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[Intermediate myocardial metabolism. Changes in ischemia, diabetes and hyperthyroidism]
D Feuvray1, N Khandoudi, D Lagadic-Gossmann
1Centre national de la recherche scientifique, Université Paris XI, Orsay.
Archives Des Maladies Du Coeur Et Des Vaisseaux
|October 1, 1988
Summary
Free fatty acids (FFA) are preferred myocardial fuel but accumulate during ischemia, especially in diabetes. This accumulation, along with metabolic byproducts, impacts cardiac membrane function and recovery after ischemia.
Area of Science:
- Cardiology
- Metabolic Research
- Cellular Physiology
Context:
- Myocardial metabolism prioritizes long-chain free fatty acids (FFA) over carbohydrates under normal oxygen supply.
- FFA utilization increases in diabetes and hyperthyroidism due to elevated plasma FFA concentrations.
- Ischemia leads to the cellular accumulation of long-chain fatty acid esters, specifically acyl-CoA and acylcarnitine.
Purpose:
- To investigate the accumulation patterns of fatty acid esters and glycolysis end-products in ischemic myocardium.
- To explore the impact of diabetes on the accumulation of acyl-CoA and acylcarnitine in ischemic heart tissue.
- To understand the relationship between cellular pH, metabolic byproduct accumulation, and functional recovery post-ischemia.
Summary:
- Under ischemic conditions, myocardial cells accumulate acyl-CoA and acylcarnitine, with accumulation levels dependent on coronary blood flow reduction.
- Diabetes exacerbates the accumulation of these amphipathic compounds in ischemic myocardium.
- High concentrations of acylcarnitine are linked to alterations in mitochondrial and sarcolemmal membrane structure and function.
- Accumulation of glycolysis end-products, such as lactates and protons, influences functional recovery after global and total ischemia.
- Decreased cellular pH is identified as a key factor in reperfusion outcomes.
Impact:
- Provides insights into the detrimental effects of altered lipid metabolism in cardiac ischemia and diabetes.
- Highlights the role of specific metabolic intermediates (acylcarnitine) in cardiac membrane dysfunction.
- Suggests potential therapeutic targets for improving myocardial recovery by modulating metabolic pathways and cellular pH during ischemia and reperfusion.