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Obesity: Original Article |
Division of Endocrinology, Diabetes and Metabolism (A.M.X., C.C.C.), Center for Cardiovascular Disease Prevention, Methodist DeBakey Heart Center, and Section of Atherosclerosis, Department of Medicine (P.H.J., R.C.H., M.-Y.L., C.M.B.), and Section of Nutrition, Department of Pediatrics (E.O.S.), Baylor College of Medicine, Houston, Texas 77030; and Methodist Wellness Services (K.W.N.), The Methodist Hospital, Houston, Texas 77030
Address all correspondence and requests for reprints to: Christie M. Ballantyne, M.D., Baylor College of Medicine, 6565 Fannin Street, MS A-601, Houston, Texas 77030. E-mail: cmb{at}bcm.tmc.edu.
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-
(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- 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- concentrations did not change. Thus, increases in plasma levels of adiponectin or reductions in TNF- are not required for marked improvements in glucose/insulin and lipid metabolism with acute weight loss.
This work was supported by National Institutes of Health General Clinical Research Center Grant 5M01RR00350 and Texas Applied Technology Program Grant 004949-0093-2001. The atherosclerosis laboratory was supported by donations from George and Cynthia Mitchell, Nijad Fares, and Jeffrey Hines.
Abbreviations: ATP III, Adult Treatment Panel III; BMI, body mass index; CI, confidence interval; GGT, 
-glutamyltransferase; HDL-C, high-density lipoprotein cholesterol; HOMA-IR, insulin resistance of the homeostasis model assessment; hs-CRP, high-sensitivity C-reactive protein; MS+, metabolic syndrome positive; MS–, metabolic syndrome negative; NEFA, nonesterified fatty acid; OR, odds ratio; PPAR-, peroxisome proliferator-activated receptor-; TG, triglyceride; VLCD, very low-calorie diet.
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