Exploring the impact of bariatric surgery on high density lipoprotein

Abstract Low HDL cholesterol is an independent cardiac risk factor. A general efficacy gradient exists for the resolution of cardiovascular risk factors after bariatric surgery (i.e., biliopancreatic diversion [BPD]>Roux-en-Y gastric bypass [RYGB]>sleeve gastrectomy [SG]>adjustable gastric banding [AGB]). However, a review of high level of evidence clinical studies shows a different hierarchy for the effect of bariatric surgery on HDL (i.e., RYGB=SG>BPD, AGB). Surgically induced weight loss effectively reverses many steps in HDL metabolism that have been altered with obesity. Furthermore, enterocytes contribute to HDL levels through the synthesis of apolipoproteins A-IV and A-I. RYGB and SG that preserve the small intestine (particularly the jejunum) lead to a significant rise in HDL. However, when the small intestinal contribution does not reinforce the weight loss dependent mechanisms (e.g., after BPD and AGB), only a modest rise in HDL occurs. Further experimental and clinical studies are required to better delineate the issue.