Abstract
Obesity is one of the major public health issues, and its prevalence is steadily increasing all the world over. The endocannabinoid system (ECS) has been shown to be involved in the intake of palatable food via activation of cannabinoid 1 receptor (CB1R). However, the involvement of lingual CB1R in the orosensory perception of dietary fatty acids has never been investigated. In the present study, behavioral tests on CB1R−/− and wild type (WT) mice showed that the invalidation of Cb1r gene was associated with low preference for solutions containing rapeseed oil or a long-chain fatty acid (LCFA), such as linoleic acid (LA). Administration of rimonabant, a CB1R inverse agonist, in mice also brought about a low preference for dietary fat. No difference in CD36 and GPR120 protein expressions were observed in taste bud cells (TBC) from WT and CB1R−/− mice. However, LCFA induced a higher increase in [Ca2+]i in TBC from WT mice than that in TBC from CB1R−/− mice. TBC from CB1R−/− mice also exhibited decreased Proglucagon and Glp-1r mRNA and a low GLP-1 basal level. We report that CB1R is involved in fat taste perception via calcium signaling and GLP-1 secretion.
Highlights
Due to the abundance of food resources in the modern era, the Western diet is comprised of more than 40% of fat, thereby contributing to the increase in the prevalence of obesity that is associated with a number of pathologies.The taste modalities represent an essential factor involved in food intake
In vivo studies were performed on male C57BL/6J wild type (WT) mice (Janvier Labs, Le Genest Saint Isle, France) and cannabinoid-1 receptors (CB1 R)–/– mice with a C57BL/6J background
CB1 R are expressed in a subset of taste bud cells [7]
Summary
Due to the abundance of food resources in the modern era, the Western diet is comprised of more than 40% of fat, thereby contributing to the increase in the prevalence of obesity that is associated with a number of pathologies (type 2 diabetes mellitus, hypertension, cancer, and others).The taste modalities represent an essential factor involved in food intake. The binding of a fatty acid to lingual CD36 in taste bud cells (TBC) leads to modifications in the membrane potential and to an increase in free intracellular calcium concentrations, [Ca2+ ]i , followed by the release of neurotransmitters [4,5]. These gustatory signals are transmitted from the oral cavity, through the cranial nerve IX (lingual branch of the glossopharyngeal), to the nucleus of the solitary tract (NST) [6]. The integration of the gustatory signals in brain triggers a behavioral and metabolic response [8]
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