Assessing palatability of long-chain fatty acids from the licking behavior of BALB/c mice

Yoneda, Tomohiro; Saitou, Katsuyoshi; Asano, Hiroki; Maekawa, Takafumi; Matsumura, Shigenobu; Eguchi, Akiyo; Manabe, Yasuko; Tsuzuki, Satoshi; Inoue, Kazuo; Fushiki, Tohru

doi:10.1016/j.physbeh.2009.01.010

Cited by 12 publications

(13 citation statements)

References 28 publications

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“…4C). This observation is consistent with previous results showing that mice exhibit high licking rates to corn oil and longchain unsaturated fatty acids, including 18:1 FA and 18:2 FA, but low responses to saturated fatty acids (37). Collectively, the available data suggest that endocannabinoid signaling in the small intestine contributes to the preference that rats display for fatty foods rich in unsaturated fatty acids (i.e., 18:2 FA and 18:1 FA), but not saturated or polyunsaturated fatty acids (i.e., 18:0 FA or 18:3 FA, respectively).…”

Section: Discussionsupporting

confidence: 93%

Endocannabinoid signaling in the gut mediates preference for dietary unsaturated fats

et al. 2013

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Dietary fat exerts a potent stimulatory effect on feeding. This effect is mediated, at least in part, by a cephalic mechanism that involves recruitment of the vagus nerve and subsequent activation of endocannabinoid signaling in the gut. Here, we used a sham-feeding protocol in rats to identify fatty-acid constituents of dietary fat that might be responsible for triggering small-intestinal endocannabinoid signaling. Sham feeding rats with a corn oil emulsion increased endocannabinoid levels in jejunum, relative to animals that received either mineral oil (which contains no fatty acids) or no oil. Sham-feeding emulsions containing oleic acid (18:1) or linoleic acid (18:2) caused, on average, a nearly 2-fold accumulation of jejunal endocannabinoids, whereas emulsions containing stearic acid (18:0) or linolenic acid (18:3) had no such effect. In a 2-bottle-choice sham-feeding test, rats displayed strong preference for emulsions containing 18:2, which was blocked by pretreatment with the peripherally restricted CB1 cannabinoid receptor antagonists, AM6546 and URB447. Our results suggest that oral exposure to the monoenoic and dienoic fatty acid component of dietary fat selectively initiates endocannabinoid mobilization in the gut, and that this local signaling event is essential for fat preference.

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Section: Discussionsupporting

confidence: 93%

Endocannabinoid signaling in the gut mediates preference for dietary unsaturated fats

et al. 2013

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“…In our experiments, this phenomenon occurred while the LCFA concentration used (i.e., 200 µM ≈ 0.005%) was undetectable by the mouse when it was presented alone during licking tests. It is consistent with the results of Yoneda et al (25) showing that mice are unable to properly detect 0.01% LCFA (ALA, OLA, or linoleic acid) during short-term behavioral tests. Therefore, the change in perceived intensity of sweet taste may not be attributed to addition of sucrose and LCFA effects.…”

Section: Discussionsupporting

confidence: 92%

Lipid-mediated release of GLP-1 by mouse taste buds from circumvallate papillae: putative involvement of GPR120 and impact on taste sensitivity

Martin

Passilly-Degrace

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et al. 2012

Journal of Lipid Research

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Glucagon-like peptide-1 (GLP-1) signaling modulates sweet-taste sensitivity in the mouse. Because circumvallate papillae (CVPs) express both GLP-1 and its receptor, a local regulation has been suggested. However, whether dietary lipids are involved in this regulation, as shown in the gut, is unknown. By using a combination of biochemical, immunohistochemical, and behavioral approaches, the present data i) confirm the role of GLP-1 signaling in the attraction for sucrose, ii) demonstrate that minute quantities of long-chain FAs (LCFAs) reinforce the attraction for sucrose in a GLP-1 receptor-dependent manner, iii) suggest an involvement of the LCFA receptor GPR120 expressed in taste buds in this system, and iv) support the existence of a regulation by GLP-1 of the lipid sensing mediated by lingual CD36. Therefore, oro-sensory detection of LCFAs may affect sweet and fatty taste responsiveness by controlling the secretion of lingual GLP-1. This regulatory loop, probably triggered by the LCFA-GPR120 interaction, might contribute to the high palatability of foods rich both in fat and sugar.

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“…When the licking behavior of the mice was tested, it was found that the mice exhibited equally strong preference for a low concentration of linoleic acid as that for 100% corn oil (29). In addition, the mice exhibited a similar strong preference for LCFAs, such as oleic, linolenic, and linoleic acid, whereas they did not display any preference for LCFA esters nor long-chain fatty alcohols (28). Moreover, ingesting linoleic acid at a low concentration increased extracellular DA release in the NAc of rats (1).…”

Section: Methodsmentioning

confidence: 99%

Behavioral palatability of dietary fatty acids correlates with the intracellular calcium ion levels induced by the fatty acids in GPR120-expressing cells

et al. 2014

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We recently reported that G-protein-coupled receptor 120 (GPR120) is expressed on taste buds, and that rodents showed preference for long-chain fatty acids (LCFA) at a low concentration. We also showed that the LCFA (1% linoleic acid) increased the extracellular dopamine (DA) level in the nucleus accumbens (NAc), which participates in reward behavior. However, the mechanism underlying the involvement of the GPR120-agonistic activity of LCFA in the palatability of dietary fat remains elusive. Therefore, we examined the association between the GPR120-agonistic activity and palatability of LCFA. First, we measured Ca(2+) signaling in HEK293 cells stably expressing GPR120 under stimulation by various LCFAs. We then assessed the palatability of the various LCFAs by testing the licking behavior in mice and measured the changes in the NAc-DA level by in vivo microdialysis. Consequently, 14- to 22-carbon unsaturated LCFAs showed strong GPR120-agonistic activity. Additionally, mice displayed high licking response to unsaturated 16- and 18-carbon LCFAs, and unsaturated 18-carbon LCFA significantly increased the DA level. The licking rate and the LCFA-dependent increase in DA level also correlated well with the GPR120- agonistic activity. These findings demonstrate that chemoreception of LCFA by GPR120 is involved in the recognition and palatability of dietary fat.

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Assessing palatability of long-chain fatty acids from the licking behavior of BALB/c mice

Cited by 12 publications

References 28 publications

Endocannabinoid signaling in the gut mediates preference for dietary unsaturated fats

Endocannabinoid signaling in the gut mediates preference for dietary unsaturated fats

Lipid-mediated release of GLP-1 by mouse taste buds from circumvallate papillae: putative involvement of GPR120 and impact on taste sensitivity

Behavioral palatability of dietary fatty acids correlates with the intracellular calcium ion levels induced by the fatty acids in GPR120-expressing cells

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