Altered cytokine secretion from dysfunctional adipose tissue or “adiposopathy” is implicated in obesity related inflammation and may mediate reduced CVD risk in response to weight loss after bariatric surgery. We hypothesized that bariatric surgery reduces CVD risk by favorably altering the pro-inflammatory profile of adipose tissue as a result of weight loss.
In this observational study with repeated measures, 142 patients underwent bariatric surgery of which 45 returned for follow up at ~6 months. At both time-points, lipid profiles and levels of plasma adiponectin, leptin, and TNF-α were obtained. Ratios of various adipokine parameters were related to pre- and post- surgical (gastric bypass vs. other restrictive bariatric procedures) lipid ratios.
Prior to surgery, circulating adiponectin and the adiponectin/TNF-α ratio was strongly associated with CVD risk characterized by levels of triglycerides, HDL, and the TC/HDL, LDL/HDL and TG/HDL ratios (all P < 0.05). Following bariatric surgery, BMI was decreased by 22%, adiponectin was increased by 93%, and leptin decreased by 50% as compared to baseline (all P < 0.01). TNF-α levels increased by 120% (P < 0.01) following surgery. Post-surgical changes in adiponectin and the leptin/adiponectin ratio were strongly associated with incremental improvements in triglycerides, HDL, and TC/HDL, LDL/HDL and TG/HDL ratios (all P < 0.05). Roux-en-y gastric bypass surgery (RYGB) as compared to other bariatric procedures was associated with more robust improvements in BMI, HDL, and leptin/adiponectin ratio than other gastric restrictive procedures (P < 0.05).
Thus, bariatric surgery, especially RYGB, ameliorates CVD risk through a partial recovery from “adiposopathy”, distinctively characterized by improved adiponectin and the leptin/adiponectin ratio.