Key result
Dietary patterns directly regulate myocardial metabolic homeostasis, substrate selection, and mitochondrial function.
Why the study?
Dietary patterns are key determinants of myocardial metabolic homeostasis, but the molecular mechanisms through which diet regulates cardiac metabolism and how chronic nutritional exposures influence the myocardial energetic phenotype require detailed synthesis.
Dietary patterns and meal timing profoundly influence myocardial metabolic flexibility and bioenergetics, highlighting the potential for targeted nutritional strategies to prevent or manage heart failure and cardiometabolic diseases.
Dietary modulation of myocardial metabolism merits exploration in cardiometabolic care; leaves open whether specific patterns improve heart failure outcomes.
The heart is a highly energy-demanding organ that depends on metabolic flexibility to adjust substrate utilization in response to changes in nutrient availability, endocrine signals, and energetic demands. Accumulating evidence demonstrates that dietary patterns are key determinants of myocardial metabolic homeostasis, affecting substrate selection, mitochondrial function, nutrient-sensing pathways, and long-term transcriptional and epigenetic regulation. This review analyzes the molecular mechanisms through which diet regulates cardiac metabolism and explores how chronic nutritional exposures influence the myocardial energetic phenotype. The physiological regulation of cardiac substrate utilization is described, with emphasis on fatty acids, glucose, ketone bodies, and branched-chain amino acids, underscoring the importance of metabolic flexibility in sustaining cardiac efficiency. The regulation of substrate transport and oxidation is examined, including the roles of the carnitine shuttle, insulin signaling, AMPK, mTOR, PPARα–PGC-1α, SIRT3, and other nutrient-sensing networks that coordinate mitochondrial ATP production. The effects of dietary composition and meal timing, such as caloric restriction and intermittent fasting, are discussed as modulators of myocardial metabolism. The adverse effects of chronic nutrient excess are reviewed, including lipotoxicity, glucotoxicity, insulin resistance, mitochondrial dysfunction, oxidative stress, pseudo-hypoxia, fetal metabolic reprogramming, and maladaptive cardiac remodeling. Recent findings on the gut–heart axis, microbiota-derived metabolites, circadian regulation, and metabolic–epigenetic interactions are also considered. Overall, current evidence supports the view that diet is an important and potentially modifiable regulator of the cardiac metabolic phenotype. Advancing the understanding of diet–metabolism interactions may enable the development of targeted nutritional strategies to maintain metabolic flexibility, enhance cardiac bioenergetics, and prevent the progression of heart failure and other cardiometabolic diseases.
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Pacinella et al. (2026) conducted a review in Cardiometabolic diseases. Dietary patterns was evaluated. Dietary patterns act as key determinants of myocardial metabolic homeostasis, affecting substrate selection, mitochondrial function, and long-term transcriptional and epigenetic regulation.
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