PubMed · 15084735
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Mitch Leslie. 2004-04-14. Lightheaded.. https://doi.org/10.1126/sageke.2004.15.nf41
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OBJECTIVE: To examine the determinants of adiponectin levels (i) in 23 women with anorexia nervosa (mean BMI 15.0 +/- 1.2) and 43 healthy normal weight females (mean BMI 22.3 +/- 2.3; cross-sectional design) as well as (ii) after six and twelve weeks of weight gain in subgroups of 18 and 11 anorectic patients (mean weight gain 5.8 kg; longitudinal design). Plasma adiponectin and leptin concentrations were measured and their relationships to body composition (fat mass by bioelectrical impedance analysis and anthropometrics), different hormones and metabolic parameters (insulin, ACTH, cortisol, glucose, FFA, lipid profile) were investigated. RESULTS: In anorectic patients, adiponectin levels were higher (+29 %) and leptin levels were lower (-75 %) than in control subjects. There was a high variance in adiponectin levels in patients ranging from 2.6 to 18 nM. Combining patients and controls, an inverse linear correlation was observed between adiponectin levels and fat mass (r = -0.36, p < 0.05), while a positive exponential relation was found between leptin levels and fat mass (r = 0.82, p < 0.001). In anorectic patients, there were no significant correlations between adiponectin and hormonal or metabolic parameters. Weight gain resulted in increasing leptin (+0.17 +/- 0.12 nM; p < 0.001) and a nonsignificant decrease in adiponectin concentrations (-1.12 +/- 2.51 nM). Changes in leptin levels were mainly explained by a gain in fat mass (r = 0.85, p < 0.001). In contrast, changes in adiponectin levels were closely linked to initial adiponectin levels (r = -0.84, p < 0.001) but not to changes in fat mass or BMI. CONCLUSION: Cross-sectionally serum adiponectin concentration followed a linear inverse function with fat mass when patients and controls were combined. Longitudinally gain in fat mass was not associated with changes in adiponectin levels suggesting other yet unidentified influences on adiponectin secretion in anorexia nervosa.
Plasma levels of adiponectin are decreased in patients with nonalcoholic fatty liver disease (NAFLD), but the relationship among plasma adiponectin, insulin sensitivity, and histological features is unclear. In 174 NAFLD patients and 42 controls, we examined plasma adiponectin concentrations in relation to 1) lipid profile, indices of insulin resistance, and features of the metabolic syndrome (n = 174); 2) hepatic insulin resistance (clamp technique with tracer infusion) (10 patients); and 3) histological features at liver biopsy (n = 116). When the data from all subjects were combined, plasma adiponectin levels were positively associated with increased age, female gender, and plasma high-density lipoprotein levels, and negatively associated with waist circumference, body mass index, triglycerides, indices of insulin resistance, and aminotransferase levels, and also predicted the presence of the metabolic syndrome. In step-wise regression, increased age, female gender, waist circumference, triglyceride levels, and homeostasis model assessment independently associated with adiponectin (adjusted R(2), 0.329). In NAFLD, adiponectin was only associated with increased age, female gender, and triglycerides (adjusted R(2), 0.245). When the measured histological parameters were included in the model, plasma adiponectin levels were also inversely proportional to the percentage of hepatic fat content (adjusted R(2), 0.221), whereas necroinflammation and fibrosis did not fit in the model. Adiponectin was negatively correlated with insulin-suppressed endogenous glucose production during the clamp (P = 0.011). The results demonstrate that decreased levels of circulating adiponectin in NAFLD are related to hepatic insulin sensitivity and to the amount of hepatic fat content. Hypoadiponectinemia in NAFLD is part of a metabolic disturbance characterized by ectopic fat accumulation in the central compartment.
There is a wide interindividual variation in peripheral insulin sensitivity at any given body mass index or percent body fat among obese adolescents with normal glucose tolerance. The goals of this study were to determine whether variability in insulin sensitivity is associated with differences in patterns of lipid partitioning or substrate use under fasting and hyperinsulinemic conditions. We compared 14 obese insulin-resistant adolescents with 14 obese insulin-sensitive controls, pair matched for age, gender, pubertal stage and body composition. Insulin sensitivity was assessed by the hyperinsulinemic-euglycemic clamp, intramyocellular lipid content by (1)H-nuclear magnetic resonance and visceral fat by magnetic resonance imaging. Obese insulin-sensitive subjects had lower intramyocellular (1.64 +/- 0.68 vs.2.26 +/- 0.62% of water peak, P = 0.017) and visceral lipid deposition (45 +/- 23 vs. 77 +/- 52 cm(2), P = 0.04) and a higher level of adiponectin, compared with their obese-resistant counterparts (8.8 +/- 3.6 vs. 6.5 +/- 1.8 mug/dl, P = 0.015). Glycerol fluxes were similar between the two obese groups yet occurred in the face of different concentrations of insulin. Intramyocellular lipid and visceral fat were negatively related to insulin sensitivity. Obese insulin-sensitive adolescents are characterized by lower lipid deposition in the intramyocellular and visceral compartments and greater levels of adiponectin, despite similar degree of adiposity.