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July 17, 2013Circulation Heart FailureOpen Access

Cardiac Insulin-Resistance and Decreased Mitochondrial Energy Production Precede the Development of Systolic Heart Failure After Pressure-Overload Hypertrophy

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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

LZLiyan ZhangJJJagdip S. JaswalJUJohn R. Ussher

Discussion

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Overview

Metabolic shifts in pressure-overload mice warrant clinical caution; leaves open causal contribution to human HF.

Structured PICO

P
Population
Mice subjected to cardiac hypertrophy secondary to pressure-overload via abdominal aortic constriction, followed for up to 3 weeks.
I
Intervention
Abdominal aortic constriction (AAC)
O
Outcome
Rates of energy substrate metabolism and cardiac functionsurrogate

Cardiac insulin resistance and decreased mitochondrial oxidative metabolism are early metabolic changes that precede the development of systolic heart failure in pressure-overload hypertrophy.

Cite This Study

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.

synapsesocial.com/papers/6a6e7d74f44fa9f079dc31behttps://doi.org/10.1161/circheartfailure.112.000228
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