title: Differences in insulin action and secretion, plasma lipids and blood pressure levels between impaired fasting glucose and impaired glucose tolerance in Japanese subjects.
abstract: We examined insulin action/secretion and cardiovascular disease risk factors in Japanese subjects with impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) who were not taking any medications known to affect glucose tolerance, blood pressure (BP) or plasma lipids (PLs). A total of 1,399 subjects received measurements of anthropometry, BP, PLs, and plasma glucose/insulin concentrations during 75 g-oral glucose tolerance test (OGTT). According to 2003 American Diabetes Association criteria, subjects were classified as having normal fasting glucose (NFG)/normal glucose tolerance (NGT) (n = 1,173), IFG (n = 128), IGT (n = 55), and IFG/IGT (n = 43). Insulin action was calculated using the HOMA-R (index of hepatic insulin resistance) and Matsuda index (reflects whole body insulin sensitivity). The ratio of the incremental area under the curve of insulin to that of glucose during OGTT (delta AUC(PI)/delta AUC(PG)) was used as an index of beta-cell function. HOMA-R was higher in IFG (2.3 +/- 0.1) and IFG/IGT (2.5 +/- 0.2) than in NFG/NGT (1.8 +/- 0.03). The Matsuda index was lower in IFG (6.5 +/- 0.3), IGT (5.4 +/- 0.4) and IFG/IGT (5.1 +/- 0.5) than in NFG/NGT (9.6 +/- 0.2). Delta AUC(PI)/delta AUC(PG) was lower in IGT (0.6 +/- 0.05) and IFG/IGT (0.5 +/- 0.05) than in IFG (1.4 +/- 0.12) or NFG/NGT (1.2 +/- 0.03). Mean BP was higher in IGT (100 +/- 1.7 mmHg) than in NFG/NGT (91 +/- 0.3) or IFG (95 +/- 1.1). The plasma triglyceride level was higher in IGT (155 +/- 14 mg/dL) and IGT/IFG (173 +/- 12) than in IFG (132 +/- 7) or NFG/NGT (122 +/- 2). In conclusion, 1) whole body insulin sensitivity is decreased in IFG and IGT, with a greater reduction in IGT, 2) hepatic insulin resistance and preserved beta-cell function are characteristics of IFG, and 3) higher BP and triglyceride levels are observed in IGT. IGT is more closely associated with risk factors for cardiovascular disease than is IFG.
authors.affiliation: 2nd Department of Internal Medicine, Sapporo Medical University School of Medicine, S-1, W-16, Chuo-ku, Sapporo 060-8543, Japan. yomiya@sapmed.ac.jp
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Miyazaki
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Akasaka
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Ohnishi
authors.forename: Shigeyuki
authors.initials: S
authors.lastname: Saitoh
authors.forename: Ralph A
authors.initials: RA
authors.lastname: DeFronzo
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Shimamoto
mesh_terms: D001786:Blood Glucose / Q000032:analysis*; D001794:Blood Pressure; D015992:Body Mass Index; D005215:Fasting / Q000097:blood*; D005260:Female; D018149:Glucose Intolerance / Q000503:physiopathology*; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance; D000078790:Insulin Secretion; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged
chemical_list: D001786:Blood Glucose; D007328:Insulin; D008055:Lipids