Population
Mice subjected to cardiac hypertrophy secondary to pressure-overload as a result of an abdominal aortic…
Design
Preclinical
Follow-up
3 weeks
Key result
Abdominal aortic constriction in mice decreased ATP production by 37% and 47% at 2 and 3 weeks, and caused cardiac insulin-resistance prior to the development of systolic dysfunction.
Authors
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Metabolic shifts in pressure-overload mice warrant clinical caution; leaves open causal contribution to human HF.
Cardiac insulin resistance and decreased mitochondrial oxidative metabolism are early metabolic changes that precede the development of systolic heart failure in pressure-overload hypertrophy.
Zhang et al. (2013) studied Cardiac hypertrophy and heart failure. Abdominal aortic constriction (AAC) was evaluated on Rates of energy substrate metabolism and cardiac function. Abdominal aortic constriction in mice decreased ATP production by 37% and 47% at 2 and 3 weeks, and caused cardiac insulin-resistance prior to the development of systolic dysfunction.