Sense of Taste in the Gastrointestinal Tract

Iwatsuki, Ken; Uneyama, Hisayuki

doi:10.1254/jphs.11r08cp

Cited by 46 publications

(35 citation statements)

References 46 publications

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“…The main signal transduction events have been identified. The binding of sweet compounds to the T1R2/T1R3 receptor results in the dissociation of the heterotrimeric G protein (α-gustducin, Gβ3, and Gγ13), leading to an increase in phospholipase C-β2 (PLC-β2) activity, which results in the inositol 1,4,5-triphosphate (IP 3 ) receptor, type 3-mediated release of Ca 2+ from intracellular stores and the opening of a transient potential ion channel, transient receptor potential cation channel subfamily M member 5 (TRPMP5) [4]. This transduction mechanism, which is common to the detection of sweet, umami, and bitter tastes, leads to membrane depolarization, generating an action potential and leading to the release of adenosine triphosphate (ATP) as a transmitter to activate gustatory afferents (Fig.…”

Section: The Sweet Taste Receptormentioning

confidence: 99%

“…The function of brush cells is currently unknown, although there is some speculation as to whether these cells might function as chemosensory detectors because of their morphological similarities with type II taste cells from taste buds and the fact that they express taste transduction molecules (Fig. 2), such as TRPM5 and PLC-β2 [4].…”

Section: Role Of the Sweet Taste Receptor In Metabolic Regulationmentioning

confidence: 99%

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Functional roles of the sweet taste receptor in oral and extraoral tissues

Laffitte

Neiers

Briand

2014

Current Opinion in Clinical Nutrition and Metabolic Care

196

170

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Purpose of reviewThis review summarizes and discusses the current knowledge about the physiological roles of the sweet taste receptor in oral and extraoral tissues.Recent findingsThe expression of a functional sweet taste receptor has been reported in numerous extragustatory tissues, including the gut, pancreas, bladder, brain and, more recently, bone and adipose tissues. In the gut, this receptor has been suggested to be involved in luminal glucose sensing, the release of some satiety hormones, the expression of glucose transporters, and the maintenance of glucose homeostasis. More recently, the sweet taste receptor was proposed to regulate adipogenesis and bone biology.SummaryThe perception of sweet taste is mediated by the T1R2/T1R3 receptor, which is expressed in the oral cavity, wherein it provides input on the caloric and macronutrient contents of ingested food. This receptor recognizes all the chemically diverse compounds perceived as sweet by human beings, including natural sugars and sweeteners. Importantly, the expression of a functional sweet taste receptor has been reported in numerous extragustatory tissues, wherein it has been proposed to regulate metabolic processes. This newly recognized role of the sweet taste receptor makes this receptor a potential novel therapeutic target for the treatment of obesity and related metabolic dysfunctions, such as diabetes and hyperlipidemia.

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Section: The Sweet Taste Receptormentioning

confidence: 99%

Section: Role Of the Sweet Taste Receptor In Metabolic Regulationmentioning

confidence: 99%

Functional roles of the sweet taste receptor in oral and extraoral tissues

Laffitte

Neiers

Briand

2014

Current Opinion in Clinical Nutrition and Metabolic Care

196

170

View full text Add to dashboard Cite

show abstract

“…The discovery that the same taste/nutrient receptors found in the mouth also exist in the gut has prompted renewed interest in the role of these receptors in the control of appetite and food intake (e.g., 2,8,10,13,14,34,36). The general view has been that nutrient sensing in the mouth promotes appetite, whereas gut sensing is responsible for inhibiting appetite by activating satiating/satiety circuits (30).…”

Section: Perspectives and Significancementioning

confidence: 99%

GPR40 and GPR120 fatty acid sensors are critical for postoral but not oral mediation of fat preferences in the mouse

Sclafani

Zukerman

Ackroff

2013

American Journal of Physiology-Regulatory, Integrative and Comp

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In addition to orosensory signals, postoral actions of fat stimulate appetite and condition flavor preferences, but the gut sensors mediating these responses are unknown. Here, we investigated the role of the fatty acid sensors GPR40 and GPR120 in postoral and oral preferences for a soybean oil emulsion (Intralipid). Mice were trained to drink a flavored solution (CS+) paired with intragastric (IG) oil infusions and another flavored solution (CS-) paired with water infusions. Knockout (KO) mice missing GPR40 or GPR120 sensors increased their CS+ intake in one-bottle tests (1 h/day) but less so than wild-type (WT) mice. The KO mice also preferred the CS+ to CS- in a two-bottle test, but the preference was attenuated in GPR40 KO mice. Double-knockout (DoKO) mice missing both GPR40 and GPR120 displayed attenuated stimulation of CS+ intake and only a marginal CS+ preference. The DoKO mice developed a more substantial CS+ preference when tested 24 h/day, although weaker than that of WT mice. The DoKO mice also consumed less of the CS+ paired with IG Intralipid, as well as less Intralipid in oral tests. However, DoKO mice, like GPR40 KO and GPR120 KO mice did not differ from WT mice in their preference for Intralipid over water at 0.001%-20% concentrations. In contrast to prior results obtained with mice missing the CD36 fatty acid sensor, these findings indicate that, together, GPR40 and GPR120 play a critical role in the postoral stimulation of appetite by fat but are not essential for oral fat preferences.

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“…5). The neurochemistry and neurophysiology of taste are beyond the scope of this review (as an example of many reviews, see [125–128]).…”

Section: Learned Responses Aversion and Preferencementioning

confidence: 99%

The Brain's Response to an Essential Amino Acid-Deficient Diet and the Circuitous Route to a Better Meal

Gietzen

Aja

2012

Mol Neurobiol

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The essential (indispensable) amino acids (IAA) are neither synthesized nor stored in metazoans, yet they are the building blocks of protein. Survival depends on availability of these protein precursors, which must be obtained in the diet; it follows that food selection is critical for IAA homeostasis. If even one of the IAA is depleted, its tRNA becomes quickly deacylated and the levels of charged tRNA fall, leading to disruption of global protein synthesis. As they have priority in the diet, second only to energy, the missing IAA must be restored promptly or protein catabolism ensues. Animals detect and reject an IAA-deficient meal in 20 min, but how? Here, we review the molecular basis for sensing IAA depletion and repletion in the brain’s IAA chemosensor, the anterior piriform cortex (APC). As animals stop eating an IAA-deficient meal, they display foraging and altered choice behaviors, to improve their chances of encountering a better food. Within 2 h, sensory cues are associated with IAA depletion or repletion, leading to learned aversions and preferences that support better food selection. We show neural projections from the APC to appetitive and consummatory motor control centers, and to hedonic, motivational brain areas that reinforce these adaptive behaviors.

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Sense of Taste in the Gastrointestinal Tract

Cited by 46 publications

References 46 publications

Functional roles of the sweet taste receptor in oral and extraoral tissues

Functional roles of the sweet taste receptor in oral and extraoral tissues

GPR40 and GPR120 fatty acid sensors are critical for postoral but not oral mediation of fat preferences in the mouse

The Brain's Response to an Essential Amino Acid-Deficient Diet and the Circuitous Route to a Better Meal

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