosterone on subsequent counterregulation in normal rats.

机译:前期低血糖,前高胰岛素血症和前皮质酮对正常大鼠后续反调节的影响。

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摘要

This study examined the effects of antecedent hypoglycemia, antecedent hyperinsulinemia, and antecedent increases in plasma corticosterone on subsequent counterregulatory responses to hypoglycemia in normal rats. Four days of intermittent treatment with antecedent hypoglycemia and antecedent hyperinsulinemia resulted in impaired epinephrine responses to subsequent hypoglycemia on the fifth day. This correlated with the diminished incremental increase of hepatic glucose production during the hypoglycemic clamp in these groups. Surprisingly, rats that had undergone antecedent corticosterone also displayed impaired glucose production response in spite of normal neuroendocrine counterregulation. We conclude that both antecedent hypoglycemia and antecedent hyperinsulinemia may cause defective hormonal counterregulation leading to impaired glucose production during subsequent hypoglycemia. This suggests that antecedent hyperinsulinemia per se plays an important role in the pathogenesis of hypoglycemia-associated autonomic failure. Moreover, antecedent increases in corticosterone may cause deficient glucose production without altering the neuroendocrine responses to hypoglycemia, implying that other mechanisms might be involved.
机译:这项研究检查了正常大鼠中先前的低血糖,先前的高胰岛素血症和血浆皮质酮的升高对随后对低血糖的反调节反应的影响。前天低血糖和前高胰岛素血症的四天间歇治疗导致肾上腺素对第五天随后的低血糖的反应受损。在这些组中,这与降血糖钳制过程中肝葡萄糖产生的增量增加减少有关。出乎意料的是,尽管神经内分泌反调节正常,但接受过皮质酮治疗的大鼠也显示出葡萄糖生成反应受损。我们得出的结论是,先前的低血糖症和先前的高胰岛素血症都可能导致激素逆调节不良,从而在随后的低血糖症中导致葡萄糖生成受损。这表明先前的高胰岛素血症本身在低血糖相关的自主神经衰竭的发病机理中起着重要作用。此外,皮质酮的前期增加可能会导致葡萄糖生成不足,而不会改变对低血糖的神经内分泌反应,这暗示可能涉及其他机制。

著录项

  • 作者

    Shum, Kar Man Kathy.;

  • 作者单位

    University of Toronto (Canada).;

  • 授予单位 University of Toronto (Canada).;
  • 学科 Animal Physiology.
  • 学位 M.Sc.
  • 年度 2000
  • 页码 126 p.
  • 总页数 126
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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