Nutritional and metabolic mechanisms linking low protein and low amino acid diets to fatty liver in laying hens.

Fatty liver is a common metabolic disorder in laying hens and is strongly influenced by dietary protein and amino acid supply. Low protein or low amino acid diets disrupt the balance between nitrogen and energy intake, enhancing hepatic de novo lipogenesis. Severe dietary protein and amino acid deficiency also impairs hepatic apolipoprotein synthesis and secretion. These metabolic alterations promote hepatic triglyceride accumulation and increase susceptibility to fatty liver. Although nutrient-sensing mechanisms in birds remain incompletely defined, evidence from mammalian studies suggests that amino acid deficiency may activate GCN2-ATF4 signaling and modulate mTORC1 activity, contributing to lipogenic reprogramming. Importantly, protein dilution alone rarely induces severe steatosis; rather, the combination of low protein and excessive dietary energy (HELP diet feeding) markedly amplifies lipogenesis, oxidative stress, inflammation, and hepatic injury, accelerating progression toward fatty liver hemorrhagic syndrome (FLHS). This review summarizes current knowledge on the physiological and molecular mechanisms linking low protein and low amino acid diets to fatty liver in laying hens, evaluates the HELP model as an experimental framework for FLHS, and outlines nutritional and functional additives shown to mitigate HELP-induced hepatic pathology. Together, these insights provide a mechanistic basis for developing safer low protein feeding strategies in modern layer production.