Jie Bai1,2, Elizabeth Greene1, Weifen Li2, Michael T Kidd1, Sami Dridi1. 1. Center of Excellence for Poultry Science, University of Arkansas, Fayetteville, AR, USA. 2. Key Laboratory of Molecular Animal Nutrition, College of Animal Science, Zhejiang University, Hangzhou, China.
Abstract
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.
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.