Naznin Dixit
University of Mississippi Medical Center, USA
Title: Smoking or use of nicotine products may enhance renal risk via augmented lipotoxicity in obese individuals
Biography
Biography: Naznin Dixit
Abstract
Obesity is currently recognized as an epidemic in both the United States and throughout the world and is linked to an increase in the incidence of chronic kidney injury both in adults and children. Obesity increases the risk of lipotoxic kidney injury, which initiates a cascade of events leading to chronic kidney injury and ultimately end-stage renal disease. Mediators of lipotoxicity are non-esterified Free Fatty Acids (FFA), levels of which are chronically elevated in obese persons. In the kidney, FFA accumulation elicits lipotoxic effects on proximal tubule cells by increasing production of Reactive Oxygen Species (ROS) and hence, oxidative stress. Several studies have confirmed adverse effects of smoking itself on kidney health. Nicotine (NIC), a major component of tobacco smoke, E-cigarettes and NIC replacement therapies-link smoking to kidney injury by inducing oxidative stress. Importantly, smoking/nicotine use increases FFA levels in the blood of smokers. Clinical studies have shown obesity and smoking as independent risk factors for renal damage, but the precise mechanism of their combined effects is not well understood. It has been propose that both obesity and smoking/nicotine use enhances renal lipid deposition leading to augmented renal oxidative stress/dysfunction. The hypothesis that chronic NIC exposure worsens renal oxidative stress in mice on High-Fat Diet (HFD) by altering the balance between expression of pro-oxidant and antioxidant genes was tested. Hence, obesity combined with nicotine product use may predict a worsening lipotoxic impact on the kidneys.