Effect of weight loss induced by gastric bypass on proinflammatory interleukin-18, soluble tumour necrosis factor-alpha receptors, C-reactive protein and adiponectin in morbidly obese patients.

OBJECTIVE: Interleukin-18 (IL-18) is a potent proinflammatory cytokine whose role in human obesity has recently been suggested. The aim of our study was to analyse in morbidly obese patients undergoing gastric bypass, the relationship of IL-18 with insulin resistance and with proinflammatory cytokines (tumour necrosis factor-alpha receptors, sTNFR), C-reactive protein (CRP) and with adiponectin.

DESIGN: Observational and prospective study.

PATIENTS: Sixty-five morbidly obese patients, aged 45 +/- 8.9 years, were studied before and 12 months after gastric bypass.

MEASUREMENTS: We analysed plasma concentrations of IL-18, sTNFR, CRP and adiponectin.

RESULTS: Plasma concentrations of sTNFR2, IL-18 and CRP were decreased and adiponectin significantly increased after bypass surgery. In the multiple regression analysis, preoperative values of IL-18 remained significantly associated with preoperative triglycerides (beta = 0.47, P = 0.005) and TNFR2 (beta = 0.47, P = 0.004). R(2) for the model = 0.38. Postoperative IL-18 concentrations in the multiple regression analysis were significantly associated with postoperative homeostasis model assessment of insulin resistance (HOMA-IR) (beta = 0.092, P = 0.019) and triglycerides (beta = 0.40, P = 0.036). R(2) for the model = 0.46. IL-18 did not correlate with body mass index, fat mass, fat-free mass or body fat. No relationship was either found between adiponectin and IL-18, TNFR1 and -2 and CRP.

CONCLUSIONS: Massive weight loss induced by gastric bypass reduces IL-18, TNFR2 and CRP. IL-18 might be a marker of the chronic inflammatory process underlying insulin resistance but its lack of association with anthropometric and body composition parameters does not support a major secretion by human adipocytes. IL-18 and sTNFR1 and -2 do not play a main role in the inhibition of the secretion of adiponectin.