Mei Zi, Song Zhenquan, Zhou Haobo, Zheng Bin, Xiong Yiwei, Sheng Zheya, Gong Yanzhang
Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction, College of Animal Science and Technology and College of Veterinary Medicine, Ministry of Education, Huazhong Agricultural University, Wuhan, 430070, China.
Hubei Shendi Agricultural science and trade Co., LTD, Jingmen, China.
BMC Genomics. 2025 Jul 2;26(1):631. doi: 10.1186/s12864-025-11832-2.
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.
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.
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.
热应激对全球家禽生产构成重大挑战，但驱动鸡多个器官急性热应激反应的分子机制仍知之甚少。本研究旨在通过建立急性热应激鸡模型并分析多组织转录组和生理反应来阐明这些机制。
暴露于36℃ 6小时会引起明显的生理变化，包括直肠温度升高、严重的多器官损伤以及能量代谢紊乱（血清葡萄糖[GLU]升高，甘油三酯[TG]和总胆固醇[TCHO]降低）。对心脏、肝脏、脾脏、肺和肾脏组织的比较转录组分析揭示了组织特异性差异基因表达，肝脏和心脏显示出差异表达基因（DEG）数量最多。KEGG富集分析确定了脂质代谢途径是多组织急性热应激反应的关键。加权基因共表达网络分析（WGCNA）进一步鉴定出58个差异模块化中心基因（DMHG），其中42个是肝脏差异表达基因，这些DMHG中的大多数在脂肪酸代谢途径中显著富集。脂肪酸代谢途径相关的DMHG与直肠温度、血清GLU、TG、乳酸脱氢酶（LDH）和天冬氨酸转氨酶（AST）显著相关。原代肝细胞中的功能验证表明，FASN的过表达减轻了热应激诱导的甘油三酯水平降低。
多组织比较转录组揭示了肝脏脂肪酸代谢在介导鸡急性热应激反应中的关键作用，并确定FASN为通过代谢干预提高家禽耐热性提供了可行的见解。
