Lack of adiponectin in mice accelerates high-fat diet-induced progression of chronic kidney disease

Obesity is an independent risk factor for the development of chronic kidney disease. The pathophysiology of the obesity-induced kidney injury is complex, but evidence suggests the involvement of reduced adiponectin levels and signaling. We investigated the extent by which adiponectin contributes to the establishment and progression of renal disease in wild type (WT) and adiponectin null (adipoKO) mice fed a control or a high-fat diet (HFD) for 16 weeks. HFD induced obesity, kidney hypertrophy, albuminuria, renal lipid accumulation and decreased nephrin expression in both mice genotypes. Notably, HFD in adipoKO mice exacerbated progression of albuminuria in comparison to WT mice. In addition, lack of adiponectin per se increased kidney weight, reduced nephrin levels, up-regulated Fabp4 expression, reduced Cpt1a expression and increased miR-130 levels in kidney. Our results demonstrate that lack of adiponectin combined with a HFD contributes to accelerated kidney dysfunction. •Lack of adiponectin reduces nephrin levels in kidney equally to obesity.•Lack of adiponectin induces kidney hyperthrophy.•Lack of adiponectin reduces fatty acid oxidation.•Higher levels of miR-130b are found in kidney of adipoKO mice compared to WT.•Adiponectin protects obese mice from accelerated progression of kidney disease.