| Literature DB >> 18025761 |
Takashi Asano1, Ryoko Yoshida, Hideaki Ogata, Kazuhiko Kokawa, Masao Ogimoto, Yuhko Akehi, Keizo Anzai, Junko Ono, Kazuo Tamura, Kiyomi Hidehira, Masahiro Kikuchi.
Abstract
Determinants of glucose intolerance were studied in 163 obese Japanese young adults, 18 to 21 years old (43 females,120 males), who underwent 75-g oral glucose tolerance testing. Type 2 diabetes was newly diagnosed in 2.9% (n = 4); impaired fasting glucose (IFG) in 5.1% (n = 7); and impaired glucose tolerance (IGT) in 10.9% (n = 15). A homeostasis model assessment of insulin resistance (HOMA-IR) was used to estimate insulin sensitivity; beta-cell function during the first 30 min of the test was measured and defined as the insulinogenic index. This index was adjusted for insulin sensitivity, since this affects both beta-cell function and glucose disposition (disposition index). The relationship between insulinogenic index and 1/HOMA-IR was not hyperbolic. However, the disposition index (DI) was useful for the estimation of beta-cell function with the correct confirmation about it validity using beta-cell function index (BI). The association between insulin sensitivity and beta-cell function to glucose disposal, as measured by the area under the glucose curve (AUCg), was examined in all subjects. Insulin sensitivity was significantly related to AUCg (log HOMA-IR; R (2) = 0.142, p<0.0001). On the other hand, an inverse curvilinear relationship was observed between beta-cell function and AUCg (log(Delta I/Delta G)/HOMA-IR, R (2) = 0.411, p<0.0001). Thus, impaired beta-cell function, when estimated as DI, was strongly associated with impaired glucose disposal. In conclusion, our study showed that both insulin sensitivity and impaired beta-cell function are associated with impaired glucose metabolism, and that beta-cell function may be more important in determining glucose disposal.Entities:
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Year: 2007 PMID: 18025761 DOI: 10.1507/endocrj.k07-016
Source DB: PubMed Journal: Endocr J ISSN: 0918-8959 Impact factor: 2.349