Suppression of fat deposition in broiler chickens by (-)-hydroxycitric acid supplementation: A proteomics perspective.

Suppression of fat deposition in broiler chickens by (-)-hydroxycitric acid supplementation: A proteomics perspective.
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补充 (-)-羟基柠檬酸抑制肉鸡脂肪沉积:蛋白质组学视角

DOI:
10.1038/srep32580
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发表时间:
2016-09-02
期刊:
影响因子:
4.6
通讯作者:
Ma H
Ma H
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Peng M;Han J;Li L;Ma H

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(-)-羟基柠檬酸(HCA)抑制动物脂肪酸合成,但其在家禽中的生化机制尚不清楚。本研究鉴定了与肉鸡脂肪代谢相关的关键蛋白,并阐明了(-)-HCA在肉鸡体内的生化机制。四个组(n = 30)分别接受添加0、1000、2000或3000 mg/kg(-)-HCA的饲料4周。在差异表达的肝脏蛋白中,线粒体和细胞质中分别鉴定出40和26个。丙酮酸脱氢酶E1组分(PDHA 1和PDHB)、二氢硫辛酰脱氢酶(DLD)、乌头酸酶(ACO 2)、α-酮戊二酸脱氢酶复合物(DLST)、烯酰辅酶A水合酶(ECHS 1)和磷酸甘油酸激酶(PGK)上调,而NADP依赖性苹果酸酶(ME 1)下调。生物网络分析表明,所鉴定的蛋白质参与糖代谢和脂质代谢,而不相容性途径分析表明,PDHA 1、PDHB、ECHS 1和ME 1参与经典途径。数据表明,(-)-HCA通过减少乙酰辅酶A的供应,通过促进三羧酸循环(上调PDHA 1,PDHB,ACO 2和DLST表达)和抑制ME 1表达来抑制脂肪酸合成。此外,(-)-HCA通过上调ECHS 1表达促进脂肪酸β-氧化。这些结果反映了(-)-HCA在肉鸡中的脂肪减少的生化相关机制。
(-)-Hydroxycitric acid (HCA) suppresses fatty acid synthesis in animals, but its biochemical mechanism in poultry is unclear. This study identified the key proteins associated with fat metabolism and elucidated the biochemical mechanism of (-)-HCA in broiler chickens. Four groups (n = 30 each) received a diet supplemented with 0, 1000, 2000 or 3000 mg/kg (-)-HCA for 4 weeks. Of the differentially expressed liver proteins, 40 and 26 were identified in the mitochondrial and cytoplasm respectively. Pyruvate dehydrogenase E1 components (PDHA1 and PDHB), dihydrolipoyl dehydrogenase (DLD), aconitase (ACO2), a-ketoglutarate dehydrogenase complex (DLST), enoyl-CoA hydratase (ECHS1) and phosphoglycerate kinase (PGK) were upregulated, while NADP-dependent malic enzyme (ME1) was downregulated. Biological network analysis showed that the identified proteins were involved in glycometabolism and lipid metabolism, whereas PDHA1, PDHB, ECHS1, and ME1 were identified in the canonical pathway by Ingenuity Pathway Analysis. The data indicated that (-)-HCA inhibited fatty acid synthesis by reducing the acetyl-CoA supply,viapromotion of the tricarboxylic acid cycle (upregulation of PDHA1, PDHB, ACO2, and DLST expression) and inhibition of ME1 expression. Moreover, (-)-HCA promoted fatty acid beta-oxidation by upregulating ECHS1 expression. These results reflect a biochemically relevant mechanism of fat reduction by (-)-HCA in broiler chickens.
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