The practice of calorie restriction involves eating fewer calories while still obtaining at least adequate levels of micronutrients. Mild calorie restriction might be a 10% reduction from recommended calorie levels, but as much as 40% is possible given sufficient diligence and attention to the details. Calorie restriction induces sweeping metabolic changes that collectively act to improve cell and tissue function. The present consensus is that the most important of these changes is enhanced autophagy. Autophagy is a collection of maintenance processes responsible for recycling damaged proteins and structures in the cell. In near all species assessed to date, calorie restriction slows aging and improves health.
Diet influences disease progression, yet the effects of fasting on acute kidney injury (AKI) and its transition to chronic kidney disease (CKD) remain unclear. This study evaluated fasting-mimicking diet (FMD) cycles versus ad libitum feeding in murine models of AKI and CKD induced by aristolochic acid or folic acid.
FMD significantly reduced serum creatinine, kidney injury, and maladaptive repair marker expression, and promoted faster recovery. It also lowered renal cytokines and pro-fibrotic genes, reduced CCL2 levels, and decreased monocyte recruitment while favoring protective monocyte phenotypes. Cycles of caloric restriction yielded similar nephroprotection. Initiating FMD at the peak of AKI enhanced repair and attenuated inflammation.
Inhibition of CCR2 abolished FMD’s protective effects, implicating the CCL2/CCR2 axis in mediating its benefits. However, broader anti-inflammatory actions may also contribute, and reduced CCL2 may reflect downstream effects. These findings highlight the potential of dietary interventions to modulate kidney injury and inflammation in AKI and CKD.
