Metabolic disturbances during acute lack of oxygen: a short overview.

Abstract

Oxygen deficiency results in several alterations in lipid metabolism in cardiac muscle. The primary events appear to involve a rise in mitochondrial NADH/NAD secondary to the low oxygen supply. The more reduced state of mitochondrial adenine nucleotides in turn inhibits β-oxidation of long chain fatty acids resulting in the accumulation of long-chain acyl CoA and acylcarnitine derivatives. These compounds accumulate in both the mitochondrial matrix and the cytosolic compartments, but acyl CoA is largely matrix and acylcarnitine is largely cytosolic. The rise in cytosolic acyl CoA may directly stimulate conversion of fatty acids to Triacylglycerol.