, Volume 21, Issue 9, pp 1413-1423
Date: 06 Feb 2011

Sleep Apnea Determines Soluble TNF-α Receptor 2 Response to Massive Weight Loss

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Abstract

Background

The effects of surgical weight loss (WL) on inflammatory biomarkers associated with sleep apnea remain unknown. We sought to determine if any biomarkers can predict amelioration of sleep apnea achieved by bariatric surgery. We hypothesized that surgical WL would substantially reduce severity of sleep apnea and levels of proinflammatory cytokines.

Methods

Twenty-three morbidly obese adults underwent anthropometric measurements, polysomnography, and serum biomarker profiling prior to and 1 year following bariatric surgery. We examined the effect of WL and amelioration of sleep apnea on metabolic and inflammatory markers.

Results

Surgical WL resulted in significant decreases in BMI (16.7 ± 5.97 kg/m2/median 365 days), apnea–hypopnea index (AHI), CRP, IL-6, sTNFαR1, sTNFαR2, and leptin levels, while ghrelin, adiponectin, and soluble leptin receptor concentrations increased significantly. Utilizing an AHI cutoff of 15 events/h, we found significantly elevated levels of baseline sTNFαR2 and greater post-WL sTNFαR2 decreases in subjects with baseline AHI ≥15 events/h compared to those with AHI <15 events/h despite no significant differences in baseline BMI, age, and ΔBMI. In a multivariable linear regression model adjusting for sex, age, impaired glucose metabolism, ΔBMI, and follow-up period, the post-WL decreases in AHI were an independent predictor of the decreases in sTNFαR2 and altogether accounted for 46% of the variance of ΔsTNFαR2 (P = 0.011) in the entire cohort.

Conclusions

Of all the biomarkers, the decrease in sTNFαR2 was independently determined by the amelioration of sleep apnea achieved by bariatric surgery. The results suggest that sTNFαR2 may be a specific sleep apnea biomarker across a wide range of body weight.

Parts of this study were presented at the Annual Congress of the European Respiratory Society, September 18–22, 2010, in Barcelona, Spain.

Research Funding Source

This study is supported by NIH HL 50381, HL80105, and NCRR UL1 RR 025005. Maria Pallayova is the recipient of a European Respiratory Society Fellowship Number LTRF 15-2008.