Why the study?
Does ethanol intake alter lipoprotein lipase activity and lipid profiles in young fasting subjects?
Does ethanol intake alter lipoprotein lipase activity and lipid profiles in young fasting subjects?
Ethanol intake interferes with carbohydrate-induced elevation of adipose tissue lipoprotein lipase activity, which may decrease the removal capacity for circulating dietary lipid and cause prolonged hyperlipemia.
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Ethanol may blunt glucose-induced adipose LPL activation and raise triglycerides; hypothesis-generating observation leaves open relevance to alcohol-related dyslipidemia.
Ethanol (ca. 1 g/kg body weight) was given alone or together with glucose or lipid (mixed triglycerides) perorally to young, fasting subjects. The changes with time (0-6 hr) of lipoprotein lipase activity (LLA) in adipose tissue, plasma glycerol, triglyceride, insulin, blood glucose, and alcohol concentrations were followed. A maximal mean blood alcohol concentration of 0.09% (w/v) was obtained 1 hr after ingestion with no apparent intoxicating effects. Ethanol intake prevented the previously observed [Nilsson-Ehle, P., S. Carlström, and P. Belfrage, Scand, J. Clin. Lab. Invest. 35:373 (1975)] glucose-induced rapid elevation of adipose tissue LLA but had small effects on this enzymatic activity when given alone or together with lipid. Confirming results by others, ethanol intake decreased plasma glycerol concentration and increased plasma triglycerides, especially after intake of lipid. It is suggested that ethanol intake interferes with the normal carbohydrate-induced elevation of adipose tissue LLA after a mixed meal, thereby decreasing the removal capacity for circulating dietary lipid and causing enhanced and prolonged alimentary hyperlipemia.
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Nilsson‐Ehle et al. (1978) studied this question.
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