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Os efeitos dietéticos de lisina digestível e zinco quelato para frangos de corte machos entre 22 e 42 dias de idade foram avaliados em dois ensaios experimentais. Adotou-se o delineamento inteiramente casualizado em arranjo fatorial 5 × 2, com cinco níveis de lisina (0,841; 0,876; 0,997; 1,022 e 1,030%) e dois de zinco (43 e 243 ppm). No primeiro ensaio, utilizaram-se 900 aves com peso médio inicial de 957,4 g distribuídas em parcelas experimentais de 30 aves e três repetições e, no segundo ensaio, 180 frangos com peso médio inicial de 866,22 g, divididos em parcelas de três aves e seis repetições. As características avaliadas foram desempenho, rendimento de cortes e composição corporal (1º ensaio), balanço de nitrogênio e digestibilidade aparente das dietas (2º ensaio). Houve interação entre os níveis de lisina e zinco para o ganho de peso, a conversão alimentar, a matéria seca ingerida e o balanço energético. Os rendimentos de peito, coxa e sobrecoxa tiveram aumentos lineares em resposta ao acréscimo no nível de lisina digestível na dieta. O melhor desempenho foi obtido com o nível de 0,997% de lisina digestível (ou 1,134% lisina total) e de 43 ppm de zinco. Para maior rendimento dos cortes, o nível de lisina digestível recomendável deve ser no mínimo 1,002% (ou 1,139% de lisina total), independentemente dos níveis de zinco quelato. A maior inclusão de zinco em dietas para frangos de corte dos 22 aos 42 dias de idade não melhora a utilização da lisina na dieta e aumenta a deposição de gordura corporal.The dietary effects of digestible lysine and chelate zinc for male broiler chickens from 22 to 42 days of age were evaluated in two experimental assays. A complete randomized block experimental design in a 5 × 2 factorial, with five lysine levels (0.841, 0.876, 0.997, 1.022 and 1.030%) and two levels of zinc (43 and 243 ppm) was used. In the first assay, it was used 900 birds with initial average weight 957.4 g distributed in experimental units with 30 birds and three replications and in the second assay, 180 broilers with initial average weight 866.22g split in plots with 3 birds and six replications were used. The characteristics evaluated were performance, cut yield and body composition (1st assay), nitrogen balance and apparent digestibility of diets (2nd assay). There was an interaction among levels of lysine and zinc for weight gain, feed conversion, ingested dry matter and energy balance. Yields of breast, thigh and drumstick had linear increases in response to increments in the level of digestible lysine in the diet. The best performance was obtained for level 0.997% of digestive lysine (or 1.134% total lysine) and level of 43 ppm zinc. For higher cut yields, the recommended level of digestible lysine has to be at least 1.002% (or 1.139% total lysine), regardless to the levels of chelate zinc. Greater inclusion of zinc in diets for broiler from 22 to 42 days of age does not improve the utilization of dietary lysine and increases body fat deposition.

Objective: Non-alcoholic fatty liver disease (NAFLD) is an aberrant lipid metabolism disease. Hypoxia inducible factor-1 (HIF-1α) is a transcription factor which plays an important part in adapting lower oxygen condition. Here, we aimed to clarify the relationship between HIF-1α and NAFLD., Methods: HepG2 cells was stimulated by oleic acid (OA) and palmitic acid (PA) to establish in vitro model of NAFLD. The expression of lipid metabolism-related genes, the binding of PPARα to HIF-1α promoter, the lipid deposition, and oxidative stress were detected by qRT-PCR, western blot, Chip assay, Oil Red O staining and ELISA assays, respectively., Results: HIF-1α silence promoted lipid accumulation in NAFLD cells, accompanying by the significantly increased contents of TG (triglyceride) and ApoB (apolipoprotein B). In HepG2 cells treated with OA/PA, the expression of lipid metabolism-related genes and proteins, including APOE, A2m, TNFRSF11B, LDLr, and SREBP2, and the intracellular lipid deposition were up-regulated and further aggravated after silencing HIF-1α. In addition, the loss of HIF-1α could remarkably elevate MDA contents while inhibit the activities of beneficial antioxidant enzymes SOD and GSH-Px to activate oxidative stress, and promote the secretion of pro-inflammatory IL-6 and TNF-α to aggravate inflammation in NDFLD cells. PPARα positively bound to HIF-1α promoter. The silence of PPARα aggravated lipid deposition under normal or hypoxic environment in NAFLD cells. In addition, PPAR-α silence could decrease the expression of HIF-1α and ANGPTL4 in NAFLD cell model; moreover, the expression of APOE, A2m and TNFRSF11B and the production of TG and MDA were increased by PPAR-α suppression., Conclusion: HIF-1α plays a crucial role in the regulation of lipid metabolism through activating PPAR-α/ANGPTL4 signaling pathway in NAFLD., (Copyright © 2020. Publicado por Elsevier España, S.L.U.)