Key result
Cardiac hypertrophy was associated with cardiac insulin resistance, reduced fatty acid oxidation, decreased p38-MAPK levels, and mitochondrial damage, independent of systemic insulin resistance.
Why the study?
Cardiac insulin resistance plays an important role in the development of heart failure, but the underlying mechanisms remain unclear.
Does myocardial hypertrophy cause cardiac insulin resistance and mitochondrial damage independent of systemic insulin resistance?
Does myocardial hypertrophy cause cardiac insulin resistance and mitochondrial damage independent of systemic insulin resistance?
Cardiac insulin resistance caused by hypertrophy is associated with mitochondrial damage and cardiac dysfunction, and occurs independently of systemic insulin resistance.
Answers are grounded in this paper and cite their sources.
Hypertrophy-linked cardiac insulin resistance and mitochondrial damage remain preclinical; leaves open p38-MAPK targeting in human HF.
Cardiac insulin resistance plays an important role in the development of heart failure, but the underlying mechanisms remain unclear. Here, we found that hypertrophic hearts exhibit normal cardiac glucose oxidation rates, but reduced fatty acid oxidation rates, compared to Sham controls under basal (no insulin) conditions. Furthermore, insulin stimulation attenuated insulin's effects on cardiac substrate utilization, suggesting the development of cardiac insulin resistance. Consistent with insulin resistance, p38-MAPK protein levels were reduced in hypertrophic hearts. By contrast, systemic hyperinsulin-euglycemic clamp indicated normal insulin sensitivity. Finally, electron microscopy revealed severe mitochondrial damage in the hypertrophic myocardium. Our results indicate that that cardiac insulin resistance caused by cardiac hypertrophy is associated with mitochondrial damage and cardiac dysfunction. Moreover, our findings suggest that cardiac insulin resistance is independent of systemic insulin resistance, which is also a risk factor for heart failure.
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Zheng et al. (2019) studied Heart failure caused by myocardial hypertrophy. Myocardial hypertrophy vs. Sham controls was evaluated on Cardiac substrate utilization, p38-MAPK protein levels, and mitochondrial damage. Cardiac hypertrophy was associated with cardiac insulin resistance, reduced fatty acid oxidation, decreased p38-MAPK levels, and mitochondrial damage, independent of systemic insulin resistance.
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