There is a constant high demand for energy to sustain the continuous contractile activity of the heart, which is met primarily by the β-oxidation of long-chain fatty acids. The control of fatty acid β-oxidation is complex and is aimed at ensuring that the supply and oxidation of the fatty acids is sufficient to meet the energy demands of the heart. The metabolism of fatty acids via β-oxidation is not regulated in isolation; rather, it occurs in response to alterations in contractile work, the presence of competing substrates (i.e., glucose, lactate, ketones, amino acids), changes in hormonal milieu, and limitations in oxygen supply. Alterations in fatty acid metabolism can contribute to cardiac pathology. For instance, the excessive uptake and β-oxidation of fatty acids in obesity and diabetes can compromise cardiac function. Furthermore, alterations in fatty acid β-oxidation both during and after ischemia and in the failing heart can also contribute to cardiac pathology. This paper reviews the regulation of myocardial fatty acid β-oxidation and how alterations in fatty acid β-oxidation can contribute to heart disease. The implications of inhibiting fatty acid β-oxidation as a potential novel therapeutic approach for the treatment of various forms of heart disease are also discussed.

Myocardial Fatty Acid Metabolism in Health and Disease

Regulation of fatty acid oxidation in the mammalian heart in health and disease.

http://msg2018.weebly.com/uploads/1/6/1/0/16101502/jaswal_2011_targeting_fatty_acid_and_carbohydrate_oxidation___a_novel_therapeutic_intervention_in_the_ischemic_and_failing_heart__.pdf

Targeting fatty acid and carbohydrate oxidation--a novel therapeutic intervention in the ischemic and failing heart.

The calcium ion (Ca2+) is the main second messenger that helps to transmit depolarization status and synaptic activity to the biochemical machinery of a neuron. These features make Ca2+ regulation a critical process in neurons, which have developed extensive and intricate Ca2+ signaling pathways. High intensity Ca2+ signaling necessitates high ATP consumption to restore basal (low) intracellular Ca2+ levels after Ca2+ influx through plasma membrane receptor and voltage-dependent ion channels. Ca2+ influx may also lead to increased generation of mitochondrial reactive oxygen species (ROS). Impaired abilities of neurons to maintain cellular energy levels and to suppress ROS may impact Ca2+ signaling during aging and in neurodegenerative disease processes. This review focuses on mitochondrial and endoplasmic reticulum Ca2+ homeostasis and how they relate to synaptic Ca2+ signaling processes, neuronal energy metabolism, and ROS generation. Also, the contribution of altered Ca2+ signaling to neurodege...

Neuronal calcium homeostasis and dysregulation.

Acylcarnitines are fatty acid metabolites that play important roles in many cellular energy metabolism pathways. They have historically been used as important diagnostic markers for inborn errors of fatty acid oxidation and are being intensively studied as markers of energy metabolism, deficits in mitochondrial and peroxisomal β-oxidation activity, insulin resistance, and physical activity. Acylcarnitines are increasingly being identified as important indicators in metabolic studies of many diseases, including metabolic disorders, cardiovascular diseases, diabetes, depression, neurologic disorders, and certain cancers. The US Food and Drug Administration-approved drug L-carnitine, along with short-chain acylcarnitines (acetylcarnitine and propionylcarnitine), is now widely used as a dietary supplement. In light of their growing importance, we have undertaken an extensive review of acylcarnitines and provided a detailed description of their identity, nomenclature, classification, biochemistry, pathophysiology, supplementary use, potential drug targets, and clinical trials. We also summarize these updates in the Human Metabolome Database, which now includes information on the structures, chemical formulae, chemical/spectral properties, descriptions, and pathways for 1240 acylcarnitines. This work lays a solid foundation for identifying, characterizing, and understanding acylcarnitines in human biosamples. We also discuss the emerging opportunities for using acylcarnitines as biomarkers and as dietary interventions or supplements for many wide-ranging indications. The opportunity to identify new drug targets involved in controlling acylcarnitine levels is also discussed. Significance Statement This review provides a comprehensive overview of acylcarnitines, including their nomenclature, structure and biochemistry, and use as disease biomarkers and pharmaceutical agents. We present updated information contained in the Human Metabolome Database website as well as substantial mapping of the known biochemical pathways associated with acylcarnitines, thereby providing a strong foundation for further clarification of their physiological roles.

Acylcarnitines: Nomenclature, Biomarkers, Therapeutic Potential, Drug Targets, and Clinical Trials

Metabolic products accumulate in ischemic myocardium secondary to reduced coronary flow, which prevents adequate washout of vascular spaces, and to reduced oxidative metabolism. The most notable products that accumulate are NADH, H+, lactate, CO2, long-chain acyl-CoA, and long-chain acyl carnitine. These products interfere with the production of ATP and the functioning of the myocardium. Glycolytic production of ATP is inhibited by accumulation of NADH, H+, and lactate. Mitochondrial and plasma membrane function may be altered by the acyl esters of CoA and carnitine. Mitochondrial membranes become structurally distorted and fragmented, and lipid-containing amorphous densities appear in the matrix. Structural alterations of mitochondria occur more frequently in hearts receiving high concentrations of fatty acids and correlate with high tissue levels of acyl esters of CoA and carnitine. Addition of acyl carnitine to mitochondria isolated from normal hearts results in nodulose-appearing cristae and fragmentation of mitochondrial membranes.

Metabolic products and myocardial ischemia

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Metabolic products and myocardial ischemia