OBJECTIVE -To examine whether decreased serum levels of adiponectin are an independent risk factor for the progression to type 2 diabetes in a Japanese population.
RESEARCH DESIGN AND METHODS -The serum levels of adiponectin and tumor necrosis factor-␣ (TNF-␣) at baseline (from 1995 to 1997) were evaluated in 1,792 individuals (1,023 women and 769 men, aged 58.5 Ϯ 12.5 years) from a cohort population (n ϭ 3,706) of the Funagata study. Glucose tolerance was evaluated at baseline and also at 5-year follow-up examinations (n ϭ 978, follow-up rate, 54.6%) according to the 1985 World Health Organization criteria. The correlation of clinical traits with serum levels of adiponectin was examined. The association of the traits with the progression to type 2 diabetes at the 5-year follow-up was also examined.RESULTS -Among the traits examined, the correlation with aging was highest (r ϭ 0.312, P Ͻ 0.001). Eighteen subjects with normal glucose tolerance (NGT) developed diabetes, and 709 remained NGT at the 5-year follow-up examinations. The subjects who became diabetic had decreased serum levels of adiponectin (7.29 Ϯ 2.35 vs. 9.13 Ϯ 2.35 10 ϫ log g/ml, P ϭ 0.009). Multiple logistic regression analysis with age, sex, waist-to-hip ratio, and 2-h plasma glucose as the variables revealed that serum adiponectin level (odds ratio [per 0.1 log g/ml] 0.766, P ϭ 0.029) was an independent risk factor for the progression to type 2 diabetes. The subjects whose serum levels of adiponectin were in the lowest tertile were 9.320 times (95% CI 1.046 -83.1) more likely to develop diabetes than those in the highest tertile (P ϭ 0.046). CONCLUSIONS -Decreased serum adiponectin level is an independent risk factor for progression to type 2 diabetes.
Diabetes Care 26:2015-2020, 2003A dipose tissue, in addition to its function as the major storage depot for lipids, plays active roles in normal metabolic homeostasis and in the development of several diseases, such as type 2 diabetes, dyslipidemia, and atherosclerosis (1,2). These roles are mediated by factors known as adipocytokines, which are secreted from adipose tissue (3). Among those factors, tumor necrosis factor-␣ (TNF-␣), leptin, and plasminogen-activator inhibitor type 1 (PAI-1) are well annotated, and the association of the dysregulated production of these factors with the pathophysiology of obesityrelated insulin resistance and thrombosis is well established (3-6).Adiponectin/ACRP30 is another adipocytokine, first identified in 1995 (7). The association of decreased plasma adiponectin levels with the presence of coronary artery disease (8) indicated the pathophysiological roles of adiponectin in the development of coronary artery disease. On the other hand, adiponectin's roles in stimulating -oxidation in muscle and decreasing insulin resistance in the liver (9) indicated its possible involvement in the development of type 2 diabetes. Indeed, its involvement was shown in many animal studies. Administration of adiponectin improved diabetes in mice (10,11), and adiponectin-knockout mice...