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Myocadium selects metabolic substrates, and energy cost efficiency is different among these substrates. The general concept that is widely accepted to date is that myocardial substrate selection (so-c...alled metabolic switch) is impaired under the pathological conditions such as heart failure and myocardial ischemia. So far, direct correlation between insulin resistance and mechanical cardiac performance has been poorly understood. Insulin resistance causes hypertension, hyperglycemia, dyslipidemia and sympathetic acceleration, and all these abnormailties increase cardiac workload. Therefore, cardiac energy demand-supply imbalance occurs due to impairment of myocardial glucose uptake and subcellular insulin signaling. Such myocardial metabolic dysregulation causes subclinical heart failure, and this situation is currently defined as insulin-resistant cardiomyopathy. This type of cardiomyopathy is visualized by cardiac imaging techniques such as positron emission tomography and magnetic resonance imaging, showing myocardial triglyceride accumulation (cardiac steatosis) and impaired glucose uptake in spite of preserved coronary perfusion. Therapeutic intervention to this cardiomyopathy is expected by life style normalization and drug intervention such as glucagon-like peptide-1 (DLP-1) agonists and dipeptidyl peptidase-4 (DPP-4) antagonists.続きを見る
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