HDL biology
Alcohol-induced HDL cholesterol rise is driven by lipoprotein lipase, not CETP, hepatic lipase, or LCAT activity (Atherosclerosis 1994)
Original title: Effects of alcohol on lipoprotein lipase, hepatic lipase, cholesteryl ester transfer protein, and lecithin:cholesterol acyltransferase in high-density lipoprotein cholesterol elevation
To identify which enzyme accounts for the HDL cholesterol (HDL-C) rise seen with alcohol consumption, 12 men consumed 0.5 g/kg body weight of alcohol per day for 4 weeks after 3 weeks of abstinence, while 13 abstaining men served as controls. Total cholesterol was unchanged in both groups. Among alcohol consumers, plasma triglycerides, HDL-C, and apolipoprotein A-I and A-II levels increased significantly after 3 weeks of loading but were unchanged in controls; HDL3 cholesterol increased significantly by 4 weeks while HDL2 cholesterol was unaffected. Postheparin plasma lipoprotein lipase (LPL) activity and mass increased significantly (P < 0.01) with alcohol, without a change in LPL specific activity. Hepatic lipase, CETP, and LCAT activities were unaffected in both groups. The authors conclude LPL contributed most to the alcohol-induced HDL-C rise.
Original abstract
The mechanism whereby alcohol increases high-density lipoprotein cholesterol (HDL-C) levels is unclear. Lipoprotein lipase (LPL), hepatic lipase (HL), cholesteryl ester transfer protein (CETP) and lecithin:cholesterol acyltransferase (LCAT) act on lipoprotein metabolism. The purpose of the present study is to determine which one or what combination of these factors is responsible for the rise in HDL-C levels following alcohol ingestion. After 3 weeks of abstinence, 12 men consumed 0.5 g/kg bw of alcohol per day for 4 weeks; 13 abstaining men served as controls. Mean plasma total cholesterol (TC) levels were unchanged in either group throughout the study. Among the alcohol consumers, plasma triglycerides (TG), HDL-C, apolipoprotein (apo) A-I and A-II levels increased significantly after 3 weeks of alcohol loading but were unchanged in the control group. High-density lipoprotein3 cholesterol (HDL3-C) levels increased significantly in the alcohol consumers after 4 weeks of alcohol loading whereas high-density lipoprotein2 cholesterol (HDL2-C) levels were unaffected. In the controls, neither HDL2-C nor HDL3-C changed significantly. Post-heparin plasma (PHP) LPL activity and mass increased significantly (P < 0.01) after the alcohol ingestion (controls remained unchanged) without changing LPL specific activity. HL, CETP and LCAT activities were unaffected in both groups. We conclude that of the factors considered, LPL contributed the most to the alcohol-induced rise in HDL-C.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.