Sympathetic inhibition after bariatric surgery.

Abstract

See related article, pp 431–437 Starting in 1967, Edward E. Mason, a surgeon at the University of Iowa, boldly advocated and performed gastric bypass for intractable morbid obesity.1 Since then, bariatric surgery has emerged as the only proven effective treatment for morbid obesity, resulting in substantial and sustained weight loss and striking beneficial effects on the metabolic syndrome, particularly type 2 diabetes mellitus. In recent years, research on the beneficial effects of gastric bypass and vertical sleeve gastrectomy (VSG) has shifted from the contribution of simple gastric diversion and restriction to an energetic pursuit of the contribution of gastrointestinal hormones, secretions, and microbiome. In this issue of Hypertension , Seravalle et al2 from Grassi’s laboratory extend their impressive body of work on the sympathetic nervous system in human hypertension and obesity with the demonstration of another beneficial effect of bariatric surgery, namely pronounced and sustained sympathoinhibition after VSG in patients with severe obesity. Using direct, intramural recording recordings of sympathetic nerve activity (SNA) to the skeletal muscle, Seravalle et al2 report that VSG produces pronounced and sustained decreases in muscle SNA, body weight, plasma leptin, and systolic blood pressure (BP) at 6 and 12 months after surgery, whereas their measure of insulin sensitivity was improved at 6 but not 12 months. Seravalle et al2 conclude that the sympathoinhibition may be related to decreases in plasma leptin attendant to reduction in adiposity. The investigators highlight the temporal dissociation of changes in muscle SNA and insulin sensitivity and suggest that changes in insulin sensitivity and SNA after VSG are …