Background: Adiponectin, a novel adipocyte-derived collagen-like protein, is the gene product of the adipose most-abundant gene transcript 1 (apM1), which has been considered to have anti-inflammatory and anti-atherogenic effects. Objective: To characterize the relationship between adiponectin and leptin, the ob gene product, in normal-weight and obese women. Design and methods: In this cross-sectional study, we measured fasting plasma adiponectin by ELISA, leptin concentrations by RIA, and related parameters such as blood pressure, body mass index (BMI), body fat mass, lipids, fasting blood glucose and insulin in 353 non-diabetic adult women with a wide range of BMI values. Results: Plasma adiponectin concentrations in women with the highest tertile of BMI (at least 25.0 kg/m
Adiponectin, the gene product of the adipose most abundant gene transcript 1, is a novel adipocyte-derived peptide that has been considered to have antiinflammatory and antiatherogenic effects. To characterize the relationship between adiponectin and lipids metabolism, we measured fasting plasma adiponectin concentration by ELISA, serum total cholesterol, high-density lipoprotein cholesterol (HDL-C), triglyceride (TG), and apolipoprotein (apo) levels in 352 nondiabetic women, 16-86 yr old, with a wide range of body weight [body mass index (BMI), 14.8-36.3 kg/m(2)]. Plasma adiponectin concentrations in women with the highest tertile of TG (1.69 mM < or approximately) were decreased, compared with the middle (1.13 < or = approximately < 1.69) or lowest tertile of TG (approximately < 1.13) (5.9 +/- 0.5 vs. 7.5 +/- 0.3, 9.2 +/- 0.2 microg/ml; P < 0.005, 0.001). Plasma adiponectin with the lowest tertile of HDL-C (approximately < 1.16 mM) was decreased, compared with the middle (1.16 < or = approximately < 1.81) or highest tertile of HDL-C (1.81 < or approximately ) (5.7 +/- 0.5 vs. 7.8 +/- 0.2, 10.1 +/- 0.4 microg/ml; both P < 0.001). These relationships had similar tendencies after adjustment for BMI, body fat mass, age, or diastolic blood pressure. Adiponectin was negatively correlated with serum TG (r = -0.33, P < 0.0001), atherogenic index [(total cholesterol - HDL-C)/HDL-C] (r = -0.34, P < 0.0001), apo B (r = -0.45, P < 0.0001), or apo E (r = -0.29, P < 0.05), and positively correlated with serum HDL-C (r = 0.39, P < 0.0001) or apo A-I levels (r = 0.42, P < 0.002). Those negative relationships became stronger after adjusting for BMI or body fat mass. The slightly positive correlation between adiponectin and age, blood urea nitrogen, or creatinine levels was also observed (all P < 0.001). These results indicate that high-TGnemia and low-HDL-Cnemia are associated with low plasma adiponectin concentrations in nondiabetic women. Further efforts must now be targeted to determine whether adiponectin causes these lipid abnormalities and thus whether it is partly responsible for the atherogenic risk seen in the metabolic syndrome.
Objective: Whether the adipocyte-derived protein adiponectin is associated with insulin resistance independently of the effects of adiposity and the diabetic state is an important question. We explored, in a cross-sectional study of 486 Japanese nondiabetic women, the relationship between the calculated insulin resistance (homeostasis model assessment ratio (HOMA-R)) and adiponectin levels determined using a validated sandwich ELISA. Design and methods: All participants were stratified into tertiles for HOMA-R (, , 1.5, 1.5 # , , 3.0, 3.0 # , ) and the differences across tertiles of continuous variables were tested with ANOVA. Two-way ANOVA was used to determine possible relationships for plasma adiponectin between tertiles of HOMA-R and several stratified parameters. Multiple regression analyses were performed with HOMA-R or fasting serum insulin as dependent variable, and diastolic blood pressure (BP), body mass index (BMI), serum triglyceride (TG), leptin and adiponectin as independent determinants. Results: Mean plasma adiponectin in the high HOMA-R group decreased compared with that in the low HOMA-R group both before (mean^S.E.M. 6:2^0:6 vs 9:2^0:3 mg=ml; P , 0:001) and after adjustment for body fat mass (BFM) as kg or percent ð0:31^0:04 vs 0:69^0:03; 0:18^0:02 vs 0:340 :01; both P , 0:001). HOMA-R was inversely associated with adiponectin levels both before ðr ¼ 20:37; P , 0:001Þ and after adjustment for BFM ðr ¼ 20:49; 20.46, both P , 0:001Þ: After covariate adjustment for age, diastolic BP, BMI and serum TG, HOMA-R retained a significant correlation with adiponectin/BFM (kg). Both adiponectin and leptin were the significant determinants of HOMA-R or fasting insulin in multiple regression models. Conclusions: Adiponectin was inversely associated with insulin resistance in nondiabetic subjects, independently from age, BP, adiposity and serum lipids. Because adiponectin is thought to have an antiatherogenic action, the presence of hypoadiponectinemia may predispose subjects to atherosclerosis, and may progress the atherogenesis in insulin resistance.
This cross sectional study was undertaken to determine whether serum leptin levels were associated with multiple risk factor (MRF) clustering syndrome. We examined the relationship between serum leptin concentrations and blood pressure (BP), serum lipids levels, calculated insulin resistance (HOMA-ratio) and adiposity among 581 Japanese adult women.
The serum uric acid level has been said to be an independent predictor of cardiovascular disease death, mainly for women, and to be linked with the metabolic Syndrome X of insulin resistance, obesity, hypertension, and dyslipidemia. Recently, it has been suggested that the elevation of serum leptin, the ob gene product, may have a role in metabolic Syndrome X. Therefore, we studied the relationship of uric acid to leptin in 822 Japanese women in a cross-sectional manner. To estimate the effect of uric acid on the variables of metabolic Syndrome X, we calculated mean values of various components of the syndrome according to tertiles of uric acid (UA < 4.0 mg/dl, 4.0 < or = UA < 5.5, 5.5 < or = UA). Age, systolic and diastolic blood pressure (BP), body mass index (BMI), percent body fat mass (BFM), serum total cholesterol, triglyceride, atherogenic index, leptin, fasting immunoreactive insulin and homeostasis model assessment-ratio (HOMA-R: calculated insulin resistance) were significantly different across the uric acid tertiles with higher levels in the highest tertile in comparison to the first (ANOVA, p < 0.001, 0.001, 0.002, 0.001, 0.001, 0.025, 0.001, 0.001, 0.001, 0.001, 0.001, respectively), while high density lipoprotein cholesterol showed lower levels (p < 0.001). Serum leptin concentrations were also elevated in hyperuricemic women after adjusting for BMI or BFM (both p < 0.001), and were weakly correlated with serum uric acid concentrations (r = 0.22, p < 0.0001). BMI, HOMA-R, serum triglyceride, diastolic BP and age-adjusted serum leptin concentrations were calculated for each tertile of serum uric acid. Compared with the lowest tertile of uric acid level, BMI, HOMA-R, serum triglyceride, diastolic BP and age-adjusted leptin concentrations were higher in the highest tertile. In the stepwise regression analysis, serum leptin was the significant independent variable for uric acid values. These results indicate an independent relationship between leptin and uric acid, further supporting the involvement of leptin in metabolic Syndrome X.
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