High protein diet worsens mitochondrial function and increases susceptibility to ROS‐induced permeability transition in pathological cardiac hypertrophy

Abstract

The goal of this study was to determine the effects of high protein intake on cardiac function, mitochondrial respiration and H2O2‐induced mitochondrial permeability transition (MPTP) in pressure overload induced heart failure. Rats underwent either transverse aortic constriction (TAC) to induce hypertrophy and heart failure, or sham surgery, and were fed a diet with either 18% or 30% of energy as protein from casein. After 14 weeks ejection fraction was lower and LV mass increased in TAC vs. Sham, with no effect of diet. Isolated mitochondria showed no effect of TAC on respiration with the 18% protein diet, however the 30% protein diet decreased state III in subsarcolemmal mitochondria (SSM) with palmitoyl carnitine (sham: 202 ± 11, TAC: 185 ± 8.1, sham protein: 209 ± 9.7 and TAC protein: 152 ± 11* p<0.05). H2O2‐induced MPTP was increased by TAC in both SSM and interfibrillar mtiochondria, and significantly worsened in SSM by the 30% protein diet in TAC animals. These results suggest that high protein intake worsens mitochondrial function in pathological hypertrophy.