Schoonderwoerd K, Hülsmann W C, Jansen H
Department of Biochemistry I, Medical Faculty, Erasmus University Rotterdam, The Netherlands.
Lipids. 1989 Dec;24(12):1039-42. doi: 10.1007/BF02544076.
Liver lipase activity was measured in EFA-deficient rats (long-term) and in control rats and rats fed an EFA-deficient diet for two weeks (short-term). Liver lipase activity was significantly enhanced by EFA deficiency, both in long-term and short-term experiments. The enhanced liver lipase activity could be normalized by feeding these rats normal laboratory chow for 14 days. Since during EFA deficiency prostaglandin synthesis is impaired, the possible involvement of prostaglandins in the observed changes in liver lipase activity during EFA deficiency was studied. Administration of the prostaglandin synthesis inhibitor indomethacin (5 mg/kg body weight, i.p.) to normally fed rats for two days led to an increase of liver lipase activity. Prostaglandin E2 was found to inhibit the secretion of liver lipase activity by freshly isolated parenchymal liver cells in vitro. These results indicate that the increase in liver lipase activity during EFA deficiency may be due to an impairment of the prostaglandin synthesis.
在长期缺乏必需脂肪酸(EFA)的大鼠、对照大鼠以及短期(两周)饲喂EFA缺乏日粮的大鼠中测量了肝脏脂肪酶活性。在长期和短期实验中,EFA缺乏均显著增强了肝脏脂肪酶活性。通过给这些大鼠饲喂正常实验室饲料14天,增强的肝脏脂肪酶活性可恢复正常。由于在EFA缺乏期间前列腺素合成受损,因此研究了前列腺素在EFA缺乏期间观察到的肝脏脂肪酶活性变化中可能的作用。给正常饲喂的大鼠腹腔注射前列腺素合成抑制剂吲哚美辛(5毫克/千克体重)两天,导致肝脏脂肪酶活性增加。发现前列腺素E2在体外可抑制新鲜分离的肝实质细胞分泌肝脏脂肪酶活性。这些结果表明,EFA缺乏期间肝脏脂肪酶活性的增加可能是由于前列腺素合成受损所致。