Impact of Insufficient Insulin Secretion on Subclinical Glucose Dysregulation

DOI Web Site 参考文献33件
  • Chizumi Yamada
    Department of Clinical Health Science, Tokai University School of Medicine
  • Toshitake Mitsuhashi
    Department of Clinical Health Science, Tokai University School of Medicine
  • Noboru Hiratsuka
    Department of Clinical Health Science, Tokai University School of Medicine Shinjuku Center Bldg. Clinic
  • Fumiyo Inabe
    Department of Clinical Health Science, Tokai University School of Medicine
  • Nami Araida
    Department of Clinical Health Science, Tokai University School of Medicine
  • Eiko Takahashi
    Department of Clinical Health Science, Tokai University School of Medicine

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Background To elucidate the impact of insufficient insulin secretion on subclinical glucose dysregulation in association with increased insulin resistance and aging.<br>Methods We conducted a cross-sectional study of 3950 Japanese subjects using homeostasis model assessment (HOMA)-derived indices. We compared β-cell function according to insulin resistance or age groups. Interaction between insulin resistance and aging on β-cell function was assessed using two-way analysis of variance (ANOVA).<br>Results Increased insulin resistance resulted in higher blood glucose levels and apparently higher insulin secretion, but compensatory insulin secretion was considered insufficient to suppress subclinical blood glucose elevation. Along with aging, fasting blood glucose became higher without changes in serum insulin levels and HOMA-derived indices for β-cell function significantly decreased. Two-way ANOVA revealed that insulin resistance and aging independently influenced β-cell function and the effects of insulin resistance on β-cell function were more dominant than those of aging.<br>Conclusion Our study shows that β-cell dysfunction is a major contributor in determining glucose disposal and insufficient insulin secretion is already present even when glucose levels rise into the “highnormal” range. Insulin secretion should be evaluated in relation to insulin resistance, as the observed insulinsecretion may be insufficient to adjust plasma glucose concentrations. (Ningen Dock 2011; 25: 37-44)

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