In Reply In his letter regarding our study,1 De Vita postulates that downregulation of the proinflammatory cytokine interleukin 32 (IL-32) could be a mechanism by which obesity-related inflammation and type 2 diabetes improve after metabolic/bariatric surgery. We do not disagree. Clearly, the mechanisms of action of bariatric surgery for achieving the profound and long-lasting diminution in appetite and body weight, along with myriad metabolic improvements, suggest that the physiologic changes induced by bariatric operations are far more complex than the relatively simple gut/anatomic changes would predict.2 However, it is also unlikely that wide-ranging anti-inflammatory effects of surgery are accounted for by the change in a single mediator.
Inge TH, Zeitler PS. Potential Effects of Bariatric Surgery and Reduced Interleukin 32 Levels on Type 2 Diabetes and Its Comorbidities—Reply. JAMA Pediatr. 2018;172(10):986–987. doi:10.1001/jamapediatrics.2018.2360
Coronavirus Resource Center
Customize your JAMA Network experience by selecting one or more topics from the list below.
Create a personal account or sign in to: