Griffin H D, Guo K, Windsor D, Butterwith S C
AFRC Institute of Animal Physiology and Genetics Research, Midlothian, Scotland, U.K.
J Nutr. 1992 Feb;122(2):363-8. doi: 10.1093/jn/122.2.363.
Rates of hepatic lipogenesis and secretion of plasma triglyceride-rich lipoproteins in 6- to 7-wk-old broiler chickens were similar to the overall rate of fat deposition in these birds, although approximately 20% of [14C]-labeled VLDL was oxidized to CO2 within 8 h. Only 6-7% of VLDL and portomicron triglyceride was taken up by the abdominal fat pad, but this proportion of total triglyceride flux could account for about 80-85% of the total fatty acids accumulating in that depot. The rate of lipogenesis in adipose tissue was much lower than that in the liver, but it could account for much of the remaining fatty acids. Lipogenesis from [14C]acetate in cultured chicken adipocytes was markedly inhibited by adding VLDL as an exogenous source of fatty acids. However, adipose tissue lipogenesis was not increased in vivo by reduction of plasma lipoprotein flux by genetic selection, by the feeding of a high protein diet or by immunological intervention. The results confirm that adipose tissue lipogenesis makes only a small contribution to adipose tissue growth in normal broilers. Its importance does not increase in response to the reductions in hepatic lipogenesis that accompany genetic or nutritional manipulation of body composition.
6至7周龄肉鸡的肝脏脂肪生成率和富含甘油三酯的血浆脂蛋白分泌率与这些鸡的总体脂肪沉积率相似，尽管约20%的[14C]标记极低密度脂蛋白（VLDL）在8小时内被氧化为二氧化碳。只有6 - 7%的VLDL和前β-脂蛋白甘油三酯被腹部脂肪垫摄取，但甘油三酯总通量的这一比例可占该脂肪库中积累的总脂肪酸的约80 - 85%。脂肪组织中的脂肪生成率远低于肝脏中的脂肪生成率，但它可占其余大部分脂肪酸。通过添加VLDL作为脂肪酸的外源来源，可显著抑制培养的鸡脂肪细胞中[14C]乙酸盐的脂肪生成。然而，通过基因选择降低血浆脂蛋白通量、饲喂高蛋白日粮或进行免疫干预，体内脂肪组织的脂肪生成并未增加。结果证实，在正常肉鸡中，脂肪组织脂肪生成对脂肪组织生长的贡献很小。随着对身体组成进行遗传或营养调控而导致肝脏脂肪生成减少时，其重要性并未增加。
