Purpose of review: Obesity is an independent risk factor for cardiovascular disease (CVD) and promotes CVD risk factors. Bariatric surgery has gained much favor because it ameliorates CVD. This review examines the current evidence for the mechanism behind this, which is currently thought to occur in part by reduction of adiposopathy, or dysfunctional adipose tissue, through modulation of adipokine secretion.
Recent findings: Increased visceral fat in obesity leads to adiposopathy, due to the chronic inflammation present in this tissue. Bariatric surgery causes weight loss as well as reduction in insulin resistance, hypertension, dyslipidemia, cardiac hypertrophy, and mortality. It also causes changes in the adipokines adiponectin, leptin, and C-reactive protein, but not in tumor necrosis factor-α. These changes contribute to improved CVD risk, possibly through decrease of chronic inflammation.
Summary: The modulations in adipokine secretion that occur after bariatric surgery are involved with reduction in CVD risk factors, CVD, and CV mortality. On the basis of the known anti-inflammatory effects of adiponectin and the pro-inflammatory effects of leptin and CRP, reduction in chronic inflammation associated with less visceral fat after surgery may contribute to the reduction in CVD. This may promote improvement of endothelial dysfunction and insulin resistance. Further work is necessary to explore these relationships.