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Clé UT : 000316202300022; International audience; Early feeding experiences, e.g. related to milk feeding, can affect later food and taste preferences. However, consequences of breast-feeding on taste acceptance are under-investigated. The objective of the present study was to examine the impact of exclusive breast-feeding duration (DEB) on taste acceptance at 6 and 12 months in the same infants (n 122). Mothers recorded the DEB. Acceptance of solutions of each of the five basic tastes relative to water was evaluated in the laboratory at 6 and 12 months by the ingestion ratio (IR). Kendall correlations were calculated between the DEB and the IR. Only 16 % completed at least 6 months of exclusive breast-feeding; 79 % had begun complementary feeding by 6 months. At 6 months, infants preferred sweet, salty and umami solutions over water and were indifferent to sour and bitter solutions. The longer an infant was breast-fed, the more s/he accepted the umami solution at 6 months. At 12 months, infants preferred sweet and salty solutions over water and were indifferent to sour, bitter and umami solutions. The relationship between the DEB and acceptance of the umami solution was not observed at 12 months. No relationship was observed between the DEB and sweet, salty, sour and bitter taste acceptance at 6 or 12 months. The association between the DEB and umami taste acceptance at 6 months may relate to the higher glutamate content of human milk compared with formula milk. Beyond the acknowledged metabolic benefits of breast-feeding, this suggests that prolonged breast-feeding could also be associated with an impact on sensory preference at the beginning of complementary feeding.

International audience; Umami is the typical taste induced by monosodium glutamate (MSG), which is thought to be detected by the heterodimeric G protein-coupled receptor, T1R1 and T1R3. Previously, we showed that MSG detection thresholds differ substantially between individuals and we further showed that nontaster and hypotaster subjects are associated with nonsynonymous single polymorphisms occurring in the T1R1 and T1R3 genes. Here, we show using functional expression that both amino acid substitutions (A110V and R507Q) in the N-terminal ligand-binding domain of T1R1 and the 2 other ones (F749S and R757C), located in the transmembrane domain of T1R3, severely impair in vitro T1R1/T1R3 response to MSG. A molecular model of the ligand-binding region of T1R1/T1R3 provides a mechanistic explanation supporting functional expression data. The data presented here support causal relations between the genotype and previous in vivo psychophysical studies in human evaluating sensitivity to MSG.