Abstract
Taste perception plays an important role in regulating food preference, eating behavior and energy homeostasis. Taste perception is modulated by a variety of factors, including gastric hormones such as ghrelin. Ghrelin can regulate growth hormone release, food intake, adiposity, and energy metabolism. Octanoylation of ghrelin by ghrelin O-acyltransferase (GOAT) is a specific post-translational modification which is essential for many biological activities of ghrelin. Ghrelin and GOAT are both widely expressed in many organs including the gustatory system. In the current study, overall metabolic profiles were assessed in wild-type (WT), ghrelin knockout (ghrelin−/−), and GOAT knockout (GOAT−/−) mice. Ghrelin−/− mice exhibited decreased food intake, increased plasma triglycerides and increased ketone bodies compared to WT mice while demonstrating WT-like body weight, fat composition and glucose control. In contrast GOAT−/− mice exhibited reduced body weight, adiposity, resting glucose and insulin levels compared to WT mice. Brief access taste behavioral tests were performed to determine taste responsivity in WT, ghrelin−/− and GOAT−/− mice. Ghrelin and GOAT null mice possessed reduced lipid taste responsivity. Furthermore, we found that salty taste responsivity was attenuated in ghrelin−/− mice, yet potentiated in GOAT−/− mice compared to WT mice. Expression of the potential lipid taste regulators Cd36 and Gpr120 were reduced in the taste buds of ghrelin and GOAT null mice, while the salt-sensitive ENaC subunit was increased in GOAT−/− mice compared with WT mice. The altered expression of Cd36, Gpr120 and ENaC may be responsible for the altered lipid and salt taste perception in ghrelin−/− and GOAT−/− mice. The data presented in the current study potentially implicates ghrelin signaling activity in the modulation of both lipid and salt taste modalities.
Highlights
Gustation is one of the fundamental chemical senses that guides organisms to identify nutrients while avoiding toxic chemicals
As expected from our previous gustometer data (Fig. 5A), we found no significant differences in the expression of leptin receptor and glucagon-like peptide-1 (GLP-1), two sweet-taste related factors, between WT and ghrelin2/2 or GOAT2/2 mice (Fig. 7A, B)
No significant differences in body weight, fat composition and glucose control were observed in ghrelin2/2 mice compared to WT controls (Fig. 1)
Summary
Gustation is one of the fundamental chemical senses that guides organisms to identify nutrients while avoiding toxic chemicals. This sensory mechanism is primarily mediated through ion channels or receptors in taste cells which are clustered into onion-shaped taste buds. Differences in ultrastructural features, stage of differentiation and diverse functioning allows taste cells within the taste buds to be classified into Type I, II, III and IV taste cells. Type I taste cells, the most abundant cells in the tongue, function as supportive glia in taste buds [2]. Type III cells, known as ‘presynaptic cells’, express multiple synaptic proteins and demonstrate functional depolarization-dependent Ca2+ transients [5,6]. Type IV taste cells are non-polarized, undifferentiated basal cells that are thought to represent a latent stem cell-like population in the tongue [7]
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