A Hypothesis-Based Framework for Chicken Meat Palatability: Proposing Indirect Roles of Arachidonic Acid and Lipid Oxidation

Chicken meat palatability is shaped by what the meat contains (e.g., intramuscular fat and fatty-acid composition), what happens to those components during storage and cooking (including oxidation and transfer into soups or meat juices), and how tastebud signaling integrates the resulting stimuli. Chicken sold in Japan as “Jidori” (premium native-line products) is often described as having a richer flavor that lingers longer than that of standard broiler chicken, and published poultry work, including reports by the author and their colleagues, has linked this phenotype to higher arachidonic acid (AA) levels in the meat; however, the mechanistic basis remains under debate and has not been overturned. In addition, intact AA is a highly hydrophobic long-chain fatty acid that partitions poorly into aqueous phases, making a direct “AA-as-tastant” mechanism unlikely. This review develops a hierarchical interpretation that separates food-level associations from tastebud mechanisms and reframes AA as a primarily downstream lipid substrate. Two complementary routes are proposed: (i) a food-chemistry route in which cooking and storage oxidation generate low-molecular-weight, water-accessible lipid-oxidation products that partition into soups, meat juices, and cooking loss, and (ii) a receptor-centered route in which kokumi-related signaling pathways, particularly those involving the calcium-sensing receptor (CaSR), amplify taste intensity, continuity, and aftertaste within tastebuds. This framework emphasizes how these routes can be linked experimentally by combining matrix/phase manipulations with targeted carbonyl profiling, fractionation–reconstitution, and pathway-perturbation assays in tastebud readouts. Overall, the model is intended to support mechanism-focused study designs beyond single-compound explanations.