安普克
内科学
脂肪生成
内分泌学
福克斯O1
脂肪酸合酶
甾醇调节元件结合蛋白
AMP活化蛋白激酶
肉鸡
生物
β氧化
过氧化物酶体增殖物激活受体
支链氨基酸
脂质代谢
新陈代谢
蛋白激酶B
蛋白激酶A
磷酸化
生物化学
氨基酸
受体
胆固醇
医学
动物科学
甾醇
亮氨酸
作者
Jie Bai,Elizabeth Greene,Weifen Li,Michael T. Kidd,Sami Dridi
标识
DOI:10.1002/mnfr.201400918
摘要
Scope The effects and roles of branched‐chain amino acids (BCAAs) in hepatic fat metabolism are still unknown. Methods and results Here, we used broiler chickens, in which lipogenesis occurs essentially in the liver as in human, to investigate the effects of three levels of BCAAs (control “C,” low “L” and exogenous supplemented diet “L+S”) on growth, carcass traits, immunity, and hepatic fat metabolism. Despite the same productive performance, immunity, and plasma BCAA levels between all groups, low BCAA levels significantly downregulated the hepatic expression of lipogenic genes particularly acetyl‐CoA carboxylase alpha (ACCα) and stearoyl‐coA desaturase 1 ( p = 0.0036 and p = 0.0008, respectively) and upregulated the hepatic expression of mitochondrial β‐oxidation‐ (uncoupling protein and NRF‐1, p < 0.05) and dynamic‐related genes (DNM1, p < 0.05). Concomitant with these changes, low BCAA levels increased the phosphorylation of AMP‐activated protein kinase (AMPK)α Thr172 , ACCα Ser79 , and forkhead box protein O1 (FoxO1 Ser256 ) and decreased the phosphorylation of mTOR Ser2481 and P70 S6 kinase Thr389 . The mRNA abundance of the transcription factors SREBP1/2, peroxisome proliferator activated receptor alpha/beta, and FoxO1 were also increased in the liver of L group compared to the control. Conclusion Together our data indicate that low BCAA levels inhibit fatty acid synthesis and enhanced fatty acid β‐oxidation in the liver of female broiler chickens and these effects were probably mediated through AMPK‐mTOR‐FoxO1 pathway.
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