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实验性甲状腺功能亢进症中的脂肪酸去饱和作用及微粒体脂质脂肪酸组成

Fatty-acid desaturation and microsomal lipid fatty-acid composition in experimental hyperthyroidism.

作者信息

Faas F H, Carter W J

出版信息

Biochem J. 1981 Mar 1;193(3):845-52. doi: 10.1042/bj1930845.

DOI:10.1042/bj1930845
PMID:7305962
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1162676/
Abstract

We have studied the influence of experimental hyperthyroidism in the rat on the synthesis of unsaturated fatty acids and on liver microsomal lipid fatty-acid composition. Tri-iodothyronine treatment (25 micrograms/100 g body weight) daily for 3 weeks caused no significant changes in delta 9 (stearate) desaturation but a 24% decrease in delta 6 (linoleate) desaturation. Much larger doses of tri-iodothyronine increased delta 9 desaturation. Liver microsomal fatty-acid composition in hyperthyroidism is altered with significantly increased proportions of stearate and arachidonate and decreased proportions of palmitate, palmitoleate, linoleate (C18:2) and eicosa-8,11,14-trienoate (C20:3). These changes, other than the decreases proportion of C20:3 fatty acid, which may be due to the diminished delta 6 desaturase activity, cannot be attributed to changes in fatty-acid desaturation. Most of these changes were also found to be due not simply to the decreased weight gain or the increased food intake of the hyperthyroid animals. Only the decreased C18:2 fatty-acid proportions could be mimicked by restricting food intake of control animals and none of the changes were prevented by restricting food intake of hyperthyroid animals. Thus most of the changes in microsomal lipid fatty-acid composition are likely to be due to a thyroid hormone effect on peripheral lipid mobilization or lipid degradation.

摘要

我们研究了大鼠实验性甲状腺功能亢进对不饱和脂肪酸合成及肝脏微粒体脂质脂肪酸组成的影响。每天给予三碘甲状腺原氨酸(25微克/100克体重),持续3周,未引起Δ9(硬脂酸)去饱和作用的显著变化,但Δ6(亚油酸)去饱和作用降低了24%。更大剂量的三碘甲状腺原氨酸可增加Δ9去饱和作用。甲状腺功能亢进时肝脏微粒体脂肪酸组成发生改变,硬脂酸和花生四烯酸的比例显著增加,棕榈酸、棕榈油酸、亚油酸(C18:2)和二十碳-8,11,14-三烯酸(C20:3)的比例降低。这些变化,除了C20:3脂肪酸比例的降低可能是由于Δ6去饱和酶活性降低外,不能归因于脂肪酸去饱和作用的变化。还发现这些变化大多并非仅仅由于甲状腺功能亢进动物体重增加减少或食物摄入量增加所致。仅通过限制对照动物的食物摄入量可模拟C18:2脂肪酸比例的降低,而限制甲状腺功能亢进动物的食物摄入量并不能阻止任何变化。因此,微粒体脂质脂肪酸组成的大多数变化可能是由于甲状腺激素对外周脂质动员或脂质降解的影响。

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