Dataset Information

Supplementing Genistein for Breeder Hens Alters the Fatty Acid Metabolism and Growth Performance of Offsprings by Epigenetic Modification.

ABSTRACT: The experiment was designed to clarify the effect and molecular mechanism of maternal genistein (GEN) on the lipid metabolism and developmental growth of offspring chicks. Laying broiler breeder (LBB) hens were supplemented with 40?mg/kg genistein (GEN), while the control group was fed with the low-soybean meal diet. The offspring chicks were grouped according to the mother generation with 8 replicates each. Hepatic transcriptome data revealed 3915 differentially expressed genes (DEGs, P adjusted < 0.05, fold change > 1.5 or fold change < 0.67) between chicks in the two groups. Maternal GEN activated the GH-IGF1-PI3K/Akt signaling pathway, which promoted the developmental processes and cellular amino acid metabolic processes, as well as inhibited the apoptotic process. GEN treatment significantly increased the weight gain, breast muscle percentage, and liver index in chicks. PANTHER clustering analysis suggested that maternal GEN enhanced the antioxidant activity of chicks by the upregulation of gene (SOD3, MT1, and MT4) expression. Accordingly, the activities of T-AOC and T-SOD in the liver were increased after GEN treatment. The overrepresentation tests revealed that maternal GEN influenced the glycolysis, unsaturated fatty acid biosynthesis, acyl-coenzyme A metabolism, lipid transport, and cholesterol metabolism in the chick livers. Hepatic cholesterol and long-chain fatty acid were significantly decreased after GEN treatment. However, the level of arachidonic acid was higher in the livers of the GEN-treated group compared with the CON group. Moreover, GEN treatment enhanced fatty acid ?-oxidation and upregulated PPAR? expression in the chick liver. ChIP-qPCR analysis indicated that maternal GEN might induce histone H3-K36 trimethylation in the promoter region of PPAR? gene (PPARD) through Iws1, methyltransferases. It also induced histone H4-K12 acetylation at the PPARD promoter through MYST2, which activated the PPAR signaling pathways in the chick livers. In summary, supplementing LBB hens with GEN can alter lipid metabolism in the offspring chicks through epigenetic modification and improve the antioxidative capability as well as growth performance.

SUBMITTER: Lv Z

PROVIDER: S-EPMC6458848 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Supplementing Genistein for Breeder Hens Alters the Fatty Acid Metabolism and Growth Performance of Offsprings by Epigenetic Modification.

Lv Zengpeng Z Fan Hao H Song Bochen B Li Guang G Liu Dan D Guo Yuming Y

Oxidative medicine and cellular longevity 20190326

The experiment was designed to clarify the effect and molecular mechanism of maternal genistein (GEN) on the lipid metabolism and developmental growth of offspring chicks. Laying broiler breeder (LBB) hens were supplemented with 40 mg/kg genistein (GEN), while the control group was fed with the low-soybean meal diet. The offspring chicks were grouped according to the mother generation with 8 replicates each. Hepatic transcriptome data revealed 3915 differentially expressed genes (DEGs, <i>P</i> ...[more]

PMID: 31049141

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Project description:Ad libitumfeeding in broiler breeder (BB) hens causes reduced egg production, lower fertility, and improper eggshell deposition. Restricted feeding (RF) is the only effective intervention available to normalize ovarian function and improve reproductive efficiency. This study aimed to assess the transcriptional changes in ovarian cortex of BB hens with free access to feed compared to those on a RF diet. RNA was isolated from the ovarian cortex of Cobb 500 pullets raised to 10 and 16 weeks of age on either a full-feeding (FF) or RF diet. Microarray analysis identified 386 differentially expressed genes between the two feeding groups at 16 weeks of age. Gene ontology enrichment identified overrepresentation of Neuroactive ligand-receptor interaction pathways, Cell adhesion molecules, Steroid hormone biosynthesis, and various KEGG pathways. From these groups, 46 genes were selected for follow-up validation by quantitative PCR. The findings show that 33 of the 46 genes had significantly different abundance by age and/or feeding level. Most of these genes were repressed in RF hens and belonged to the steroid biosynthesis and neuropeptide signaling groups. The VIPR2 receptor was higher in the FF group leading us to hypothesize that vasoactive intestinal peptide (VIP) is an important regulator of small cortical follicles. Culture of hen cortical follicles with VIP increased Star, an indication of increased steroidogenic activity, although did not elevate Cyp11a1. These results offer insights and suggest the possible mechanisms and pathways responsible for the increases in cortical follicle growth associated with excess feed intake in BB hens.Lay summaryGiving breeder hens unrestricted access to feed can lead to problems with their ovaries, including excessive growth of the ovary and reduced fertility. Giving a limited amount of feed is the only effective way to reduce this growth of the ovaries and improve fertility. This study aimed to assess the changes in the molecules that make proteins in the body in hens fed unrestricted and restricted diets. In the hens fed a limited amount of feed, there were more of one type of molecules, while there were more of another type in the ovaries of hens with unrestricted access to feed. These results show that how much a hen eats can alter the number of these molecules in the ovary and this could help us understand why their ovaries grow excessively and why their eggs are less fertile.

Project description:Sperm storage tubules (SSTs) in the uterovaginal junction (UVJ) of the oviduct are major sites of sperm storage after artificial insemination or mating. Female birds may regulate sperm motility in the UVJ. Heat stress can decrease the reproductive ability of broiler breeder hens. However, its effects on UVJ remain unclear. Changes in gene expression aid in understanding heat stress-affected molecular mechanisms. Herein, we wanted to conduct a comparative transcriptomic analysis to identify the differentially expressed genes (DEGs) in the UVJ of breeder hens under thermoneutral (23°C) and heat stress (36°C for 6 h) conditions. The results indicated that cloacal temperatures and respiratory rates were significantly increased in heat-stressed breeder hens (P < 0.05). Total RNA was extracted from the hen UVJ tissues containing SSTs after heat exposure. Transcriptome analysis identified 561 DEGs, including 181 upregulated DEGs containing heat shock protein (HSP) transcripts and 380 downregulated DEGs containing immune-related genes, such as interleukin 4-induced 1, radical S-adenosyl methionine domain containing 2, and 2'-5'-oligoadenylate synthetase like, in heat-stressed hens. Gene Ontology analysis revealed the significantly enriched terms involving HSPs. Kyoto Encyclopedia of Genes and Genomes analysis identified 9 significant pathways, including the protein processing in endoplasmic reticulum (11 genes including HSPs), neuroactive ligand-receptor interaction (13 genes including luteinizing hormone/choriogonadotropin receptor), biosynthesis of amino acids (4 genes including tyrosine aminotransferase), ferroptosis (3 genes including heme oxygenase 1), and nitrogen metabolism (carbonic anhydrase [CA]-12 and CA6) pathways. Protein-protein interaction network analysis of DEGs revealed 2 large networks, one containing upregulated HSPs and the other containing downregulated interferon-stimulating genes. Overall, heat stress inhibits innate immunity in the UVJ tissues of broiler chickens, and heat-stressed chickens protect their cells by increasing the expression levels of HSPs. The identified genes are potential candidates for further exploration of the UVJ in heat-stressed hens. The identified molecular pathways and networks increase our understanding of the sperm storage reservoirs (UVJ containing SSTs) within the reproductive tract and may be used to prevent heat stress-induced fertility loss in breeder hens.

Dataset Information

Supplementing Genistein for Breeder Hens Alters the Fatty Acid Metabolism and Growth Performance of Offsprings by Epigenetic Modification.

Publications

Supplementing Genistein for Breeder Hens Alters the Fatty Acid Metabolism and Growth Performance of Offsprings by Epigenetic Modification.

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