Taste Receptor Cells in Mice Express Receptors for the Hormone Adiponectin

AbstractThe metabolic hormone adiponectin is secreted into the circulation by adipocytes, and mediates key biological functions including insulin sensitivity, adipocyte development, and fatty acid oxidation. Adiponectin is also abundant in saliva, where its functions are poorly understood. Here we report that murine taste receptor cells express adiponectin receptors, and may be a target for salivary adiponectin. Analysis of a transcriptome dataset obtained by RNA-seq analysis of purified circumvallate taste buds, revealed high expression levels for three adiponectin receptor types. Immunohistochemical studies showed that two of these receptors, AdipoR1 and T-cadherin, are localized to subsets of taste receptor cells. Immunofluorescence for T-cadherin was primarily co-localized with the Type 2 taste receptor cell marker phospholipase β2, suggesting that adiponectin signaling could impact sweet, bitter, or umami taste signaling. However, adiponectin null mice showed no differences in taste responsiveness compared to wildtype controls in brief-access taste testing. AAV-mediated overexpression of adiponectin in the salivary glands of adiponectin null mice did result in a small but significant increase in behavioral taste responsiveness to the fat emulsion Intralipid. Together, these results suggest that salivary adiponectin can effect taste receptor cell function, though its impact on taste responsiveness and peripheral taste coding remains unclear.

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Taste Receptor Cells in Mice Express Receptors for the Hormone Adiponectin

Chemical Senses ◽

10.1093/chemse/bjz030 ◽

2019 ◽

Vol 44 (6) ◽

pp. 409-422 ◽

Cited By ~ 2

Author(s):

Sean M Crosson ◽

Andrew Marques ◽

Peter Dib ◽

Cedrick D Dotson ◽

Steven D Munger ◽

...

Keyword(s):

Taste Receptor ◽

Immunohistochemical Analysis ◽

Acid Oxidation ◽

Rna Seq ◽

Adiponectin Receptors ◽

Umami Taste ◽

Receptor Cells ◽

Taste Receptor Cells ◽

Adipocyte Development

Abstract The metabolic hormone adiponectin is secreted into the circulation by adipocytes and mediates key biological functions, including insulin sensitivity, adipocyte development, and fatty acid oxidation. Adiponectin is also abundant in saliva, where its functions are poorly understood. Here we report that murine taste receptor cells (TRCs) express specific adiponectin receptors and may be a target for salivary adiponectin. This is supported by the presence of all three known adiponectin receptors in transcriptomic data obtained by RNA-seq analysis of purified circumvallate (CV) taste buds. As well, immunohistochemical analysis of murine CV papillae showed that two adiponectin receptors, ADIPOR1 and T-cadherin, are localized to subsets of TRCs. Immunofluorescence for T-cadherin was primarily co-localized with the Type 2 TRC marker phospholipase C β2, suggesting that adiponectin signaling could impact sweet, bitter, or umami taste signaling. However, adiponectin null mice showed no differences in behavioral lick responsiveness compared with wild-type controls in brief-access lick testing. AAV-mediated overexpression of adiponectin in the salivary glands of adiponectin null mice did result in a small but significant increase in behavioral lick responsiveness to the fat emulsion Intralipid. Together, these results suggest that salivary adiponectin can affect TRC function, although its impact on taste responsiveness and peripheral taste coding remains unclear.

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Effects of osmolarity on taste receptor cell size and function

AJP Cell Physiology ◽

10.1152/ajpcell.1999.277.4.c800 ◽

1999 ◽

Vol 277 (4) ◽

pp. C800-C813 ◽

Cited By ~ 33

Author(s):

Vijay Lyall ◽

Gerard L. Heck ◽

John A. DeSimone ◽

George M. Feldman

Keyword(s):

Cell Volume ◽

Receptor Cell ◽

Taste Receptor ◽

Chorda Tympani ◽

Taste Receptor Cell ◽

Salt Taste ◽

Receptor Cells ◽

Enhanced Ct ◽

And Function ◽

Osmotic Effects

Osmotic effects on salt taste were studied by recording from the rat chorda tympani (CT) nerve and by measuring changes in cell volume of isolated rat fungiform taste receptor cells (TRCs). Mannitol, cellobiose, urea, or DMSO did not induce CT responses. However, the steady-state CT responses to 150 mM NaCl were significantly increased when the stimulus solutions also contained 300 mM mannitol or cellobiose, but not 600 mM urea or DMSO. The enhanced CT responses to NaCl were reversed when the saccharides were removed and were completely blocked by addition of 100 μM amiloride to the stimulus solution. Exposure of TRCs to hyperosmotic solutions of mannitol or cellobiose induced a rapid and sustained decrease in cell volume that was completely reversible, whereas exposure to hypertonic urea or DMSO did not induce sustained reductions in cell volume. These data suggest that the osmolyte-induced increase in the CT response to NaCl involves a sustained decrease in TRC volume and the activation of amiloride-sensitive apical Na+ channels.

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Responses to Di-Sodium Guanosine 5′-Monophosphate and Monosodiuml-Glutamate in Taste Receptor Cells of Rat Fungiform Papillae

Journal of Neurophysiology ◽

10.1152/jn.00994.2002 ◽

2003 ◽

Vol 89 (3) ◽

pp. 1434-1439 ◽

Cited By ~ 16

Author(s):

Weihong Lin ◽

Tatsuya Ogura ◽

Sue C. Kinnamon

Keyword(s):

Patch Clamp ◽

Monosodium Glutamate ◽

Taste Receptor ◽

Intracellular Camp ◽

Fungiform Papillae ◽

Simultaneous Application ◽

Umami Taste ◽

Receptor Cells ◽

Imaging Results ◽

Taste Receptor Cells

The 5′-ribonucleotide guanosine 5′-monophosphate (GMP) is used widely as an umami taste stimulus and a potent flavor enhancer as it synergistically increases the umami taste elicited by monosodium glutamate. Transduction mechanisms for GMP and its synergy with glutamate are largely unknown. Using whole-cell patch-clamp and Ca2+ imaging, we examined responses to GMP, glutamate, and a mixture of GMP and glutamate in taste-receptor cells of rat fungiform papillae. Our electrophysiological results showed that GMP induces responses that are similar to those of glutamate, e.g., an outward current, an inward current, or a biphasic response. Our Ca2+ imaging results showed that applications of GMP, glutamate, and the mixture increased intracellular Ca2+ levels. Interestingly, both patch-clamp and Ca2+ imaging showed that some taste cells can respond to GMP and glutamate independently, indicating that glutamate and GMP likely activate different receptors. Simultaneous application of GMP and glutamate resulted in synergistic responses in a subset of cells; both response intensity and number of responding cells were increased. Most responses to GMP, as well as the synergy between GMP and glutamate, were suppressed by 8bromo-adenosine 3′,5′-cyclic monophosphate (8-bromo-cAMP) in patch-clamp recordings. Together, our results suggest that intracellular cAMP- and Ca2+-mediated pathways are involved in umami taste transduction for GMP and its synergistic responses with glutamate.

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Inactivation of taste receptor cell function by two cationic protein modification reagents

Journal of Neurobiology ◽

10.1002/neu.480080303 ◽

1977 ◽

Vol 8 (3) ◽

pp. 193-206 ◽

Cited By ~ 8

Author(s):

Gregory Mooser ◽

Nancy Lambuth

Keyword(s):

Protein Modification ◽

Cell Function ◽

Receptor Cell ◽

Taste Receptor ◽

Taste Receptor Cell ◽

Cationic Protein

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Changes in taste receptor cell [Ca2+]i modulate chorda tympani responses to bitter, sweet, and umami taste stimuli

Journal of Neurophysiology ◽

10.1152/jn.00129.2012 ◽

2012 ◽

Vol 108 (12) ◽

pp. 3221-3232 ◽

Cited By ~ 10

Author(s):

John A. DeSimone ◽

Tam-Hao T. Phan ◽

ZuoJun Ren ◽

Shobha Mummalaneni ◽

Vijay Lyall

Keyword(s):

Receptor Cell ◽

Synergistic Effects ◽

Monosodium Glutamate ◽

Taste Receptor ◽

Chorda Tympani ◽

Taste Receptor Cell ◽

Acetoxymethyl Ester ◽

Umami Taste ◽

Before And After ◽

Intracellular Ca

The relationship between taste receptor cell (TRC) intracellular Ca2+ ([Ca2+]i) and rat chorda tympani (CT) nerve responses to bitter (quinine and denatonium), sweet (sucrose, glycine, and erythritol), and umami [monosodium glutamate (MSG) and MSG + inosine 5′-monophosphate (IMP)] taste stimuli was investigated before and after lingual application of ionomycin (Ca2+ ionophore) + Ca2+, 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′-tetraacetic acid acetoxymethyl ester (BAPTA-AM; Ca2+ chelator), U73122 (phospholipase C blocker), thapsigargin (Ca2+-ATPase blocker), and diC8-PIP2 (synthetic phosphatidylinositol 4,5-bisphosphate). The phasic CT response to quinine was indifferent to changes in [Ca2+]i. However, a decrease in [Ca2+]i inhibited the tonic part of the CT response to quinine. The CT responses to sweet and umami stimuli were indifferent to changes in TRC [Ca2+]i. However, a decrease in [Ca2+]i attenuated the synergistic effects of ethanol on the CT response to sweet stimuli and of IMP on the glutamate CT response. U73122 and thapsigargin inhibited the phasic and tonic CT responses to bitter, sweet, and umami stimuli. Although diC8-PIP2 increased the CT response to bitter and sweet stimuli, it did not alter the CT response to glutamate but did inhibit the synergistic effect of IMP on the glutamate response. The results suggest that bitter, sweet, and umami taste qualities are transduced by [Ca2+]i-dependent and [Ca2+]i-independent mechanisms. Changes in TRC [Ca2+]i in the BAPTA-sensitive cytosolic compartment regulate quality-specific taste receptors and ion channels that are involved in the neural adaptation and mixture interactions. Changes in TRC [Ca2+]i in a separate subcompartment, sensitive to inositol trisphosphate and thapsigargin but inaccessible to BAPTA and ionomycin + Ca2+, are associated with neurotransmitter release.

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