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. Author manuscript; available in PMC: 2014 Apr 1.
Published in final edited form as: Biochim Biophys Acta. 2012 Aug 31;1833(4):840–847. doi: 10.1016/j.bbamcr.2012.08.015

Figure 1.

Figure 1

Divergent substrate utilization in the hypertensive, hypertrophic and insulin resistant, diabetic hearts. The specific etiology of heart disease promotes different substrate utilization in the cardiac myocyte. Cardiac hypertrophy frequently associated with hypertension and ischemia promotes glucose utilization while obesity and diabetes favors increased fatty acid oxidation (FAO). PPARα activity is central to the control of FAO and its modulation in hypertrophy (down) or diabetes (up) contributes to the observed changes in fuel source. However, both substrate switches eventually lead to mitochondrial dysfunction contributing to the progression of clinical heart failure. LVH, left ventricular hypertrophy; PPARα, peroxisome proliferator- activated receptor alpha; PCr, phosphocreatine; TAG, triacylglycerol.