Present study investigated which diet, high-carbohydrate (HCD) or high-fat (HFD), most effectively induces classical characteristics of obesity in mice. Mice were fed commercial chow (control), an HCD, or an HFD for 12 weeks. HFD and HCD increased body weight, fat mass, and glycaemia, whereas the HFD augmented insulinemia. In the kidney, the HFD caused albuminuria, and reductions in fractional Na+ excretion, Thromboxane B2 (TXB2) excretion, and urinary flow, whereas the HCD reduced glomerular filtration, plasma osmolality, and TXB2 and Prostaglandin E2 excretion. The consumption of HFD and HCD modified parameters that indicate histopathological changes, such as proliferation (proliferating-cell-nuclear antigen), inflammation (c-Jun N-terminal-protein), and epithelial-mesenchymal transition (vimentin, and desmin) in renal tissue, but the HCD group presents fewer signals of glomerular hypertrophy or tubule degeneration. In summary, the HCD generated the metabolic and renal changes required for an obesity model, but with a delay in the development of these modifications concerning the HFD.
Keywords: Renal function; epithelial–mesenchymal transition; high-fat diet; inflammation; obesity.