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Metformin alters liver metabolism to sustain egg production in the reproductively aging broiler breeder hen

ABSTRACT: The liver plays a critical role in avian reproduction as it is the primary site of de novo lipogenesis and yolk precursor synthesis. Broiler breeder hens, the parents of commercial broiler chickens, often experience poor reproductive efficiency primarily due to declining egg production beginning around 45 weeks of age. Metformin, an antidiabetic drug, exerts its primary effects in the liver by increasing insulin sensitivity and reducing hepatic glucose production in humans. This study aimed to characterize the liver transcriptomic profile of broiler breeder hens supplemented with metformin in the diet at 0 or 75 mg/kg body weight for 40 weeks (25-65 weeks of age; n=45 hens/treatment). Liver tissue was collected from a subset of hens (n=12 hens/treatment group) at 65 weeks of age, RNA was extracted and sequenced using next-generation sequencing. Differential gene abundance analysis revealed that metformin treatment led to the most significant changes in gene expression, with 552 genes differentially expressed compared to the control group. Further transcriptomic analysis highlighted increased expression of genes related to estrogen-stimulated yolk precursor synthesis, insulin-stimulated de novo lipogenesis, and AMPK-mediated glucose homeostasis. qPCR analysis revealed increased expression of ESR1, APOB, APOV1, VTG2, ADIPOQ, ADIPOR2 and ACACA mRNA and decreased expression of PCK1 mRNA validating the transcriptomic data. Collectively, the present study suggests that metformin supplementation supports prolonged egg production in aging broiler breeder hens by sustaining yolk precursor and fatty acid synthesis that are typically diminished in aging broiler breeder hens.

ORGANISM(S): Gallus gallus

PROVIDER: GSE286522 | GEO | 2025/01/14

REPOSITORIES: GEO

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Project description:Heat stress (HS) can damage the integrity of the intestinal mucosal barrier, leading to decreased poultry productivity. This study aimed to identify candidate genes related to acute HS in breeder hens and provide insight into the molecular mechanisms underlying acute HS in gut health. Fifty 28-week-old breeder hens were divided into two groups (25 hens each) raised under thermoneutral zone (23 °C) and acute HS (36 °C, 6 hours) conditions. The heart rate and cloacal temperature were measured in all hens, and jejunal mucosa tissues were randomly collected from 12 hens per treatment for RNA-sequencing analysis. The results indicated a significant increase in the heart rate and cloacal temperature in hens exposed to acute HS (P < 0.05). Transcriptome analysis identified 138 differentially expressed genes (DEGs) in heat-stressed breeder hens, including 75 upregulated DEGs containing heat shock protein (HSP), energy homeostasis metabolism-related gene (PDK4), and fat metabolism-related genes (PPARA and CD36), and 63 downregulated DEGs containing the bile acid transporter gene (SLC10A2). Gene ontology analysis revealed significant enrichment in biological processes related to heat response and cholesterol biosynthesis. Kyoto Encyclopedia of Genes and Genomes analysis highlighted several significant pathways, including steroid biosynthesis, steroid hormone biosynthesis, protein processing in endoplasmic reticulum, the peroxisome proliferator-activated receptor (PPAR) signaling pathway, and the adipocytokine signaling pathway. Protein-protein interaction network analysis involving two large networks: one containing several upregulated HSPs and genes related to energy homeostasis and fat metabolism (PDK4, PPARA, and CD36) and glucose transporter (SLC2A5), and the other containing downregulated DEGs related to cholesterol biosynthesis. Overall, acute HS might affect energy metabolism, fat metabolism, and glucose transport in the jejunal mucosa of breeder hens. Heat-stressed hens could restore the nutritional function of the jejunal mucosa by increasing the expression of HSPs. These findings provide a theoretical framework for further investigation into the molecular regulatory mechanisms responsible for HS-induced changes in the gut health of poultry.

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Metformin alters liver metabolism to sustain egg production in the reproductively aging broiler breeder hen

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