Betaine, Taurine and α-Ketoglutarate in Broiler Nutrition: Linking Metabolic Homeostasis, Nutrient Utilization and Growth Efficiency

Abstract

Modern broiler chickens are selected for rapid growth, high breast-muscle accretion and low feed conversion ratio, a phenotype that requires continuous coordination among intestinal nutrient acquisition, hepatic intermediary metabolism, mitochondrial energy production, redox control and skeletal-muscle protein deposition. Functional nutrients that regulate metabolic pathways rather than merely supply substrate have therefore attracted increasing attention in poultry nutrition. Betaine, taurine and α-ketoglutarate (AKG) are chemically distinct metabolites that enter broiler metabolism at different but interconnected nodes. Betaine (trimethylglycine) is a zwitterionic quaternary ammonium compound that acts as a compatible osmolyte and a methyl donor for betaine-homocysteine methyltransferase, thereby supporting methionine regeneration and S-adenosylmethionine-dependent methyl transfer. Taurine (2-aminoethanesulfonic acid) is a non-proteinogenic sulfur-containing metabolite produced downstream of cysteine; it contributes to bile-acid conjugation, membrane stability, mitochondrial function and antioxidant signaling, and recent broiler work has linked it to Nrf2, AMPK/SIRT1/CPT1, lipid metabolism and tissue-specific responses to methionine replacement. AKG (2-oxoglutarate) is a five-carbon keto-dicarboxylate positioned at the junction of the tricarboxylic-acid cycle and amino-group transfer; recent poultry studies have connected AKG with intestinal morphology, antioxidant defense, Nrf2 signaling, microbiota, growth and UCP2-associated control of intestinal oxidative phosphorylation. This review integrates the three nutrients through a methyl–sulfur–carbon metabolic framework rather than treating them as independent feed additives. We trace each compound from chemical structure and gastrointestinal handling to cellular signaling, organ physiology, nutrient partitioning and growth efficiency, while clearly distinguishing direct broiler evidence from avian support and cross-species mechanistic inference. Particular attention is paid to one-carbon metabolism, transsulfuration, bile-acid physiology, Nrf2–Keap1 redox signaling, AMPK/SIRT1 lipid sensing, UCP2-mediated mitochondrial regulation, gut–liver–muscle communication, nitrogen efficiency and context-dependent dose responses. The synthesis identifies major gaps in head-to-head comparison, combination studies, tissue-resolved metabolomics, phosphoproteomics, mitochondrial phenotyping and stable-isotope tracing. A future precision-nutrition framework is proposed in which betaine, taurine or AKG is selected according to the metabolic node that limits nutrient retention and biological efficiency rather than according to generic feed-additive claims.