Diet-induced obese mouse hearts tolerate an acute high-fatty acid exposure that also increases ischemic tolerance

Abstract

An acute myocardial fat-load leads to oxidative stress, oxygen wasting, mechanical inefficiency, hyperacetylation, and impaired mitochondrial function, which can contribute to reduced ischemic tolerance. Following obesity/insulin resistance, hearts were less affected by a high fat-load, which subsequently also improved ischemic tolerance. This study highlights that an acute fat-load affects normal and obese hearts differently and that obesity renders hearts less vulnerable to the disadvantageous effects of an acute fat-load.