Carbohydrate metabolism in cardiovascular disease.
Carbohydrate metabolism is temporarily disturbed in acute myocardial infarction. The degree of hyperglycaemia and failure of response of insulin appears to be related to the severity of the infarction. The underlying hormonal changes probably include increased secretion of catecholamines and of glucagon. Circulating free fatty acids (FFA) are generally increased by the same metabolic and hormonal factors which promote glucose intolerance. In the zone of developing infarction in the heart, there is a complex metabolic situation with glucose metabolism both being accelerated and inhibited by different factors. Continued uptake of FFA is associated with intracellular accumulation of activated long-chain FFA, acyl CoA, which tends to inhibit mitochondrial metabolism. The metabolism of glucose is thought to be beneficial and that of FFA detrimental to the infarcting tissue. Thus the glucose intolerance and the high circulating FFA occurring as part of the general metabolic response to myocardial infarction, are thought to be harmful to the ischaemic tissue. Increased provision of glucose by dichloroacetate, and inhibition of FFA metabolism by nicotinic acid analogues decrease the extent of experimental infaraction, while glucose--insulin--potassium and propranolol act both by increasing glucose uptake and decreasing that of FFA. Glucose intolerance is also common in peripheral vascular disease. The reasons for this are obscure. However, the alterations in circulating insulin concentration which accompany this intolerance may be involved in the development of arterial lesions either directly through an effect on arterial wall synthesis or indirectly through an effect on circulating lipid levels. Defects may also be found in arterial wall mucopolysaccharide or sorbitol metabolism. The role of sex hormones and catecholamines remains speculative. At present the most cogent view is that in peripheral vascular disease a multi-hormonal disorder exists which may be contributing to the development of arteriosclerosis.
D000208:Acute Disease; D001158:Arteries / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D050260:Carbohydrate Metabolism; D002318:Cardiovascular Diseases / Q000378:metabolism*; D003327:Coronary Disease / Q000378:metabolism; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000378:metabolism; D004837:Epinephrine / Q000652:urine; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005947:Glucose / Q000627:therapeutic use; D005951:Glucose Tolerance Test; D006019:Glycolysis; D006029:Glycosuria / Q000150:complications / Q000378:metabolism; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000378:metabolism; D050356:Lipid Metabolism; D008954:Models, Biological; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy / Q000378:metabolism*; D009638:Norepinephrine / Q000652:urine
D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D005947:Glucose; D009638:Norepinephrine; D004837:Epinephrine