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给予α-六氯环己烷后大鼠血清极低密度脂蛋白的增加。

Increase of serum very low density lipoproteins in rats after administration of alpha-hexachlorocyclohexane.

作者信息

Grajewski O, Oberdisse E

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1977 Jun;298(2):129-35. doi: 10.1007/BF00508619.

Abstract

After enteral administration of 200 mg/kg alpha-hexachlorocyclohexane (alpha-HCH) female Wistar rats develop a hyperlipemia. 48 h after administration of alpha-HCH, serum triglycerides are increased by 300%, whereas both serum cholesterol and serum total phospholipids only increase by about 45%. Serum free fatty acids are not significantly altered. Fractionation of the serum lipoproteins by ultracentrifugation shows that the hyperlipemia is due to a fivefold increase in serum very low density lipoproteins. Hepatic triglyceride secretion, calculated after i.v. injection of Triton WR 1339, is increased in animals pretreated wtih alpha-HCH. Corresponding to this observation, drugs known to diminish the triglyceride secretion of the liver, such as actinomycin D, cycloheximide; glucagon, orotic acid, CFT 1201, and CFT 1042 reduce the alpha-HCH-induced hyperlipemia. We concluded from the results that hyperlipoproteinemia after alpha-HCH is due to an increased hepatic very low density lipoprotein secretion. At the same time, the blood sugar level was decreased in fasting animals after treatment with alpha-HCH. Earlier experiments suggest that this effect is due to a decreased gluconeogenesis in the liver.

摘要

经肠内给予200mg/kg的α-六氯环己烷(α-HCH)后,雌性Wistar大鼠会出现高脂血症。给予α-HCH后48小时,血清甘油三酯增加了300%,而血清胆固醇和血清总磷脂仅增加约45%。血清游离脂肪酸无明显变化。通过超速离心对血清脂蛋白进行分级分离表明,高脂血症是由于血清极低密度脂蛋白增加了五倍所致。经静脉注射曲拉通WR 1339后计算得出,经α-HCH预处理的动物肝脏甘油三酯分泌增加。与此观察结果一致,已知能减少肝脏甘油三酯分泌的药物,如放线菌素D、环己酰亚胺、胰高血糖素、乳清酸、CFT 1201和CFT 1042,可减轻α-HCH诱导的高脂血症。我们从这些结果得出结论,α-HCH后的高脂蛋白血症是由于肝脏极低密度脂蛋白分泌增加所致。同时,用α-HCH处理后的禁食动物血糖水平降低。早期实验表明,这种作用是由于肝脏糖异生减少所致。

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