Influence of smoking on cellular lipid metabolism.
Smoking and hyper-beta-lipoproteinemia, are well-established risk factors for the early development of atherosclerotic disease. The presence of both factors augments the potential risk. Since the influence of smoking on the plasma lipoprotein profile in humans seems to be either absent or minor, we were interested in whether cigarette smoking develops a direct influence on lipid metabolism at the cellular level. Our findings showed that smoking has no effect on either the high affinity LDL receptor activity or on the activity of HMG-CoA reductase, acid lipase, or cholesterol ester hydrolase.
D000328:Adult; D001161:Arteriosclerosis / Q000209:etiology; D006801:Humans; D006903:Hydroxymethylglutaryl CoA Reductases / Q000097:blood; D025782:Hydroxymethylglutaryl-CoA-Reductases, NADP-dependent; D008049:Lipase / Q000097:blood; D008055:Lipids / Q000097:blood*; D008214:Lymphocytes / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D011973:Receptors, LDL / Q000097:blood; D012306:Risk; D012907:Smoking; D002787:Sterol Esterase / Q000097:blood
D008055:Lipids; D011973:Receptors, LDL; D006903:Hydroxymethylglutaryl CoA Reductases; D025782:Hydroxymethylglutaryl-CoA-Reductases, NADP-dependent; D002787:Sterol Esterase; D008049:Lipase