Interleukin-16 is increased in obesity and alters adipogenesis and inflammation in vitro

Abstract

Introduction: Obesity is a chronic condition associated with low-grade</p><p>inflammation mainly due to immune cell infiltration of white adipose tissue</p><p>(WAT). WAT is distributed into two main depots: subcutaneous WAT (sWAT)</p><p>and visceral WAT (vWAT), each with different biochemical features and metabolic</p><p>roles. Proinflammatory cytokines including interleukin (IL)-16 are secreted by</p><p>both adipocytes and infiltrated immune cells to upregulate inflammation. IL-16</p><p>has been widely studied in the peripheral proinflammatory immune response;</p><p>however, little is known about its role in adipocytes in the context of obesity.</p><p>Aim & Methods: We aimed to study the levels of IL-16 in WAT derived from sWAT</p><p>and vWAT depots of humans with obesity and the role of this cytokine in</p><p>palmitate-exposed 3T3-L1 adipocytes.</p><p>Results: The results demonstrated that IL-16 expression was higher in vWAT</p><p>compared with sWAT in individuals with obesity. In addition, IL-16 serum levels</p><p>were higher in patients with obesity compared with normal-weight individuals,</p><p>increased at 6 months after bariatric surgery, and at 12 months after surgery</p><p>decreased to levels similar to before the intervention. Our in vitro models showed</p><p>that IL-16 could modulate markers of adipogenesis (Pref1), lipid metabolism</p><p>(Plin1, Cd36, and Glut4), fibrosis (Hif1a, Col4a, Col6a, and Vegf), and inflammatory</p><p>signaling (IL6) during adipogenesis and in mature adipocytes. In addition, lipid</p><p>accumulation and glycerol release assays suggested lipolysis alteration.</p><p>Discussion: Our results suggest a potential role of IL-16 in adipogenesis, lipid and</p><p>glucose homeostasis, fibrosis, and inflammation in an obesity context.