Co-expression patterns of the neuropeptides vasoactive intestinal peptide and cholecystokinin with the transduction molecules α-gustducin and T1R2 in rat taste receptor cells

Shen, Ting; Kaya, Namik; Zhao, Fuqing; Lu, Shicheng; Cao, Yang; Herness, Scott

doi:10.1016/j.neuroscience.2004.09.017

Cited by 85 publications

(57 citation statements)

References 49 publications

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“…Third, a subset of TBC, mainly type II cells, also expresses multiple gastrointestinal hormones including glucagon-like peptide-1 (GLP-1) (194), cholecystokinin (CCK) (73,190), neuropeptide Y (NPY) (82,232), vasoactive intestinal polypeptide (VIP) (119,190), and ghrelin (195), known to regulate digestive tract function, glucose homeostasis, and appetite/satiety (for an exhaustive review, see Ref. 234) (FIGURE 3).…”

Section: Taste Bud Cells Stratified Non-gustatory Epitheliummentioning

confidence: 99%

Taste of Fat: A Sixth Taste Modality?

Besnard

Passilly-Degrace

Khan

2016

Physiological Reviews

203

170

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An attraction for palatable foods rich in lipids is shared by rodents and humans. Over the last decade, the mechanisms responsible for this specific eating behavior have been actively studied, and compelling evidence implicates a taste component in the orosensory detection of dietary lipids [i.e., long-chain fatty acids (LCFA)], in addition to textural, olfactory, and postingestive cues. The interactions between LCFA and specific receptors in taste bud cells (TBC) elicit physiological changes that affect both food intake and digestive functions. After a short overview of the gustatory pathway, this review brings together the key findings consistent with the existence of a sixth taste modality devoted to the perception of lipids. The main steps leading to this new paradigm (i.e., chemoreception of LCFA in TBC, cell signaling cascade, transfer of lipid signals throughout the gustatory nervous pathway, and their physiological consequences) will be critically analyzed. The limitations to this concept will also be discussed in the light of our current knowledge of the sense of taste. Finally, we will analyze the recent literature on obesity-related dysfunctions in the orosensory detection of lipids ("fatty" taste?), in relation to the overconsumption of fat-rich foods and the associated health risks.

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Section: Taste Bud Cells Stratified Non-gustatory Epitheliummentioning

confidence: 99%

Taste of Fat: A Sixth Taste Modality?

Besnard

Passilly-Degrace

Khan

2016

Physiological Reviews

203

170

View full text Add to dashboard Cite

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“…Twenty immunopositive taste buds from each rat were randomly selected to count the number of DPP4-immunopositive cells. Data were analyzed quantitatively by cell counts according to the protocol described previously (Shen et al 2005).…”

Section: Immunohistochemistrymentioning

confidence: 99%

Liraglutide alters DPP4 in the circumvallate papillae of type 2 diabetic rats

Cao¹,

Zhou²,

Liu³

et al. 2016

Journal of Molecular Endocrinology

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Liraglutide, a human glucagon-like peptide (GLP1) analog that partially inhibits dipeptidyl-peptidase 4 (DPP4), can decrease glucose levels and suppress appetite in patients with type 2 diabetes (T2DM). GLP1 and its receptor (GLP1R) also exist in the taste buds of rodents and regulate taste sensitivity. DPP4, a protease, functions in homeostasis of blood glucose, lipids, and body weight. Interactions among GLP1, GLP1R, and DPP4 likely affect taste and food-intake behavior. The aim of the present study was to investigate DPP4 expression in the taste buds of the circumvallate papillae (CV) in T2DM rats, and determine the effects of liraglutide treatment. Rats were divided into diabetic control (T2DM-C), normal control (NC), and liraglutide-treated diabetic (T2DM + LIR) groups. DPP4 localization and gene expression levels were evaluated by immunohistochemistry and quantitative reverse transcription-polymerase chain reaction (RT-qPCR), respectively. DPP4 immunoreactive cells were localized in the taste buds of the rat CV. RT-qPCR showed significantly higher expression of Dpp4 mRNA in both the taste buds and hypothalamus of T2DM-C rats compared with NC rats. However, in the T2DM + LIR group, Dpp4 expression differed between the taste buds and hypothalamus, with significantly higher and lower levels compared with the T2DM-C group, respectively. Dpp4 mRNA expression is increased in the taste buds of the CV of T2DM rats. Liraglutide simultaneously upregulated (taste buds) and downregulated (hypothalamus) Dpp4 expression in T2DM rats. Therefore, DPP4 may be closely associated with the anorexigenic signaling and weight loss induced by the treatment of liraglutide in type 2 diabetic patients.

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“…Likewise, receptors for wellknown gut hormones [i.e., serotonin (5-HT), cholecystokinin (CCK) and VIP] are also expressed in taste buds of the oral cavity, and it has been proposed that those gut hormones could modulate taste perception too (13,15,16,38). Taking all these observations together, it seems as if the tongue and the upper GI tract share common systems for nutrient sensing.…”

mentioning

confidence: 99%

Luminal amino acid sensing in the rat gastric mucosa

Uneyama¹,

Niijima²,

Gabriel³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

145

151

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. Luminal amino acid sensing in the rat gastric mucosa. Am J Physiol Gastrointest Liver Physiol 291: G1163-G1170, 2006. First published June 29, 2006 doi:10.1152/ajpgi.00587.2005.-Recent advancements in molecular biology in the field of taste perception in the oral cavity have raised the possibility for ingested nutrients to be "tasted" in the upper gastrointestinal tract. The purpose of this study was to identify the existence of a nutrient-sensing system by the vagus in the rat stomach. Afferent fibers of the gastric branch increased their firing rate solely with the intragastric application of the amino acid glutamate. Other amino acids failed to have the same effect. This response to glutamate was blocked by the depletion of serotonin (5-HT) and inhibition of serotonin receptor 3 (5-HT3) or nitric oxide (NO) synthase enzyme. Luminal perfusion with the local anesthesia lidocaine abolished the glutamate-evoked afferent activation. The afferent response was also mimicked by luminal perfusion with a NO donor, sodium nitroprusside. In addition, the NO donorinduced afferent activation was abolished by 5-HT 3 blockade as well. Altogether, these results strongly suggest the existence of a sensing system for glutamate in the rat gastric mucosa. Thus luminal glutamate would enhance the electrophysiological firing rate of afferent fibers from the vagus nerve of the stomach through the production of mucosal bioactive substances such as NO and 5-HT. Assuming there is a universal coexistence of free glutamate with dietary protein, a glutamate-sensing system in the stomach could contribute to the gastric phase of protein digestion.visceral nutrient sensing; rat vagal gastric afferent; serotonin; nitric oxide THE NUMBER OF ARTICLES DEDICATED to the abdominal vagus nerve that were focused in gut nutrient sensing has increased dramatically over the last decade (33,36,42). This is due to the advancement of techniques that facilitated the study of visceral afferent fibers and their function and characteristic electrophysiological patterns and also due to recognition that these fibers are important for body nutrient homeostasis. Psychophysiological approaches for the understanding of ingestive behavior have demonstrated that the presence of food in the upper gastrointestinal (GI) tract plays a critical role in determining meal size. The vagus nerve is extensively distributed throughout the GI tract, from the posterior region of oral cavity and esophagus to the lowest part of the colon, and functions as the primary neuroanatomical circuit in the gut-brain axis to transmit meal-related signals from the GI mucosa to the central nervous system. This is where regulatory processes (e.g., ingestive behavior, nutrient absorption, GI secretion, and stomach emptying) as well as conscious sensations (e.g., satiety, nausea, and discomfort) take place (5, 22, 37).Recently, it has been shown that taste transduction-related molecules, such as ␣-gustducin and a family of bitter-sensing taste receptors (T 2 Rs), were also expressed at the GI mu...

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Co-expression patterns of the neuropeptides vasoactive intestinal peptide and cholecystokinin with the transduction molecules α-gustducin and T1R2 in rat taste receptor cells

Cited by 85 publications

References 49 publications

Taste of Fat: A Sixth Taste Modality?

Taste of Fat: A Sixth Taste Modality?

Liraglutide alters DPP4 in the circumvallate papillae of type 2 diabetic rats

Luminal amino acid sensing in the rat gastric mucosa

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