Adiponectin, Inflammation, and the Expression of the Metabolic Syndrome in Obese Individuals: The Impact of Rapid Weight Loss through Caloric Restriction

Abstract

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 microg/ml; P = 0.003) and significantly higher TNF-alpha (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-alpha 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-alpha concentrations did not change. Thus, increases in plasma levels of adiponectin or reductions in TNF-alpha are not required for marked improvements in glucose/insulin and lipid metabolism with acute weight loss.

Weight loss effect on inflammation and LDL oxidation in metabolically healthy but obese (MHO) individuals: low inflammation and LDL oxidation in MHO women

“…25,26 Given that the subjects remained obese after the present study's 12-week weight loss period, it seems likely that a critical amount of total adiposity must be lost before the weight loss effect on this cytokine is observed, so the adipocyte resumes a more balanced function. 27 At this time, the mechanisms regarding the different effects of weight loss shown in MHO and MAO individuals have not been elucidated. Although the MHO individuals' clinical markers did not reflect the beneficial effects of weight loss in the present study, these results should not persuade us to underestimate the positive effects of lifestyle modifications, including weight loss, on MHO individuals.…”

Effects of marked weight loss on plasma levels of adiponectin, markers of chronic subclinical inflammation and insulin resistance in morbidly obese women

“…26 Circulating adiponectin concentrations are reduced in patients with T2D and are associated with the metabolic syndrome. 9,27 Data from human cross-sectional studies have shown intra-abdominal adipose tissue as an important determinant of plasma adiponectin, implying that adiponectin might link visceral obesity and insulin resistance. Findings of Lihn et al 28 describing lower adiponectin gene expression in visceral adipose tissue support this hypothesis.…”

The Sir David Cuthbertson Medal Lecture Hunting for new pieces to the complex puzzle of obesity

“…Interestingly, in rodent models of atherosclerosis, such as ob/ob and apoEdeficient mice, adiponectin reportedly exerts a protective effect on the development of both atherosclerosis and type 2 diabetes mellitus (Frühbeck, 2004a;Lau et al 2005). The findings in animals have a certain clinical parallel in human subjects, evidenced by a negative correlation between adiponectinaemia and markers of inflammation (Pischon et al 2004;Xydakis et al 2004). Circulating adiponectin levels have been observed to be inversely correlated with insulin resistance and C-reactive protein concentrations (Ouchi et al 2003).…”