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Circulation adiponectine levels in male adult patients: Influence of abdominal obesity and hypertriglyceridemia (pp. 145-158) $100.00
Authors:  (T. Meroño, L. Gómez Rosso, M. Menafra, G. Giunta, L. Boero, L. Schreier, L. Cuniberti, Fernando D. Brites)
Abstract:
Recent studies have revealed that adiponectin facilitates insulin action and presents antiatherogenic properties. However, data on the regulation of adiponectin plasma concentration and its relationship with abdominal obesity, with hypertriglyceridemia (HTG) and other metabolic characteristics are still insufficient.
To describe the main factors conditioning plasma adiponectin concentration and to evaluate its association with abdominal obesity and biomarkers of insulin resistance and vascular inflammation in a cohort of male adults attending a health centre.
Male adults attending Favaloro Hospital, Buenos Aires, Argentina, at time of a health control were enrolled. Patients were excluded if they presented diabetes, thyroid, renal or hepatic diseases, previous history of cardiovascular disease, or actual treatment with drugs known to affect carbohydrate or lipid metabolism. Plasma levels of glucose, insulin, triglycerides (TG), total cholesterol, HDL-C, remnant lipoproteins (RLP)-C and LDL-C were measured by standardized methods. CETP activity and the concentrations of adiponectin and endothelial-derived cell adhesion molecules (VCAM-1, ICAM-1 and E-
selectin) were also determined. Subjects were divided according to WC quartiles: Q1) WC < 90cm (n = 22); Q2) WC 90-98cm (n = 26); Q3) WC 99-103cm (n = 18); and Q4) WC > 103cm (n = 20). Linear trends across WC quartiles were analyzed. Effects of abdominal obesity and HTG (TG>150mg/dl) on adiponectin were evaluated in a linear model adjusted by confounders.
Across WC quartiles, positive linear trends were evidenced for age, hypertensive and HTG subjects, insulin concentration, HOMA-IR, TG, RLP-C, CETP activity and VCAM-1 levels; while, negative ones for HDL-C, RLP-C/TG ratio and adiponectin (all p < 0.05). Furthermore, adiponectin levels were correlated with WC (r = -0.28, p < 0.01), glucose (r= -0.25, p < 0.05), HOMA-IR (r = -0.40, p < 0.001), TG (r = -0.31, p < 0.005), HDL-C (r = 0.26, p < 0.05), RLP-C (r = -0.29, p < 0.01), VCAM-1 levels (r = -0.48, p < 0.001) and CETP activity (r = -0.28, p < 0.01). Furthermore, abdominal obesity did not exert a significant effect on circulating adiponectin concentration while HTG did (F = 4.69, p < 0.05). In addition, subjects with HTG displayed lower adiponectin than non-HTG ones, only when they fitted the Q1 and Q2 (4.7 [2.8-6.2] vs. 6.7 [5.3-10.7] μg/ml, p < 0.001 for Q1 and Q2 individuals and 4.6 [3. 2-6.0] vs. 5. 1 [3.9-7.1]μg/ml, p > 0.05, for Q3 and Q4 subjects). Moreover, adiponectin antiatherogenic properties were evidenced as its concentration explained a 22% of VCAM-1 levels total variance.
Patients with higher grade of abdominal obesity, in addition to increment in markers of insulin resistance, presented higher levels of biomarkers of vascular inflammation and atherosclerosis. Adiponectin plasma levels remained high only in patients with low WC and without HTG. TG concentration might be a better tool than WC for easily identifying subjects with low adiponectin concentration, whose vascular beds might be less protected. 


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Circulation adiponectine levels in male adult patients: Influence of abdominal obesity and hypertriglyceridemia (pp. 145-158)