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Poultry Science 2017-Jun

Effect of Chinese herbal medicine treatment on plasma lipid profile and hepatic lipid metabolism in Hetian broiler.

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Z Xie
J Zhang
S Ma
X Huang
Y Huang

Ключевые слова

абстрактный

The purpose of this study was to investigate whether adding a Chinese herbal hedicine (CHM, including astragalus membranaceus, codonopsis pilosula, poria cocos, bighead atractylodes rhizome, fructus crataegi, folium epimedii, radix saposhnikoviae, and pericarpium citri reticulatae) diet has effects on lipid metabolism in the liver of the broiler. Six-hundred-thirty Hetian broilers were divided into 3 groups including base diet (control), 0.3%, or 1% CHM diets, for 130 days. The results showed that CHM treatment significantly increased the slaughter performance. CHM treatment decreased plasma triglyceride (TG) and nonesterified fatty acid (NEFA) concentrations; up-regulated the expression of peroxisome proliferator activated receptor (PPAR), the transcription factor sterol regulatory element binding protein-1c (SREBP-1c) and its downstream proteins involved in NEFA oxidation including carnitine palmitoyltransferase-1, liver fatty acid binding protein, and PPARα; and it significantly decreased fatty acid synthetase, stearoyl-CoA desaturase, acyl-CoA synthetase long-chain family member 1 and acetyl-CoA carboxylase expression to inhibit NEFA synthesis. In addition, the CHM treatment increased plasma insulin (INS) levels and up-regulated insulin receptors (INSR) glycerol-3-phosphate acyltransferase and mitochondrial and 1-acylglycerol-3-phosphate O-acyltransferase 6 mRNA expression to enhance TG synthesis. The protein levels of phosphatidylinositol 3-hydroxy kinase (PI3K), serine/threonine protein kinase (Akt), S6 kinase (S6K), phospho-serine/threonine protein kinase (p-Akt), and phospho-S6 kinase (p-S6K) also were increased. PI3K, p-Akt, and p-S6K were significantly up-regulated in the liver. These data suggest that the CHM may be a beneficial compound to decrease plasma NEFA and TG levels by activating the INS/INSR-PI3K-Akt-SREBP1c pathway resulting in fat content reduction in the carcass.

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