# Ovariectomy Enhances Carcass Performance and Meat Quality by Modulating Muscle Development and Lipid Metabolism in Wuding Hens

**Authors:** Le Zhang, Xiaoqi Xu, Wenbin Dao, Yongwang Miao

PMC · DOI: 10.3390/ani15213183 · Animals : an Open Access Journal from MDPI · 2025-10-31

## TL;DR

Removing ovaries in hens increases meat quality and body weight by altering muscle and fat metabolism.

## Contribution

A novel estrogen-deficient model in Wuding hens reveals how estrogen affects muscle growth and meat quality through multi-omics analysis.

## Key findings

- Ovariectomized hens had higher body weight and carcass yield than controls.
- Thigh muscle tenderness improved in estrogen-deficient hens despite no changes in muscle fiber structure.
- Estrogen withdrawal altered lipid metabolism and activated key signaling pathways like MAPK and mTOR.

## Abstract

Estrogen is an important hormone that shapes muscle growth and function, but its role in female chickens has not been fully clarified. To address this, we used Wuding hens, a traditional Chinese breed, and surgically removed the ovaries to establish an estrogen-deficient model. Growth performance, muscle quality, and lipid metabolism were then compared with intact hens that retained normal estrogen production. By the end of the growth cycle, the ovariectomized hens showed greater body weight and higher carcass yield than controls. Their leg muscles were also more tender, even though the morphology of muscle fibers did not differ between groups. Lipid analysis revealed that intramuscular triglycerides increased at specific growth stages, pointing to altered fat deposition. At the molecular level, transcriptomic and proteomic profiling indicated that estrogen influences both muscle development and energy metabolism through changes in signaling pathways and gene expression. Taken together, these findings demonstrate that estrogen has a complex role in regulating muscle traits in hens. Beyond advancing our understanding of hormone action in poultry, this work also provides insights that may be useful for improving meat quality in female chickens.

Estrogen is a key regulator of skeletal muscle growth and metabolism in birds, yet its specific roles in female chickens remain poorly defined. To address this gap, we established an estrogen-deficient model by surgically removing the ovaries of Wuding hens, a Chinese indigenous slow-growing breed. Growth traits, carcass yield, and meat quality were evaluated across different ages, complemented by histological examination, serum biochemical analysis, and multi-omics approaches (transcriptomics, proteomics, and lipidomics). Ovariectomized hens maintained somatic growth for a longer period and reached greater body weight and carcass yield at 330 days compared with intact controls. Thigh muscle tenderness was also enhanced in the absence of estrogen, despite no long-term differences in muscle fiber morphology. Lipidomic analysis revealed a transient increase in intramuscular triglyceride content at mid-growth (240 days), pointing to altered lipid storage and distribution. Integrated omics profiling further demonstrated significant changes in the mitogen-activated protein kinase (MAPK) and mechanistic target of rapamycin (mTOR) signaling pathways, accompanied by differential expression of key metabolic and structural genes, including mitogen-activated protein kinase 8 (MAPK8), fatty acid binding protein 4 (FABP4), ankyrin 1 (ANK1), and coenzyme Q6 monooxygenase (COQ6). These molecular adjustments suggest that estrogen withdrawal triggers broad reprogramming of muscle signaling and lipid metabolism. Overall, this study highlights the multifaceted role of estrogen in coordinating growth, muscle quality, and lipid homeostasis in hens and provides a functional model for studying estrogen deficiency in poultry with implications for meat quality improvement.

## Linked entities

- **Genes:** MAPK8 (mitogen-activated protein kinase 8) [NCBI Gene 5599], FABP4 (fatty acid binding protein 4) [NCBI Gene 2167], ANK1 (ankyrin 1) [NCBI Gene 286], COQ6 (coenzyme Q6, monooxygenase) [NCBI Gene 51004]

## Full-text entities

- **Genes:** ANK1 (ankyrin 1) [NCBI Gene 396311] {aka CHANK1}, MAPK8 (mitogen-activated protein kinase 8) [NCBI Gene 423778], FABP4 (fatty acid binding protein 4) [NCBI Gene 374165] {aka A-FABP, AFABP, FABP}, MTOR (mechanistic target of rapamycin) [NCBI Gene 419455] {aka FRAP1}, COQ6 (coenzyme Q6, monooxygenase) [NCBI Gene 423342]
- **Diseases:** estrogen deficiency (MESH:D056828), muscle tenderness (MESH:D063806)
- **Chemicals:** triglyceride (MESH:D014280), Lipid (MESH:D008055)
- **Species:** Gallus gallus (bantam, species) [taxon 9031]

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12607552/full.md

## References

36 references — full list in the complete paper: https://tomesphere.com/paper/PMC12607552/full.md

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Source: https://tomesphere.com/paper/PMC12607552