Modification of nicotinic acid and prostaglandin E1 antilipolytic action in vitro.
In epididymal adipose tissue from rats, human serum antagonizes inhibition of basal lipolysis by nicotinic acid in vitro. Under similar conditions caffeine-stimulated lipolysis was unaffected by the presence of human serum. Very low density (VLDL), low density (LDL) and high density (HDL) lipoproteins were all found to antagonize the action of nicotinic acid on basal lipolysis. VLDL also antagonized prostaglandin E1 (PGE1)-inhibition of basal lipolysis in vitro. The fat cell membrane was suggested as the site at which human serum lipoproteins antagonize nicotinic acid or PGE1 antilipolytic action on basal lipolysis in vitro.
D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D002384:Catalysis; D005990:Glycerol / Q000378:metabolism; D006801:Humans; D006868:Hydrolysis; D008053:Lipid Mobilization / Q000187:drug effects*; D008071:Lipoprotein Lipase / Q000378:metabolism; D008079:Lipoproteins, VLDL / Q000494:pharmacology; D008297:Male; D008968:Molecular Conformation; D009539:Nicotinic Acids / Q000037:antagonists & inhibitors / Q000097:blood / Q000494:pharmacology*; D011448:Prostaglandin Antagonists / Q000097:blood; D011458:Prostaglandins E / Q000097:blood / Q000494:pharmacology*; D011485:Protein Binding; D051381:Rats; D014280:Triglycerides / Q000097:blood
D008079:Lipoproteins, VLDL; D009539:Nicotinic Acids; D011448:Prostaglandin Antagonists; D011458:Prostaglandins E; D014280:Triglycerides; D008071:Lipoprotein Lipase; D005990:Glycerol