TY - JOUR
T1 - Adiponectin, inflammation, and the expression of the metabolic syndrome in obese individuals
T2 - The impact of rapid weight lose through caloric restriction
AU - Xydakis, Antonios M.
AU - Case, Christopher C.
AU - Jones, Peter H.
AU - Hoogeveen, Ron C.
AU - Liu, Mine Yine
AU - O'Brian Smith, E.
AU - Nelson, Kathleen W.
AU - Ballantyne, Christie M.
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2004/6
Y1 - 2004/6
N2 - Severe obesity increases the prevalence of the metabolic syndrome, and moderate acute weight loss with a very low-calorie diet in obese subjects with the metabolic syndrome leads to significant metabolic benefits. Adiponectin has been implicated in both the pathogenesis of obesity-related insulin resistance and increased inflammation. We analyzed the relationship of the adipocyte-derived hormone adiponectin with indices of inflammation, adiposity, and insulin resistance in obese subjects with (MS+, n = 40) and without (MS-, n = 40) the metabolic syndrome and examined the acute effects of rapid weight loss. MS+ subjects had significantly lower adiponectin (7.6 ± 0.6 vs. 10.4 ± 0.6 μg/ml; P = 0.003) and significantly higher TNF-α (3.3 ± 0.2 vs. 2.8 ± 0.3 pg/ml; P = 0.004) levels compared with MS- subjects matched for age and body mass index. Plasma adiponectin and TNF-α levels were inversely related to the number of metabolic syndrome factors in a stepwise manner. After 4-6 wk of weight loss, there was marked improvement in glucose, insulin, leptin, and triglycerides, whereas adiponectin and TNF-α concentrations did not change. Thus, increases in plasma levels of adiponectin or reductions in TNF-α are not required for marked improvements in glucose/insulin and lipid metabolism with acute weight loss.
AB - Severe obesity increases the prevalence of the metabolic syndrome, and moderate acute weight loss with a very low-calorie diet in obese subjects with the metabolic syndrome leads to significant metabolic benefits. Adiponectin has been implicated in both the pathogenesis of obesity-related insulin resistance and increased inflammation. We analyzed the relationship of the adipocyte-derived hormone adiponectin with indices of inflammation, adiposity, and insulin resistance in obese subjects with (MS+, n = 40) and without (MS-, n = 40) the metabolic syndrome and examined the acute effects of rapid weight loss. MS+ subjects had significantly lower adiponectin (7.6 ± 0.6 vs. 10.4 ± 0.6 μg/ml; P = 0.003) and significantly higher TNF-α (3.3 ± 0.2 vs. 2.8 ± 0.3 pg/ml; P = 0.004) levels compared with MS- subjects matched for age and body mass index. Plasma adiponectin and TNF-α levels were inversely related to the number of metabolic syndrome factors in a stepwise manner. After 4-6 wk of weight loss, there was marked improvement in glucose, insulin, leptin, and triglycerides, whereas adiponectin and TNF-α concentrations did not change. Thus, increases in plasma levels of adiponectin or reductions in TNF-α are not required for marked improvements in glucose/insulin and lipid metabolism with acute weight loss.
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U2 - 10.1210/jc.2003-031826
DO - 10.1210/jc.2003-031826
M3 - Article
C2 - 15181044
AN - SCOPUS:2942677231
VL - 89
SP - 2697
EP - 2703
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
SN - 0021-972X
IS - 6
ER -