Sutherland W H, Larking P W, Nye E R
Atherosclerosis. 1976 Oct;25(1):45-53. doi: 10.1016/0021-9150(76)90046-0.
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.
在大鼠附睾脂肪组织中,人血清在体外可拮抗烟酸对基础脂解作用的抑制。在相似条件下,咖啡因刺激的脂解作用不受人血清存在的影响。超低密度脂蛋白(VLDL)、低密度脂蛋白(LDL)和高密度脂蛋白(HDL)均可拮抗烟酸对基础脂解作用的影响。VLDL在体外也可拮抗前列腺素E1(PGE1)对基础脂解作用的抑制。有人提出,脂肪细胞膜是人血清脂蛋白在体外拮抗烟酸或PGE1对基础脂解作用的抗脂解作用的位点。