Chronic exposure to hyperpalatable diet promotes a subclinical kidney disease associated with tubular proteinuria and proximal tubule epithelial cell injury in a murine model

Obesity became a prevalent condition around the world over the past few decades. There are many causes for obesity development, but one important factor is the increased consumption and wide availability of highly palatable foods, rich in sugar and fat, such as: the cafeteria diet, a hyperpalatable diet. Also, the excess of weight is an important risk factor for the development of chronic diseases. Furthermore, high fat diets (HFD) are accompanied by increased oxidative stress in liver, kidney and heart tissues, as well as functional and metabolic changes. In addition, obesity is also considered to be an independent risk factor for chronic kidney disease (CKD). The pathological features of obesity-induced kidney disease are complex, and the main mechanisms are poorly understood. A large body of evidence shows that obesity induced by HFD promotes significant glomerular and tubular dysfunction. Although the deleterious consequences of HFD have been documented, changes in kidney morphology and function after chronic use are still unclear. Interestingly, some studies using cafeteria diets showed that they are good candidates to induce obesity and significant changes in kidney structure and function. However, mechanisms underlying this process need to be investigated.