BACKGROUND

Obesity may be regarded as a low-grade inflammatory state.

OBJECTIVE

The aim of this study was to evaluate changes in pro-inflammatory adipocytokines and the innate immune system, cardiovascular risk, and insulin sensitivity after massive weight loss.

METHODS

This was a longitudinal study.

METHODS

The study was conducted at Catholic University, Rome.

METHODS

There were 10 normoglucose-tolerant obese women evaluated before and 36 months after bilio-pancreatic diversion (BPD). Glucose sensitivity (M value) was estimated using the euglycemic-hyperinsulinemic clamp. Mannan-binding lectin (MBL), bactericidal/permeability increasing protein (BPI), alpha-defensins, soluble CD14 receptor (sCD14), C-reactive protein, adiponectin, leptin, visfatin, IL-6, and TNF-alpha were assayed.

RESULTS

After massive weight loss (53% of excess body weight), leptin (P <or= 0.0001), IL-6 (P <or= 0.0001), alpha-defensins (P <or= 0.001), and C-reactive protein (P <or= 0.0001) decreased significantly. Adiponectin increased significantly (P <or= 0.001). Of the nine subjects who lost more than 20% of body mass index, sCD14 (2.87 +/- 0.5 to 2.55 +/- 0.5; P = 0.016) and visfatin levels (12.20 +/- 0.93 to 10.63 +/- 1.93 ng/ml; P = 0.045) decreased significantly. No significant changes were observed in TNF-alpha, BPI, or MBL. Insulin sensitivity more than doubled after BPD (P <or= 0.0001). sCD14 changes were significantly associated with body mass index (r0 = 0.80; P = 0.003) and M changes (r0 = -0.59; P = 0.03). MBL correlated with insulin sensitivity in obese (r0 = 0.93; P = 0.0001) and post-BPD women (r(0) = 0.66; P = 0.038). Adiponectin correlated negatively with cardiovascular risk (r0 = -0.709; P = 0.02) and IL-6 (r0 = -0.634; P = 0.05). Multiple linear regression analysis showed that changes in sCD14 were also significantly related to changes in insulin sensitivity.

CONCLUSIONS

Surgically induced weight loss is capable of reversing low-grade inflammation, at least partially. The relationships between sCD14, MBL, BPI, and glucose sensitivity, and the role of TNF-alpha in obesity warrant further investigation.