Evans R D, Ilic V, Williamson D H
Nuffield Department of Anaesthetics, Radcliffe Infirmary, Oxford, U.K.
Biochem J. 1991 Dec 1;280 ( Pt 2)(Pt 2):541-3. doi: 10.1042/bj2800541.
Administration of platelet-activating factor (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine; PAF) did not alter the rate of triacylglycerol entry into the plasma. The gastrointestinal absorption of [1-14C]triolein was, however, inhibited by PAF, yet there was increased accumulation of [14C]lipid in the plasma and hypertriglyceridaemia. The half-life of injected [9,10(n)-3H]triolein in the plasma increased by 47%, and there was decreased accumulation of [3H]lipid in brown adipose tissue. This was accompanied by a decrease in lipoprotein lipase activity. The hypertriglyceridaemia induced by PAF appears to be mainly due to decreased peripheral removal, one important site affected being brown adipose tissue.
给予血小板活化因子(1-O-烷基-2-乙酰基-sn-甘油-3-磷酸胆碱;PAF)并未改变三酰甘油进入血浆的速率。然而,PAF抑制了[1-14C]三油精的胃肠道吸收,与此同时,血浆中[14C]脂质的蓄积增加,出现了高甘油三酯血症。注射的[9,10(n)-3H]三油精在血浆中的半衰期增加了47%,并且棕色脂肪组织中[3H]脂质的蓄积减少。这伴随着脂蛋白脂肪酶活性的降低。PAF诱导的高甘油三酯血症似乎主要是由于外周清除减少,棕色脂肪组织是受影响的一个重要部位。