To provide a perspective by investigating the potential cross-talk between the adipose tissue and the kidney during obesity.
It is well established that excessive caloric intake contributes to organ injury. The associated increased adiposity initiates a cascade of cellular events that leads to progressive obesity-associated diseases such as kidney disease. Recent evidence has indicated that adipose tissue produces bioactive substances that contribute to obesity-related kidney disease, altering the renal function and structure. In parallel, proinflammatory processes within the adipose tissue can also lead to pathophysiological changes in the kidney during the obese state.
Despite considerable efforts to better characterize the pathophysiology of obesity-related metabolic disease, there are still a lack of efficient therapeutic strategies. New strategies focused on regulating adipose function with respect to AMP-activated protein kinase activation, NADPH oxidase function, and TGF-β may contribute to reducing adipose inflammation that may also provide renoprotection.
aCenter for Renal Translational Medicine, La Jolla, California, USA
bLaboratory of Experimental Nephrology, Faculty of Medicine, Université Libre de Bruxelles (ULB), Brussels, Belgium
cInstitute for Metabolomic Medicine, University of California San Diego, Veterans Affairs San Diego Healthcare System, La Jolla, California, USA
Correspondence to Kumar Sharma, MD, Center for Renal Translational Medicine, University of California San Diego, Veterans Affairs San Diego Healthcare System, Stein Clinical Research Building, 4th Floor, 9500 Gilman Drive, La Jolla, CA 92093-0711, USA. Tel: +1 858 822 0870; fax: +1 858 822 7483; e-mail: email@example.com