Insulin Secretory Defect and Insulin Resistance in Isolated Impaired Fasting Glucose and Isolated Impaired Glucose Tolerance.

نویسندگان

  • Sae Aoyama-Sasabe
  • Mitsuo Fukushima
  • Xin Xin
  • Ataru Taniguchi
  • Yoshikatsu Nakai
  • Rie Mitsui
  • Yoshitaka Takahashi
  • Hideaki Tsuji
  • Daisuke Yabe
  • Koichiro Yasuda
  • Takeshi Kurose
  • Nobuya Inagaki
  • Yutaka Seino
چکیده

OBJECTIVE To investigate the characteristics of isolated impaired glucose tolerance (IGT) and isolated impaired fasting glucose (IFG), we analyzed the factors responsible for elevation of 2-hour postchallenge plasma glucose (2 h PG) and fasting plasma glucose (FPG) levels. METHODS We investigated the relationship between 2 h PG and FPG levels who underwent 75 g OGTT in 5620 Japanese subjects at initial examination for medical check-up. We compared clinical characteristics between isolated IGT and isolated IFG and analyzed the relationships of 2 h PG and FPG with clinical characteristics, the indices of insulin secretory capacity, and insulin sensitivity. RESULTS In a comparison between isolated IGT and isolated IFG, insulinogenic index was lower in isolated IGT than that of isolated IFG (0.43 ± 0.34 versus 0.50 ± 0.47, resp.; p < 0.01). ISI composite was lower in isolated IFG than that of isolated IGT (6.87 ± 3.38 versus 7.98 ± 4.03, resp.; p < 0.0001). In isolated IGT group, insulinogenic index showed a significant correlation with 2 h PG (r = -0.245, p < 0.0001) and had the strongest correlation with 2 h PG (β = -0.290). In isolated IFG group, ISI composite showed a significant correlation with FPG (r = -0.162, p < 0.0001) and had the strongest correlation with FPG (β = -0.214). CONCLUSIONS We have elucidated that decreased early-phase insulin secretion is the most important factor responsible for elevation of 2 h PG levels in isolated IGT subjects, and decreased insulin sensitivity is the most important factor responsible for elevation of FPG levels in isolated IFG subjects.

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عنوان ژورنال:
  • Journal of diabetes research

دوره 2016  شماره 

صفحات  -

تاریخ انتشار 2016