ATGL-Mediated Fat Catabolism Regulates Mitochondrial Function Via PPAR- and PGC-1

A recent study unveils a fascinating role for an intra-cellular lipase in cardiac myocytes. The new results demonstrate that liberation of lipid species from myocyte neutral lipid stores results in activation of the nuclear receptor peroxisome proliferator-activated receptor (PPAR) and the transcriptional coactivators, PPAR coactivator 1 (PGC-1) and , chief regulators of cardiac mitochondrial fat burning capacity. Deficiency of this lipase in mice causes a cardiomyopathy with myocyte lipid accumulation and mitochondrial dysfunction. The adult mammalian heart burns enormous quantities of fatty acids (FA) to meet its high energy demand. FA import, storage, and oxidation must be tightly coordinated to maintain cardiac myocyte lipid balance while yielding sufficient fuel supply. Significant progress has been made in the delineation of gene regulatory networks involved in the coordinat