Beta cell dysfunction and low insulin sensitivity (SI) are causally related to the development of diabetes mellitus (DM). The existence of this relationship has been established by a number of cross-sectional and longitudinal studies [1][2][3][4][5]. However, the predisposing factors for non-diabetic hyperglycemia (NDH) have not been established. More precisely, the significance of attenuated glucose-stimulated insulin secretion (GSIS), SI and beta cell function (BCF) for the worsening of glucose metabolism from normal glucose tolerance (NGT) to impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) has not been fully clarified [5][6][7][8][9]. Especially, a longitudinal analysis in Japanese subjects aiming at clarification of the predisposing factors for NDH has been lacking. The eluci- Follow-up glucose tolerance status was determined by 75 g OGTT performed 3.7 yrs later. Glucose-stimulated insulin secretion (GSIS), whole body insulin sensitivity (SI) and beta cell function (BCF) were estimated by Stumvoll indices, ISI Matsuda, and a product of Stumvoll 1 st and ISI Matsuda , respectively, and hepatic SI by quantitative insulin sensitivity check index. Logistic regression analysis revealed that attenuated BCF due to low GSIS was an independent risk factor for IFG. Low whole body SI was an additional risk for IGT. Male gender and high BMI were independently related to the progression to both IFG and IGT, whereas a positive diabetes family history was independently related to IGT. The worsening of glucose tolerance at large was predicted with 66% sensitivity by risk engine with GSIS, whole body SI, gender, BMI and glucose. This finding may help when implementing early intervention strategies for diabetes.
Aim: To identify predictors of coronary heart disease (CHD) in Japanese patients with type 2 diabetes (T2DM).Methods: A matched case-control study was performed using 800 patients with T2DM admitted for treatment of hyperglycemia from January
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