With the transformation of modern poultry farming towards a high-density and high-energy diet mode, fatty liver syndrome (FLS) has become an important metabolic disease restricting production performance. Its core pathological feature is the abnormal accumulation of triglycerides (TG) in liver cells, and the essence is the imbalance of lipid metabolism in the liver: when fat synthesis (such as the activation of the de novo fatty acid synthesis pathway) exceeds the capacities of decomposition (such as limited mitochondrial β-oxidation) and transportation (such as insufficient secretion of very low-density lipoprotein VLDL), excessive lipids are deposited in the form of lipid droplets, leading to damage to the liver cell membrane, oxidative stress, and inflammatory responses. Eventually, it results in a decrease in feed intake, a sharp decline in egg production rate, or liver rupture and bleeding. Studies have shown that for every 1% increase in the abdominal fat rate of broilers, the feed conversion ratio increases by 2.3%; there is a significant negative correlation between the incidence of fatty liver in laying hens and the duration of the peak egg production period.
The Core Molecular Mechanism of Bile Acids Regulating Lipid Metabolism
As an endogenous bioactive molecule synthesized by the liver, bile acids construct a lipid metabolism regulation network through the “liver-gallbladder-intestine” axis, and its functions can be summarized into three core pathways:
1.The Key Initiating Factor for Intestinal Lipid Digestion
After being secreted into the intestine with bile, bile acids (mainly composed of hyodeoxycholic acid, chenodeoxycholic acid, and cholic acid) emulsify the triglycerides in the diet into micelles with a diameter of < 200nm by virtue of their amphiphilic molecular structure (hydrophilic hydroxyl groups and hydrophobic steroid rings), increasing the surface area for the action of lipase by more than 100 times and significantly improving the efficiency of lipid digestion (in vitro experiments show that adding bile acids can increase the activity of lipase). At the same time, as a carrier, it mediates the transportation of fatty acids and fat-soluble vitamins (A/D/E/K) in intestinal epithelial cells, and completes transmembrane absorption through the apical membrane transporter ASBT and the basolateral transporter OSTα/β, ensuring the efficient utilization of nutrients.
2.The Nuclear Receptor Regulation Network for Liver Lipid Homeostasis
Bile acids reconstruct the liver metabolic pathway by activating the farnesoid X receptor (FXR) and peroxisome proliferator-activated receptor α (PPARα):
Promoting Decomposition: PPARα induces the expression of carnitine palmitoyltransferase 1 (CPT-1), accelerates the entry of fatty acids into mitochondria for β-oxidation, and at the same time inhibits the activities of key enzymes in fat synthesis, such as acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), reducing the synthesis of TG from the source.
>Promoting Transportation: FXR activates the liver X receptor (LXR)-sterol regulatory element-binding protein 1c (SREBP-1c) pathway, promotes the assembly and secretion of VLDL, and transports the excess lipids in the liver to peripheral tissues.
>Antioxidant Stress: By regulating the gene expression of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), it reduces oxidative damage and repairs the integrity of the liver cell membrane (electron microscopy observation shows that the swelling rate of liver cell mitochondria in the group supplemented with bile acids is reduced by 65%).
3.The Bidirectional Regulatory Effect of the Enterohepatic Axis
Bile acids in the intestine reduce the liver inflammatory response induced by lipopolysaccharide (LPS) by regulating the balance of the microbiota (such as inhibiting the proliferation of gram-negative bacteria that produce endotoxins). At the same time, secondary bile acids (such as lithocholic acid LCA) act as ligands for the G protein-coupled receptor TGR5, promoting the secretion of glucagon-like peptide-1 (GLP-1) in the intestine, indirectly enhancing the insulin sensitivity of the liver, and inhibiting gluconeogenesis and fat synthesis.
According to experimental data, the content of triglycerides (TG) in the liver of the high-fat model group increased by 150% compared with the normal group, while after adding 200 mg/kg of bile acids, the liver lipid content decreased to 120% of that in the normal group.
Recommended Dosage and Synergistic Effects
*Laying Hens: 200-300 g/t of feed can extend the peak egg production period and reduce the incidence of fatty liver. For example, when adding 300 g/t of bile acids and reducing 4 kg/t of oil, the egg production rate of laying hens increases by 4-8%, and the eggshell quality is significantly improved.
*Broilers: 300-400 g/t of feed can reduce the feed conversion ratio by 6-10% and at the same time reduce the fat dosage by 16-31%.
