Markers of chronic inflammation and obesity: a prospective study on the reversibility of this association in middle-aged women undergoing weight loss by surgical intervention

Abstract

BACKGROUND: Human adipose tissue expresses and releases proinflammatory cytokines and these measures of chronic inflammation have recently been associated with obesity. HYPOTHESIS: To test whether the proinflammatory state is reversible in subjects undergoing weight loss by surgical measures. SUBJECTS AND METHODS: Twenty morbidly obese women participated in this prospective study. Subjects were examined for fat mass, high-sensitive C-reactive protein (hs-CRP), interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-a) before and 1 y after Swedish adjustable gastric banding. RESULTS: Anthropometric measures displayed a significant reduction of the body mass index (BMI) from 41.6 AE 5.4 to 30.8 AE 6.1 kg=m 2 and the fat mass from 53.9 AE 10.3 to 29.8 AE 12.1 kg (mean AE s.d.). Hs-CRP levels decreased significantly from 1.33 AE 1.21 mg=dl in pre-gastric banding subjects to 0.40 AE 0.61 mg=dl in post-gastric banding subjects, respectively. IL-6 and TNF-a levels did not differ significantly between pre-and post-gastric banding subjects. CONCLUSIONS: We speculate that in these patients the marked reduction in C-reactive protein might be beneficial in reducing their cardiovascular risk and is not solely mediated by IL-6 and TNF-a.

Effect of weight loss on inflammatory and endothelial markers and FMD using two low-fat diets

“…16,36 CRP is positively associated with BMI and we and others have shown that energy striction and weight loss lowers CRP. 16,37,38 Ziccardi et al 7 found reductions in IL-6, VCAM-1 and ICAM-1 following weight loss of 10 kg however we demonstrated reductions in the ICAM-1 but not VCAM or IL-6. The reason for these differences is not clear although other studies with much greater weight loss have shown no change in IL-6, 38 whereas Nicoletti et al 9 and Esposito et al 39 observed reduction in IL-6 after weight loss.…”

Effect of diet-induced energy deficit and body fat reduction on high-sensitive CRP and other inflammatory markers in obese subjects

“…38,39,[52][53][54][55] The adipokines adiponectin and leptin have previously been connected with pro-inflammatory markers. A reduction in FM has been shown to induce a decline in leptin concentration 28,35,40,41 and a rise in adiponectin concentration. 14,15,29,40 However, the present study failed to provide the expected increase in adiponectin as a response to the fat loss possibly due to the study being simply underpowered.…”

“…16,28,29,35,36 However, only hs-CRP and IL-6 were Figure 2 Loading plot of factor structure of the pro-inflammatory markers high-sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), fibrinogen, haptoglobin, transferrin and the adipokines leptin and adiponectin. Factor 1 was related to fibrinogen (0.81), CRP (0.63), haptoglobin (0.71), IL-6 (0.64) whereas adiponectin, leptin and transferrin were not.…”

An immune origin of type 2 diabetes?

“…Here, again, polymorphisms in immune genes modulate risk, implying a pathogenetic significance for immune gene products Table 4 Interventions that have an impact on the inflammatory state Inflammatory mediators whose concentrations are reduced by weight loss and/or physical exercise [190][191][192][193][194][195][196][197][198][199][200][201][202][203][204][205][206][207] CRP, TNF-α, soluble TNF-α receptor 2, IL-6, IL-18, MCP-1, PAI-1, t-PA, soluble ICAM-1, soluble VCAM-1, P-selectin Inflammatory mediators whose concentrations are reduced by glucose-lowering drugs [186,188,[208][209][210][211][212][213][214][215][216][217] Sulphonylurea: TNF-α Metformin: CRP Glitazones: CRP, SAA, TNF-α, soluble CD40 ligand, PAI-1 Insulin: CRP, IL-1, IL-6, TNF-α, soluble ICAM-1, MCP-1, PAI-1 SAA Serum amyloid A, t-PA tissue plasminogen activator, VCAM-1 vascular cell adhesion molecule-1 [171][172][173]. Where studied, the upregulation of inflammatory mediators was linked to increased oxidative stress, impaired mitochondrial function and abnormal cholesterol metabolism [174][175][176].…”