BACKGROUND: Metabolic syndrome is associated with an increased risk of major cardiovascular events. Decreased high-molecular-weight (HMW) adiponectin levels are associated with metabolic syndrome and its components. Changes in γ-glutamyl transferase (GGT) levels are also associated with metabolic syndrome and could be modulated by HMW adiponectin. METHODS: From a single community, we recruited 822 men (mean age, 61±14 years) and 1,097 women (63±12 years) during their annual health examination. We investigated whether increased GGT and decreased HMW adiponectin levels are synergistically associated with metabolic syndrome and insulin resistance as evaluated by homeostasis of model assessment of insulin resistance (HOMA-IR). RESULTS: Of these subjects, 141 men (17.2%) and 170 women (15.5%) had metabolic syndrome. In men, the odds ratios (ORs) [(95% confidence interval (CI)] for metabolic syndrome across tertiles of GGT and HMW adiponectin were 1.00, 2.31 (1.25-4.24) and 3.39 (1.75-6.55) and 1.00, 0.51 (0.32-0.82) and 0.30 (0.17-0.54), respectively. In women, the ORs (95% CI) for metabolic syndrome across tertiles of GGT and HMW adiponectin were 1.00, 1.39 (0.81-2.40) and 1.79 (1.06-3.01) and 1.00, 0.35 (0.22-0.55) and 0.27 (0.15-0.46), respectively. The ORs for insulin resistance were increased in relation to GGT only in women, and decreased significantly in relation to HMW adiponectin in both genders. The interaction between increased GGT and decreased HMW adiponectin was a significant and independent determinant for metabolic syndrome and insulin resistance. CONCLUSIONS: These results suggested that higher GGT and lower HMW adiponectin levels are synergistically associated with metabolic syndrome and insulin resistance.
BACKGROUND:Metabolic syndrome is associated with an increased risk of major cardiovascular events. Decreased high-molecular-weight (HMW) adiponectin levels are associated with metabolic syndrome and its components. Changes in γ-glutamyl transferase (GGT) levels are also associated with metabolic syndrome and could be modulated by HMW adiponectin. METHODS: From a single community, we recruited 822 men (mean age, 61±14 years) and 1,097 women (63±12 years) during their annual health examination. We investigated whether increased GGT and decreased HMW adiponectin levels are synergistically associated with metabolic syndrome and insulin resistance as evaluated by homeostasis of model assessment of insulin resistance (HOMA-IR). RESULTS: Of these subjects, 141 men (17.2%) and 170 women (15.5%) had metabolic syndrome. In men, the odds ratios (ORs) [(95% confidence interval (CI)] for metabolic syndrome across tertiles of GGT and HMW adiponectin were 1.00, 2.31 (1.25-4.24) and 3.39 (1.75-6.55) and 1.00, 0.51 (0.32-0.82) and 0.30 (0.17-0.54), respectively. In women, the ORs (95% CI) for metabolic syndrome across tertiles of GGT and HMW adiponectin were 1.00, 1.39 (0.81-2.40) and 1.79 (1.06-3.01) and 1.00, 0.35 (0.22-0.55) and 0.27 (0.15-0.46), respectively. The ORs for insulin resistance were increased in relation to GGT only in women, and decreased significantly in relation to HMW adiponectin in both genders. The interaction between increased GGT and decreased HMW adiponectin was a significant and independent determinant for metabolic syndrome and insulin resistance. CONCLUSIONS: These results suggested that higher GGT and lower HMW adiponectin levels are synergistically associated with metabolic syndrome and insulin resistance.