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https://www.selleckchem.com/products/fenretinide.html The present study was conducted to investigate effects and mechanism of quercetin on lipids metabolism in broilers. 480 AA broilers were randomly allotted to four treatments (0, 0.2, 0.4, and 0.6 g/kg quercetin) for 42 days. Compared with the control, 0.6 g/kg quercetin significantly decreased percentage of abdominal fat (P less then 0.05); 0.2, 0.4, and 0.6 g/kg quercetin significantly decreased relative abundance of Lachnospiraceae and Desulfovibrionaceae (P less then 0.05, P less then 0.05, P less then 0.01; P less then 0.01, P less then 0.01, P less then 0.01); 0.2 g/kg quercetin significantly increased mRNA expression of PI3K, AMPKα1, AMPKα2, AMPKβ2, LKB1 (P less then 0.01, P less then 0.01, P less then 0.05, P less then 0.01, P less then 0.05), and significantly reduced mRNA expression of SREBP1 and PPARγ (P less then 0.01, P less then 0.05); 0.4 g/kg quercetin significantly increased mRNA expression of LKB1 and PKB (P less then 0.05, P less then 0.01) and significantly r 0.01, P less then 0.01). In conclusion, quercetin improved lipid metabolism by modulating gut microbial and AMPK/PPAR signaling pathway in broilers.Proper targeting of the urate and xenobiotic transporter ATP-binding transporter subfamily G member 2 (ABCG2) to the plasma membrane (PM) is essential for its normal function. The naturally occurring Q141K and M71V polymorphisms in ABCG2, associated with gout and hyperuricemia, affect the cellular routing of the transporter, rather than its transport function. The cellular localization of ABCG2 variants was formerly studied by immunolabeling, which provides information only on the steady-state distribution of the protein, leaving the dynamics of its cellular routing unexplored. In the present study, we assessed in detail the trafficking of the wild-type, M71V-, and Q141K-ABCG2 variants from the endoplasmic reticulum (ER) to the cell surface using a dynamic approach, the so-called Retention Usin

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