Modulation of energy metabolism in prevention of cardiac remodeling: Stimulation of peroxisome proliferator-activated alpha receptor (Project - 5198)

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Hypertension-induced pathological cardiac hypertrophy is an important risk factor for cardiac failure. In the hypertrophic heart, there is a switch in energy substrate preference from fatty acids to glucose. Alteration in energy metabolism is considered to play a role in the development of cardiac hypertrophy and its progression to failure, although the sequence of events remains to be elucidated. Long-term low rates of fatty acid oxidation will lead to energy deficit and accumulation of free radical species that might be toxic to the heart. The metabolic shift is facilitated by down regulation of the nuclear hormone receptor, peroxisome proliferator-activated receptor (PPAR)α. Hence, it was hypothesized that, “Stimulation of PPARα can reestablish a more ‘normal’ metabolic physiology, thereby maintaining cardiac function and preventing cardiac failure.” The aim of the study was to examine whether stimulation of fatty acid metabolism using PPARα agonists can prevent pathological cardiac remodeling.
Hypertension, Cardiac hypertrophy, Cardiac failure, PPAR, Fenofibrate, Medium chain triglycerides