Acute and chronic effect of bariatric surgery on circulating autotaxin levels.

Autotaxin (ATX), an adipose tissue‐derived lysophospholipase, has been involved in the pathophysiology of cardiometabolic diseases. The impact of bariatric surgery on circulating ATX levels is unknown. We examined the short‐ (24 h, 5 days) and longer‐term (6 and 12 months) impact of bariatric surgery; as well as the short‐term effect of caloric restriction (CR) on plasma ATX levels in patients with severe obesity. We measured ATX levels in 69 men and women (mean age: 41 ± 11 years, body mass index: 49.8 ± 7.1 kg/m2), before and after biliopancreatic diversion with duodenal switch surgery (BPD‐DS) as well as in a control group (patients with severe obesity without surgery; n = 34). We also measured ATX levels in seven patients with severe obesity and type 2 diabetes who underwent a 3‐day CR protocol before their BPD‐DS. At baseline, ATX levels were positively associated with body mass index, fat mass, insulin resistance (HOMA‐IR) as well as insulin and leptin levels and negatively with fat‐free mass. ATX concentrations decreased 26.2% at 24 h after BPD‐DS (342.9 ± 152.3 pg/mL to 253.2 ± 68.9 pg/mL, P < 0.0001) and by 16.4% at 12 months after BPD‐DS (342.9 ± 152.3 pg/mL to 286.8 ± 182.6 pg/mL, P = 0.04). ATX concentrations were unchanged during follow‐up in the control group (P = 0.4), and not influenced by short‐term CR. In patients with severe obesity, bariatric surgery induced a rapid and sustained decrease in plasma ATX levels. Acute changes in ATX may not be explained by bariatric surgery‐induced CR. Autotaxin (ATX) is an adipose tissue‐secreted enzyme involved in the pathophysiology of cardiometabolic diseases. The association between obesity and ATX levels is controversial. Whether bariatric surgery and/or caloric restriction influence plasma ATX levels is unknown. We asked whether bariatric surgery and/or caloric restriction influenced plasma ATX levels in patients with severe obesity. We found that bariatric surgery induced a rapid and sustained decrease in plasma ATX levels. Short‐term caloric restriction also did not influence ATX levels. Our results improve our understanding of the factors that influence ATX, a potential therapeutic target for the prevention and management of cardiometabolic diseases. [ABSTRACT FROM AUTHOR]