title: Beta-cell function is a major contributor to oral glucose disposition in obese Japanese students.
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.
authors.affiliation: Medical Health Center, Fukuoka University, Fukuoka, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Asano
authors.forename: Ryoko
authors.initials: R
authors.lastname: Yoshida
authors.forename: Hideaki
authors.initials: H
authors.lastname: Ogata
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Kokawa
authors.forename: Masao
authors.initials: M
authors.lastname: Ogimoto
authors.forename: Yuhko
authors.initials: Y
authors.lastname: Akehi
authors.forename: Keizo
authors.initials: K
authors.lastname: Anzai
authors.forename: Junko
authors.initials: J
authors.lastname: Ono
authors.forename: Kazuo
authors.initials: K
authors.lastname: Tamura
authors.forename: Kiyomi
authors.initials: K
authors.lastname: Hidehira
authors.forename: Masahiro
authors.initials: M
authors.lastname: Kikuchi
mesh_terms: D000284:Administration, Oral; D000293:Adolescent; D000328:Adult; D019540:Area Under Curve; D001786:Blood Glucose / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D005947:Glucose / Q000008:administration & dosage / Q000378:metabolism*; D018149:Glucose Intolerance; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000378:metabolism / Q000502:physiology*; D007564:Japan; D008297:Male; D009765:Obesity / Q000097:blood / Q000378:metabolism*; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D007328:Insulin; D014280:Triglycerides; D002784:Cholesterol; D005947:Glucose