Due to high basal temperatures, rapid growth, and the absence of sweat glands, chickens are highly susceptible to heat stress, which systematically reprograms hepatic lipid metabolism. Current physiological and multi-omics data highlight three primary effects: increased de novo lipogenesis, suppressed β-oxidation, and impaired very-low-density lipoprotein (VLDL) assembly and export. These metabolic shifts are driven by mitochondrial dysfunction, oxidative stress, and endoplasmic reticulum (ER) stress, leading to hepatic triglyceride accumulation. Consequently, heat stress results in altered carcass fat distribution, changes in fatty acid composition, and reduced meat quality and productivity. Effective mitigation requires an integrated approach combining environmental control, nutritional strategies, and genetic interventions such as thermal conditioning. This review summarizes these mechanisms to identify targets for mitigation strategies for restoring hepatic lipid homeostasis and maintaining poultry performance in a warming climate.
Yang Soo Moon (Mon,) studied this question.