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吉非贝齐可改变豚鼠肝脏微粒体磷脂的酰基组成,而不会促进过氧化物酶体增殖。

Gemfibrozil modifies acyl composition of liver microsomal phospholipids from guinea-pigs without promoting peroxisomal proliferation.

作者信息

Vázquez M, Alegret M, Adzet T, Merlos M, Laguna J C

机构信息

Unidad de Farmacología y Farmacognosia, Facultad de Farmacia, Universidad de Barcelona, Spain.

出版信息

Biochem Pharmacol. 1993 Oct 19;46(8):1515-8. doi: 10.1016/0006-2952(93)90121-c.

Abstract

Treatment with gemfibrozil modifies acyl composition of hepatic microsomal phosphatidylcholine and phosphatidylethanolamine in guinea-pigs. Palmitic (16:0) and palmitoleic (16:1) fatty acids are increased, and stearic (18:0) and oleic (18:1) are decreased; further, while linoleic acid [18:2 (n-6)] is increased by gemfibrozil treatment, the other constituents of the n-6 fatty acids family, including arachidonic acid [20:4 (n-6)], are decreased. As gemfibrozil is a potent inhibitor of fatty acid elongation in vitro (Sánchez et al., FEBS Lett 300: 89-92, 1992), the inhibition of this enzyme system by gemfibrozil treatment could be responsible for the observed results in vivo. These changes in fatty acid composition are accompanied by a decrease in serum lipids and, more important, are independent of peroxisomal proliferation.

摘要

用吉非贝齐治疗可改变豚鼠肝脏微粒体磷脂酰胆碱和磷脂酰乙醇胺的酰基组成。棕榈酸(16:0)和棕榈油酸(16:1)脂肪酸增加,而硬脂酸(18:0)和油酸(18:1)减少;此外,虽然吉非贝齐治疗可使亚油酸[18:2(n-6)]增加,但n-6脂肪酸家族的其他成分,包括花生四烯酸[20:4(n-6)]却减少。由于吉非贝齐在体外是一种有效的脂肪酸延长酶抑制剂(桑切斯等人,《欧洲生物化学学会联合会快报》300:89-92,1992),因此吉非贝齐治疗对该酶系统的抑制作用可能是体内观察到的结果的原因。脂肪酸组成的这些变化伴随着血脂的降低,更重要的是,与过氧化物酶体增殖无关。

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