Article

Obesity alters the gustatory perception of lipids in the mouse: plausible involvement of the lingual CD36.

Physiologie de la Nutrition et Toxicologie (NUTox) UMR U866 INSERM/uB/AgroSup Dijon, France.
The Journal of Lipid Research (Impact Factor: 4.73). 07/2013; DOI: 10.1194/jlr.M039446
Source: PubMed

ABSTRACT A relationship between oro-sensory detection of dietary lipids, regulation of fat intake and body mass index was recently suggested. However, involved mechanisms are poorly understood. Moreover, whether obesity can directly modulate preference for fatty foods remains unknown. To address this question, exploration of the oral lipid sensing system was undertaken in diet-induced obese (DIO) mice. By using a combination of biochemical, physiological and behavioral approaches, we found that i) the attraction for lipids is decreased in obese mice, ii) this behavioral change has an oro-sensory origin, iii) it is reversed in calorie-restricted DIO mice, revealing an inverse correlation between fat preference and adipose tissue size, iv) obesity suppresses the lipid-mediated down-regulation of the lipid-sensor CD36 in circumvallate papillae, usually found during the refeeding of lean mice and v) the CD36-dependent signaling cascade controlling the intracellular calcium levels ([Ca2+]i) in taste bud cells is decreased in obese mice. Therefore, obesity alters the lipid sensing system responsible for the oral perception of dietary lipids via a CD36-mediated mechanism, leading to changes in the eating behavior.

1 Follower
 · 
98 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Evidence supporting a “taste” cue from fat in the oral cavity continues to accrue. The proposed stimuli for fat taste, non-esterified fatty acids (NEFA), are released from food through hydrolytic rancidity and lipase activity derived from foods or saliva. NEFA must then be released from the food matrix, negotiate the aqueous environment to reach taste cell surfaces, and interact with receptors such as CD36 and GPR120 or diffuse across cell membranes to initiate a taste signal. Knowledge of these processes in non-gustatory tissues should inform understanding of taste responses to NEFA. Additionally, downstream effects of oral triglyceride exposure have been observed in numerous studies. Data specific to effects of NEFA versus triglyceride are scarce, but modified sham feeding trials with triglyceride document cephalic phase responses including elevations in serum lipids and insulin as well as potential, but debated, effects on gut peptides, appetite, and thermogenesis. In this review, we highlight the mechanisms by which NEFA migrate to and interact with taste cells, and then we examine physiological responses to oral fat exposure. © 2014 BioFactors, 2014
    BioFactors 05/2014; 40(3). DOI:10.1002/biof.1162 · 3.00 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Implication of the long-chain fatty acid (LCFA) receptor GPR120, also termed free fatty acid receptor 4 (FFAR4), in the taste-guided preference for lipids is a matter of debate. To further unravel the role of GPR120 in the "taste of fat", the present study was conducted on GPR120-null mice and their wild-type littermates. Using a combination of morphological (i.e. immunohistochemical staining of circumvallate papillae - CVP), behavioral (i.e. two-bottle preference tests, licking tests and conditioned taste aversion) and functional studies (i.e. calcium imaging in freshly isolated taste bud cells - TBC), we show that absence of GPR120 in oral cavity was not associated with changes in i) the gross anatomy of CVP, ii) the LCFA-mediated increases in [Ca2+]i, iii) the preference for oily and LCFA solutions and iv) the conditioned avoidance of LCFA solutions. In contrast, the rise in [Ca2+]i triggered by grifolic acid (GA), a specific GPR120 agonist, was dramatically curtailed when GPR120 gene was lacking. Taken together these data demonstrate that activation of lingual GPR120 and preference for fat are disconnected, suggesting that GPR120 expressed in TBC is not absolutely required for the oral fat detection in the mouse. Copyright © 2014, The American Society for Biochemistry and Molecular Biology.
    The Journal of Lipid Research 12/2014; DOI:10.1194/jlr.M055202 · 4.73 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Mounting evidence suggests that gustation is important for the orosensory detection of dietary fats, and might contribute to preferences that humans, rodents, and possibly other mammals exhibit for fat-rich foods. In contrast to sweet, sour, salty, bitter, and umami, fat is not widely recognized as a primary taste quality. Recent investigations, however, provide a wealth of information that is helping to elucidate the specific molecular, cellular, and neural mechanisms required for fat detection in mammals. The latest evidence supporting a fat taste will be explored in this review, with a particular focus on recent studies that suggest a surprising role for gut-brain endocannabinoid signaling in controlling intake and preference for fats based on their proposed taste properties.
    Physiology & Behavior 03/2014; 136. DOI:10.1016/j.physbeh.2014.03.002 · 3.03 Impact Factor

Full-text (2 Sources)

Download
25 Downloads
Available from
Jan 8, 2015
Available from

Similar Publications