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Background <p>Heat stress poses a major challenge to global poultry production, but the molecular mechanisms driving the acute heat stress response in multiple organs of chickens remain poorly understood. The present study aimed to elucidate these mechanisms by establishing an acute heat stress chicken model and analyzing the multi-tissue transcriptome and physiological responses.</p> Results <p>Exposure to 36℃ for 6&#xa0;h induced marked physiological changes, including elevated rectal temperatures, severe multi-organ damage, and disrupted energy metabolism (increased serum glucose [GLU] and decreased triglycerides [TG] and total cholesterol [TCHO]). Comparative transcriptomic analysis of heart, liver, spleen, lung, and kidney tissues revealed tissue-specific differential gene expression, with the liver and heart showing the highest number of differentially expressed genes (DEGs). KEGG enrichment analyses identified lipid metabolism pathways that are key to the multi-tissue acute heat stress response. Weighted gene co-expression network analysis (WGCNA) further identified 58 differentially modularized hub genes (DMHGs), of which 42 were hepatic differentially expressed genes, and most of these DMHGs were significantly enriched for fatty acid metabolic pathways. Fatty acid metabolic pathway-associated DMHGs were significantly correlated with rectal temperature, serum GLU, TG, lactate dehydrogenase (LDH), and aspartate aminotransferase (AST). Functional validation in primary hepatocytes demonstrated that overexpression of <i>FASN</i> attenuated heat stress-induced reductions in triglyceride levels.</p> Conclusions <p>The critical role of hepatic fatty acid metabolism in mediating the acute heat stress response in chickens was revealed by a multi-tissue comparative transcriptome, and it was determined that <i>FASN</i> provides actionable insights into improving heat tolerance in poultry through metabolic interventions.</p>

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Comparative transcriptomic analysis reveals the important role of hepatic fatty acid metabolism in the acute heat stress response in chickens

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月2日

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  • Zi Mei,
  • Zhenquan Song,
  • Haobo Zhou,
  • Bin Zheng,
  • Yiwei Xiong,
  • Zheya Sheng,
  • Yanzhang Gong

摘要

Background

Heat stress poses a major challenge to global poultry production, but the molecular mechanisms driving the acute heat stress response in multiple organs of chickens remain poorly understood. The present study aimed to elucidate these mechanisms by establishing an acute heat stress chicken model and analyzing the multi-tissue transcriptome and physiological responses.

Results

Exposure to 36℃ for 6 h induced marked physiological changes, including elevated rectal temperatures, severe multi-organ damage, and disrupted energy metabolism (increased serum glucose [GLU] and decreased triglycerides [TG] and total cholesterol [TCHO]). Comparative transcriptomic analysis of heart, liver, spleen, lung, and kidney tissues revealed tissue-specific differential gene expression, with the liver and heart showing the highest number of differentially expressed genes (DEGs). KEGG enrichment analyses identified lipid metabolism pathways that are key to the multi-tissue acute heat stress response. Weighted gene co-expression network analysis (WGCNA) further identified 58 differentially modularized hub genes (DMHGs), of which 42 were hepatic differentially expressed genes, and most of these DMHGs were significantly enriched for fatty acid metabolic pathways. Fatty acid metabolic pathway-associated DMHGs were significantly correlated with rectal temperature, serum GLU, TG, lactate dehydrogenase (LDH), and aspartate aminotransferase (AST). Functional validation in primary hepatocytes demonstrated that overexpression of FASN attenuated heat stress-induced reductions in triglyceride levels.

Conclusions

The critical role of hepatic fatty acid metabolism in mediating the acute heat stress response in chickens was revealed by a multi-tissue comparative transcriptome, and it was determined that FASN provides actionable insights into improving heat tolerance in poultry through metabolic interventions.