HADP-61HK Sigma-AldrichHuman Adiponectin RIA

Objective. n-3 long-chain polyunsaturated fatty acids (LCPUFAs) have shown potential to increase lipid oxidation and prevent obesity. Subjects. Seventy-eight boys aged 13-15?y with whole-body fat% of 30 ± 9% were randomly assigned to consume bread with fish oil (FO) (1.5?g n-3 LCPUFA/d) or vegetable oil for 16 weeks. All boys were counselled to improve diet and exercise habits. Results. Lifestyle counselling resulted in decreased sugar intake but did not change the physical activity level. Whole-body fat% decreased 0.7 ± 2.5% and 0.6 ± 2.2%, resting metabolic rate after the intervention was 7150 ± 1134?kJ/d versus 7150 ± 1042?kJ/d, and the respiratory quotient was 0.89 ± 0.05 versus 0.88 ± 0.05, in the FO and control group, respectively. No group differences were significant. Conclusion. FO-supplementation to slightly overweight teenage boys did not result in beneficial effects on RMR, lipid oxidation, or body composition.

OBJECTIVES: The aim of the study was to assess the association between visceral and subcutaneous fat with glucose intolerance, adipocytokines, inflammatory markers and carotid IMT in Asian Indians.DESIGN AND METHODS: Subjects with NGT (n=85), IGT (n=49) and T2DM (n=93) were randomly selected from CURES. Total abdominal, visceral and subcutaneous fat were measured using Helical CT scan. Adiponectin, hs-CRP, TNF-alpha, oxidized LDL, visfatin and leptin and IMT and insulin resistance were assessed.RESULTS: Total abdominal fat (p=0.041) and the visceral fat (p=0.039) but not subcutaneous fat progressively increased from NGT, IGT and T2DM subjects. With increasing quartiles of visceral fat, there was a significant increase in insulin resistance (p=0.040); significant decrease in adiponectin (p=0.043) and increase in TNF-alpha (p=0.028), hs-CRP (p=0.043), OX-LDL (p=0.034) and visfatin (p=0.040), and carotid IMT (p=0.047) was observed.CONCLUSION: Visceral fat levels increased with increasing glucose intolerance and are associated with decreased levels of adiponectin and increased levels of hs-CRP, TNF-alpha, oxidized LDL, visfatin, HOMA-IR and IMT.Copyright © 2010 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.

Summary The aim of this cross-sectional study was to find possible relationships between insulin-like growth factor-1 (IGF-1), adipocytokines (leptin and adiponectin) and twitch contraction (TC) characteristics of the knee extensor (KE) muscles in healthy physically active postmenopausal women (n = 28, 64-78 years old). We hypothesized that IGF-1 is related at least to isometric TC peak torque (Pt) as the highest value of isometric torque production and maximal voluntary contraction (MVC) torque, and there will not be any relationships between TC characteristics and leptin and adiponectin. During the measurement of MVC torque and twitch contractile properties of KE muscles, the subjects sat in a custom-made dynamometric chair with the knee and hip angles equal to 90 degrees and 100 degrees , respectively. To assess the contractile properties of the KE muscles, electrically evoked isometric twitch was elicited by percutaneous electrical nerve stimulation. Serum leptin, adiponectin, IGF-1, insulin-like growth factor-binding protein-3 (IGFBP-3) and insulin were determined. There were a very few significant relationships between the measured muscle contractile parameters and fasting blood hormones. TC Pt correlated significantly with IGFBP-3 (r = 0.652, P = 0.001) and insulin (r = 0.495, P = 0.007). In conclusion, this study suggests that only TC peak torque correlated positively with serum fasting IGFBP-3 and insulin concentration. Adipocytokines leptin and adiponectin not correlated significantly with measured strength parameters in physically active postmenopausal women.

Adiponectin may play a role in the development of type 2 diabetes and cardiovascular disease (CVD). However, little is known about the relationship between adiponectin and impaired glucose tolerance (IGT). We investigated the association between adiponectin and IGT and between adiponectin and cardiovascular risk factors among subjects with IGT.

The association between premature pubarche (PP) and metabolic syndrome is controversial and not supported by some authors. The aim of this study was to determine insulin resistance syndrome, plasma adiponectin, and fatty acid profile in PP girls to discern potential confounder variables and markers of metabolic disturbances. We studied 22 prepubertal girls with a diagnosis of PP and 20 healthy controls who differed in body mass index (BMI) (19.33 +/- 0.71 vs 17.30 +/- 0.60). We evaluated insulin resistance syndrome components and postprandial response of adiponectin, nonesterified fatty acids, and fatty acid profile after consumption of a standardized breakfast. No lipid disturbances were detected in the PP group. High-density lipoprotein to low-density lipoprotein cholesterol ratio tended to be lower in PP girls (P = .052), but this effect disappeared when data were adjusted for both BMI and age (P = .480). Insulin levels tended to be higher at 2 hours in PP girls, who showed significantly higher C-peptide area under the curve. In contrast, adiponectin at 3 hours after the meal and postprandial adiponectin area under the curve were significantly lower. The PP girls showed significantly higher percentages of eicosapentaenoic acid in total plasma and plasma phospholipids. No differences were found in the postprandial fatty acid clearance rate. In conclusion, PP girls and controls differed in postprandial plasma adiponectin response and in postprandial plasma C-peptide response after both BMI and age adjustment. Cholesterol plasma disturbances were mainly attributable to their higher BMI, although n-3 polyunsaturated fatty acids were higher because of the PP.

OBJECTIVE-Observations of elevated circulating concentrations of visfatin (PBEF/Nampt) in obesity and diabetes suggest that this recently described adipokine is involved in the regulation of body weight and metabolism. We examined in humans whether visfatin is found in cerebrospinal fluid (CSF) and, if so, how CSF visfatin concentrations relate to adiposity and metabolic parameters. RESEARCH DESIGN AND METHODS-We measured visfatin concentrations in the plasma and CSF of 38 subjects (18 men and 20 women; age 19-80 years) with a wide range of body weight (BMI 16.24-38.10 kg/m(2)). In addition, anthropometric parameters and endocrine markers were assessed. Bivariate correlation coefficients were determined and stepwise multiple regression analyses were performed to detect associations of CSF and plasma visfatin levels with relevant parameters. RESULTS-Plasma visfatin levels increased with rising BMI (P 0.0001) and body fat mass (P 0.0001). In contrast, CSF visfatin levels decreased with increasing plasma visfatin concentrations (P 0.03), BMI (P 0.001), body fat mass (P 0.0001), and insulin resistance (P 0.05). Body fat was the only factor independently associated with CSF visfatin, explaining 58% of the variation of CSF visfatin levels (P 0.0001). Neither plasma (P 0.13) nor CSF (P 0.61) visfatin concentrations differed between men and women. CONCLUSIONS-Our data indicate that visfatin concentrations in human CSF decrease with rising body fat, supporting the assumption that visfatin transport across the blood-brain barrier is impaired in obesity and that central nervous visfatin insufficiency or resistance are linked to pathogenetic mechanisms of obesity.

Abstract. Henneman P, Janssens ACJW, Carola Zillikens M, Frolich M, Frants RR, Oostra BA, van Duijn CM, van Dijk KW (Leiden University Medical Center, Leiden; Erasmus Medical Center, Rotterdam, The Netherlands). Menopause impacts the relation of plasma adiponectin levels with the metabolic syndrome. J Intern Med 2009; doi: 10.1111/j.1365-2796.2009.02162.xObjective. Plasma adiponectin is negatively correlated with metabolic syndrome (MetS) components obesity and insulin sensitivity. Here, we set out to evaluate the effect of menopause on the association of plasma adiponectin with MetS. Design. Data on plasma adiponectin and MetS were available from 2256 individuals participating in the Erasmus Rucphen Family study. Odds ratios for MetS were calculated by logistic regression analysis using plasma adiponectin quartiles. The discriminative accuracy of plasma adiponectin for MetS was determined by calculating the area under the curve (AUC) of receiver operator. Analyses were performed in women and men, pre- and postmenopausal women and younger and older men. Results. Virtually all determinants of MetS differed significantly between groups. Low plasma adiponectin showed the highest risk for MetS in postmenopausal women (odds ratio = 18.6, 95% CI = 7.9-44.0). We observed a high discriminative accuracy of age and plasma adiponectin for MetS not only in postmenopausal women (AUC = 0.76) but also in other subgroups (AUC from 0.67 to 0.87). However, in all groups, the discriminative accuracy of age and body mass index (BMI) for MetS was similar to the discriminative accuracy of age and plasma adiponectin. Conclusions. Low plasma levels of adiponectin are associated with increased prevalence of MetS, especially in postmenopausal women. Age and BMI have similar discriminatory accuracies for presence of MetS when compared with age and plasma adiponectin. Thus, we conclude that the association of plasma adiponectin with MetS is significantly affected by menopause but challenge the additional value of adiponectin for the discriminatory accuracy for presence of MetS.

The goal of this study was to determine the magnitude by which acute consumption of fructose in a morning bolus would stimulate lipogenesis (measured by infusion of 13C1-acetate and analysis by GC-MS) immediately and after a subsequent meal. Six healthy subjects [4 men and 2 women; aged (mean +/- SD) 28 +/- 8 y; BMI, 24.3 +/- 2.8 kg/m(2); and serum triacylglycerols (TG), 1.03 +/- 0.32 mmol/L] consumed carbohydrate boluses of sugars (85 g each) in a random and blinded order, followed by a standardized lunch 4 h later. Subjects completed a control test of glucose (100:0) and a mixture of 50:50 glucose:fructose and one of 25:75 (wt:wt). Following the morning boluses, serum glucose and insulin after 100:0 were greater than both other treatments (P 0.05) and this pattern occurred again after lunch. In the morning, fractional lipogenesis was stimulated when subjects ingested fructose and peaked at 15.9 +/- 5.4% after the 50:50 treatment and at 16.9 +/- 5.2% after the 25:75 treatment, values that were greater than after the 100:0 treatment (7.8 +/- 5.7%; P 0.02). When fructose was consumed, absolute lipogenesis was 2-fold greater than when it was absent (100:0). Postlunch, serum TG were 11-29% greater than 100:0 and TG-rich lipoprotein-TG concentrations were 76-200% greater after 50:50 and 25:75 were consumed (P 0.05). The data demonstrate that an early stimulation of lipogenesis after fructose, consumed in a mixture of sugars, augments subsequent postprandial lipemia. The postlunch blood TG elevation was only partially due to carry-over from the morning. Acute intake of fructose stimulates lipogenesis and may create a metabolic milieu that enhances subsequent esterification of fatty acids flowing to the liver to elevate TG synthesis postprandially.

The aim of the present study was to assess the plasma fatty acid composition of the total plasma lipids and lipid fractions in obese prepubertal children with and without metabolic syndrome (MS). Thirty-four obese prepubertal children were recruited: 17 who met MS criteria and 17 who did not; and twenty prepubertal children of normal weight. MS characteristics, insulin resistance (by homeostasis model assessment [HOMA-IR]), and plasma adiponectin (by radioimmunoassay) were recorded. Separation of lipid fractions was performed by liquid chromatography and the concentration of fatty acids in total plasma lipids and fractions was determined by gas-liquid chromatography. Concentrations of 16:1n-7, 16:1n-9, 18:3n-3, 22:6n-3, and n-3 PUFA in total plasma lipids (P 0.05) and of 16:0, 16:1n-7, 18:1n-9, 18:2n-6, and n-6 PUFA in triacylglycerols (TG) (P 0.05) were significantly higher in obese MS versus normal-weight children. Increased risk of MS was positively associated with plasma concentration of 16:1n-7 and negatively associated with proportion of 20:4n-6 (OR 2.76; P = 0.004; OR 0.56, P = 0.030, respectively). Saturated FA in TG were associated with HOMA-IR (R = 0.349, P = 0.017) and 22:5n-6 with adiponectin (R = 0.336, P = 0.05). In conclusion, increased concentrations of 16:1n-7 and decreased proportions of 20:4n-6 and 22:5n-6 in plasma lipids appear to be early markers of MS in children at prepubertal age.

The association of body fat mass (FM) with bone mineral mass (BMC) and bone mineral density (BMD) has been attributed to a mechanical load exerted on the skeleton by FM and by the effect of different hormones. The aim of the present study was to determine whether there is a relationship between ghrelin, adiponectin, and leptin with BMC and BMD in healthy postmenopausal women (n = 88; age, 68.9 +/- 6.8 years; body mass index, 27.4 +/- 3.6 kg/m(2)). Body composition, BMC, and BMD were derived by dual-energy X-ray absorptiometry. Waist-to-hip (WHR) and waist-to-thigh (WTR) ratios were also obtained. Ghrelin was associated with total BMC (beta = -0.945; P = 0.0001), total BMD (beta = -0.959; P = 0.0001), lumbar spine BMD (beta = -0.945; P = 0.0001), and femoral neck BMD (beta = -0.957; P = 0.0001), and remained associated (P 0.041) in different analyses that controlled for measured body composition and hormonal and insulin resistance values. However, the associations between ghrelin and measured bone mineral values were no longer significant (P 0.149) when adjusted for body fat distribution values (WHR, WTR). Adiponectin was significantly related to total BMC (beta = -0.931; P = 0.0001), total BMD (beta = -0.940; P = 0.0001), lumbar spine BMD (beta = -0.937; P = 0.0001), and femoral neck BMD (beta = -0.940; P = 0.0001) values, and these relationships remained significant (P 0.019) after adjusting for measured body fat, hormonal, and insulin resistance values but not when adjusted for fat-free mass (FFM; P 0.106). In addition, significant associations of leptin with total BMC (beta = 0.912; P = 0.0001), total BMD (beta = 0.907; P = 0.0001), lumbar spine BMD (beta = 0.899; P = 0.0001), and femoral neck BMD (beta = 0.906; P = 0.0001) were found. These associations remained significant (P 0.010) in different analyses that controlled for hormonal and insulin resistance values, but the associations between leptin and bone mineral values were no longer significant (P 0.145) when adjusted for specific body composition values (WHR, WTR, FM, and FFM). In conclusion, it appears that the influence of plasma ghrelin, adiponectin, and leptin levels on BMC and BMD values is mediated or confounded by the specific body composition parameters in healthy postmenopausal women.