Donaldson W E
Ann N Y Acad Sci. 1985;447:105-11. doi: 10.1111/j.1749-6632.1985.tb18429.x.
Data are summarized from several papers on the effects of biotin deficiency on lipid metabolism, especially fatty acid synthesis, in chicks. Biotin deficiency inhibits in vivo lipogenesis and hepatic acetyl-CoA carboxylase (ACC) activity. Although acetate incorporation into fatty acids is inhibited in biotin-deficient chicks, malonate incorporation is not inhibited. In fact, dietary malonic acid stimulates lipogenesis during biotin deficiency as measured by total carcass fatty acid content. Biotin-deficient chicks exhibit altered hepatic and whole body fatty acid composition in comparison with control chicks. The deficiency results in an increased proportion of the 16-carbon to 18-carbon fatty acids, and the most striking increase is for palmitoleic (16:1) acid. Biotin deficiency increases the relative incorporation of palmitate and stearate into phospholipids and decreases the relative incorporation of these fatty acids into triglycerides. Finally, mercury stimulates lipogenesis in biotin-deficient, but not in control, chicks by an unknown mechanism.
数据总结自几篇关于生物素缺乏对雏鸡脂质代谢,尤其是脂肪酸合成影响的论文。生物素缺乏会抑制体内脂肪生成和肝脏乙酰辅酶A羧化酶(ACC)活性。虽然在生物素缺乏的雏鸡中,乙酸盐掺入脂肪酸的过程受到抑制,但丙二酸盐掺入不受抑制。事实上,通过全胴体脂肪酸含量测定,在生物素缺乏期间,日粮中的丙二酸会刺激脂肪生成。与对照雏鸡相比,生物素缺乏的雏鸡肝脏和全身脂肪酸组成发生改变。这种缺乏导致16碳脂肪酸与18碳脂肪酸的比例增加,最显著的增加是棕榈油酸(16:1)。生物素缺乏会增加棕榈酸和硬脂酸相对掺入磷脂的量,并减少这些脂肪酸相对掺入甘油三酯的量。最后,汞通过未知机制刺激生物素缺乏的雏鸡的脂肪生成,但对对照雏鸡无此作用。