Dataset Information

Quercetin Improving Lipid Metabolism by Regulating Lipid Metabolism Pathway of Ileum Mucosa in Broilers.

ABSTRACT: This study is aimed at evaluating the regulatory mechanism of quercetin on lipid metabolism in the ileum of broilers to better understand these pathways decreasing abdominal fat. 480 chickens were randomly divided into 4 groups (control, 0.02% quercetin, 0.04% quercetin, and 0.06% quercetin). Breast muscle, thigh muscle, and abdominal fat pad were removed and weighed at 42?d of age. Serum was obtained by centrifuging blood samples from the jugular vein (10?ml) to determine high-density lipoprotein (HDL), total cholesterol (TC), low-density lipoprotein (LDL), triglyceride (TG), leptin, and adiponectin using ELISA. About 5?g of the ileum was harvested and immediately frozen in liquid nitrogen for RNA-seq. Then, the confirmation of RNA-seq results by the Real-Time Quantitative PCR (RT-qPCR) method was evaluated using Pearson's correlation. Compared with control, abdominal fat percentage was significantly decreased with increasing quercetin supplementation, and the best result was obtained at 0.06% dietary quercetin supplementation (P < 0.01). Breast muscle percentage was significantly decreased at 0.02% quercetin (P < 0.01), and thigh muscle percentage tended to increase (P = 0.078). Meanwhile, 0.04% and 0.06% quercetin significantly decreased TG (P < 0.01), TC (P < 0.01), and LDL content (P < 0.05) in serum. Serum leptin and adiponectin contents were significantly increased by 0.04% and 0.06% dietary quercetin supplementation, compared with the control (P < 0.01). Analyses of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) database were used to identify differently expressed genes and lipid metabolism pathways. Quercetin decreased abdominal fat percentage through regulating fat digestion and absorption, glycerophospholipid metabolism, AMPK signaling pathway, fatty acid degradation, and cholesterol metabolism.

SUBMITTER: Wang M

PROVIDER: S-EPMC7520004 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Quercetin Improving Lipid Metabolism by Regulating Lipid Metabolism Pathway of Ileum Mucosa in Broilers.

Wang Mi M Mao Yanjun Y Wang Bo B Wang Shanshan S Lu Han H Ying Linlin L Li Yao Y

Oxidative medicine and cellular longevity 20200918

This study is aimed at evaluating the regulatory mechanism of quercetin on lipid metabolism in the ileum of broilers to better understand these pathways decreasing abdominal fat. 480 chickens were randomly divided into 4 groups (control, 0.02% quercetin, 0.04% quercetin, and 0.06% quercetin). Breast muscle, thigh muscle, and abdominal fat pad were removed and weighed at 42 d of age. Serum was obtained by centrifuging blood samples from the jugular vein (10 ml) to determine high-density lipoprote ...[more]

PMID: 33014279

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Project description:The purpose of the experiment was to investigate the Toll-like receptor signaling pathway of quercetin regulating avian beta-defensin (AvBD) in the ileum of Arbor Acre (AA) broilers. Four hundred and eighty one-day-old Arbor Acre broilers with similar body weight, half male and female, were randomly allotted to four treatments; the control treatment and three dietary treatments were fed with the basal diets supplemented with 0, 0.02%, 0.04, and 0.06% quercetin, respectively. The results showed that dietary quercetin supplementation did not significantly influence growth performance (p > 0.05), but significantly decreased the mortality rate of broilers by 85.74%, 85.74, and 71.28%, respectively (p < 0.05, F = 9.06). Compared with control, dietary supplementation with 0.04 and 0.06% quercetin significantly upregulated mRNA expression of total AvBD (p < 0.05), and there were no significant differences in the mRNA expression of AvBD1, AvBD2, and AvBD14 in three quercetin supplementation groups in the ileum of AA broilers (p > 0.05). Dietary supplementation with 0.02 and 0.06% quercetin significantly downregulated the mRNA expression of total Toll-like receptors (p < 0.05). Dietary quercetin supplementation significantly downregulated the mRNA expression of TLR1A, TLR1B, and TLR2A (p < 0.05); however, there were no significant differences in the mRNA expression of TLR2B, TLR5, and TLR15 (p > 0.05). Dietary quercetin supplementation significantly downregulated the mRNA expression of myeloid differentiation primary response protein 88 (MyD88) and TIR domain-containing adaptor protein/MyD88-adaptor-like (TIRAP/MAL) (p < 0.05), 0.02% quercetin significantly downregulated the mRNA expression of tank-binding kinase1 (TBK1), IκB kinase complex-α (IKKα), IKKβ, IKKε, nuclear factor-kappa B (NF-κB), NF-κB inhibitor-alpha (IκBα), IκBα, IκBβ, TNF-receptor-associated factor 3 (TRAF3), and interferons regulatory factor 7 (IRF7) (p < 0.05), 0.04% quercetin significantly downregulated the mRNA expression of IKKβ, IKKε, NF-κB, IκBα, IκBβ, TRAF3, and TRAF6 (p < 0.05), and 0.06% quercetin significantly downregulated the mRNA expression of TBK1 and IKKα (p < 0.05). 0.02% quercetin significantly decreased the relative abundance of Escherichia, Staphylococcus (p < 0.05), and Salmonella (p < 0.01), 0.04% quercetin significantly decreased the relative abundance of Staphylococcus (p < 0.05), Escherichia, and Salmonella (p < 0.01), and 0.06% quercetin significantly decreased the relative abundance of Salmonella (p < 0.05) and Staphylococcus (p < 0.01) in the ileum of AA broilers. These findings suggested that dietary quercetin supplementation regulated the mRNA expression of AvBD, TLR, and the TLR signaling pathways and NF-κB signalling pathways, thereby maintaining the microecological balance of the intestinal tract and decreasing the mortality of broilers, and the optimum addition amount of quercetin is 0.04% under the test conditions.

Project description:This study was conducted to investigate the effects and mechanism of quercetin on chicken quality in broilers. We selected 480 AA broilers (1 day old) and randomly allotted those to four treatments (negative control and 0.2, 0.4, or 0.6 g of quercetin per kg of diet) for 42 days. Compared with the control group, the supplementation with 0.4 g of quercetin significantly increased the pH45min and L * value of the thigh muscle and decreased the shearing force of the thigh muscle and breast muscle and drip loss of the thigh muscle (P < 0.05). The supplementation with 0.6 g/kg of quercetin significantly increased the pH45min and L * value of the thigh muscle, and pH45min of breast muscle and decreased the drip loss of the thigh muscle (P < 0.05). Sensory scores of meat color, tenderness, and juiciness also were improved with increasing quercetin concentration (P < 0.05). The inosinic acid (IMP) content of the breast and thigh muscles of broilers was significantly increased by supplementation with 0.6 g/kg of quercetin (P < 0.05). Supplementation with 0.2, 0.4, and 0.6 g of quercetin significantly reduced mRNA expression of L-FABP (P < 0.05, P < 0.05, and P < 0.05); supplementation with 0.4 and 0.6 g/kg of quercetin significantly increased mRNA expression of PKB and AMPKα1 (P < 0.05 and P < 0.05); supplementation with 0.6 g/kg of quercetin in the diet significantly reduced mRNA expression of SREBP1 and HMGR (P < 0.05 and P < 0.05) and significantly increased mRNA expression of CPT1 and PPARγ (P < 0.05 and P < 0.05); and supplementation with 0.2, 0.4, and 0.6 g/kg of quercetin significantly increased mRNA expression of PI3K, LPL, and Apo A1 and significantly reduced mRNA expression of ACC and FATP1 in the breast muscle of broilers (P > 0.05). PI3k, PKB, AMPK, SREBP1, and L-FABP were significantly and positively correlated with pH45min (P < 0.05); PPARγ was significantly and positively correlated with shear force (P < 0.05); CPT1 was significantly and positively correlated with the L * value (P < 0.05); and HMGR was significantly and positively correlated with drip loss (P < 0.05). In conclusion, quercetin improved the meat quality, protecting it against lipid oxidation and deposition by regulating the PI3K/PKB/AMPKα1 signaling pathway in the breast muscle of broilers.

Project description:Quercetin, the main component of flavonoids, has a wide range of biological actions. Quercetin can be made into a variety of additives for practice, because of the stable chemical structure and water-soluble derivatives. This study was intended to explore the effects of quercetin on immune function and its regulatory mechanism in Arbor Acre broiler to provide a practical basis for improving poultry immune function and figure out the optimum supplementation as functional feed additives. A total of 240 one-day-old healthy Arbor Acre broilers, similar in body weight, were randomly allotted to 4 treatments with 6 replicates, 10 broilers in each replicate and fed with diets containing quercetin at 0, 0.02, 0.04, and 0.06% for 6 wk. Blood and immune organs (spleen, thymus, and bursa) were collected from chickens at the end of the experiment. Growth performance, immune organs indexes, contents of serum immune molecules, splenic T lymphocyte proliferative responses, and expression of immune related genes were evaluated. The results showed that dietary quercetin had no significant effect (P > 0.05) on growth performance of broilers. Compared with control, 0.06% quercetin supplementation in diet significantly increased spleen index and thymus index (P < 0.05). It also increased the secretion of immune molecules including immunoglobulin A (IgA), interleukin-4 (IL-4) (P < 0.001), immunoglobulin M (IgM) (P = 0.007), complement component 4 (C4) (P = 0.001), and tumor necrosis factor-α (TNF-α) (P < 0.05). On the other hand, 0.02% quercetin supplementation significantly increased complement component 3 (C3) (P < 0.05). Additionally, both 0.04 and 0.06% quercetin supplementation significantly increased expression of TNF-α, TNF receptor associated factor-2 (TRAF-2), TNF receptor superfamily member 1B (TNFRSF1B), nuclear factor kappa-B p65 subunit (NF-κBp65), and interferon-γ (IFN-γ) mRNA (P < 0.05), and expression of NF-κB inhibitor-alpha (IκB-α) mRNA were significantly decreased (P < 0.05). Thus, quercetin improved immune function via NF-κB signaling pathway triggered by TNF-α.

Project description:The objective of this study was to determine the effects of angiopoietin-like protein 4 (ANGPTL4) on breast muscle lipid metabolism in broilers. In experiment 1, 36 thirty-five-day-old male Arbor Acres broilers were randomly allocated into 6 treatment groups with 6 birds in a completely randomized design. The broilers were subjected to intravenous injection of His-SUMO-ANGPTL4 at the dose of 0 (injection of normal saline [NS]), 20, 100, 500, 2,500, or 12,500 ng/kg BW, respectively. The results showed that broilers at 30 min after His-SUMO-ANGPTL4 at the level of 12,500 ng/kg BW intravenous injection had higher (P < 0.05) concentrations of triglyceride and non-esterified fatty acid in the serum, higher (P < 0.05) adipose triglyceride lipase and carnitine palmitoyltransferase 1 mRNA expression in the breast muscle, but lower (P < 0.05) lipoprotein lipase (LPL) mRNA expression in the breast muscle. In experiment 2, 18 thirty-five-day-old male Arbor Acres broilers were randomly allocated into 3 treatment groups with 6 birds in a completely randomized design. The broilers were subjected to intravenous injection of NS, His-SUMO, or His-SUMO-ANGPTL4 (12,500 ng/kg BW) in order to rule out the effect of His-SUMO tag. It's confirmed that ANGPTL4 could increase (P < 0.05) concentrations of triglyceride and non-esterified fatty acid in the serum, enhance (P < 0.05) adipose triglyceride lipase mRNA expression in the breast muscle, and decrease (P < 0.05) LPL mRNA expression in the breast muscle. In experiment 3 and 4, co-culture experiments of chicken primary myoblasts and NS, His-SUMO, or His-SUMO-ANGPTL4 (250 pg/mL, physiological dose) were set up to monitor the cytotoxicity of ANGPTL4 and the changes of lipid metabolism-related genes expression. It was found that cell viability was not affected but LPL mRNA expression in chicken primary myoblasts was highly reduced (P < 0.05) by ANGPTL4. In conclusion, ANGPTL4 could promote lipodieresis and inhibit LPL in the breast muscle of broilers.

Project description:BackgroundSalvia-Nelumbinis naturalis (SNN), the extract of Chinese herbal medicine, has shown effects on NAFLD. This study aims to explore the underlying mechanism of SNN for regulating the lipid metabolism disorder in NAFLD based on the SIRT1/AMPK signaling pathway.MethodsMale C57BL/6J mice fed with a high-fat diet (HFD) were used to establish the NAFLD model. Dynamic changes of mice including body weight, liver weight, serological biochemical indexes, liver histopathological changes, and protein level of AMPK and SIRT1 were monitored. After18 weeks, SNN treatment was administrated to the NAFLD mice for another 4 weeks. Besides the aforementioned indices, TC and TG of liver tissues were also measured. Western blot and quantitative RT-PCR were used to detect the expression and/or activation of SIRT1 and AMPK, as well as the molecules associated with lipid synthesis and β-oxidation. Furthermore, AML12 cells with lipid accumulation induced by fatty acids were treated with LZG and EX527 (SIRT1 inhibitor) or Compound C (AMPK inhibitor ) to confirm the potential pharmacological mechanism.ResultsDynamic observation found the mice induced by HFD with gradually increased body and liver weight, elevated serum cholesterol, hepatic lipid accumulation, and liver injury. After 16 weeks, these indicators have shown obvious changes. Additionally, the hepatic level of SIRT1 and AMPK activation was identified gradually decreased with NAFLD progress. The mice with SNN administration had lower body weight, liver weight, and serum level of LDL-c and ALT than those of the NAFLD model. Hepatosteatosis and hepatic TG content in the liver tissues of the SNN group were significantly reduced. When compared with control mice, the NAFLD mice had significantly decreased hepatic expression of SIRT1, p-AMPK, p-ACC, ACOX1, and increased total Acetylated-lysine, SUV39H2, and SREBP-1c. The administration of SNN reversed the expression of these molecules. In vitro experiments showed the effect of SNN in ameliorating hepatosteatosis and regulating the expression of lipid metabolism-related genes in AML12 cells, which were diminished by EX527 or Compound C co-incubation.ConclusionsTaken together, the SIRT1/AMPK signaling pathway, involved in hepatic lipid synthesis and degradation, plays a pivotal role in the pathogenesis of NAFLD development. The regulation of SIRT1/AMPK signaling greatly contributes to the underlying therapeutic mechanism of SNN for NAFLD.

Dataset Information

Quercetin Improving Lipid Metabolism by Regulating Lipid Metabolism Pathway of Ileum Mucosa in Broilers.

Publications

Quercetin Improving Lipid Metabolism by Regulating Lipid Metabolism Pathway of Ileum Mucosa in Broilers.

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