RESUMO
Recently, a sweet taste receptor family, the T1R family, that recognizes some carbohydrates including sucrose was identified. Although the T1R3 molecule is known to participate in heterodimers that are used as sweet- and umami-tasting receptors, there is no evidence that T1R3 alone recognizes similar ligands. We demonstrate for the first time that the candidate sweet taste receptor T1R3 is essential for the recognition and response to the disaccharide trehalose. Our system is a valuable tool not only for understanding the relationship between sweeteners and their receptors but also for exploring the diversities of their receptors, resulting in the design of new high-potency sweeteners.
Assuntos
Receptores de Superfície Celular/metabolismo , Edulcorantes/metabolismo , Paladar/fisiologia , Trealose/metabolismo , Animais , Cálcio/metabolismo , Linhagem Celular , Humanos , Ionomicina/metabolismo , Ionóforos/metabolismo , Ligantes , Camundongos , Camundongos Endogâmicos C57BL , Receptores de Superfície Celular/genética , Receptores Acoplados a Proteínas G , Proteínas Recombinantes de Fusão/genética , Proteínas Recombinantes de Fusão/metabolismo , Sacarose/metabolismoRESUMO
The disaccharide trehalose has been shown to inhibit both bone loss in ovariectomized mice and excessive osteoclastogenesis in lipopolysaccharide-injected mice. However, the mechanism of osteoclastogenesis inhibition by oral administration of trehalose is still unclear. We report here for the first time that a human intestinal epithelial cell line, FHs74Int, also produces osteoprotegerin (OPG) and that trehalose augments OPG production by this cell line. Thus, these results suggest that trehalose promotes the production of OPG by intestinal epithelial cells, which then acts on bone marrow cells, resulting in the suppression of osteoclastogenesis.