Implication of TRPC3 channel in gustatory perception of dietary lipids

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985904%3A_____%2F21%3A00541169" target="_blank" >RIV/67985904:_____/21:00541169 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216224:14310/21:00121009

Výsledek na webu

<a href="https://onlinelibrary.wiley.com/doi/full/10.1111/apha.13554" target="_blank" >https://onlinelibrary.wiley.com/doi/full/10.1111/apha.13554</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1111/apha.13554" target="_blank" >10.1111/apha.13554</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Implication of TRPC3 channel in gustatory perception of dietary lipids

Popis výsledku v původním jazyce

Aim The pathogenesis of obesity has been associated with high intake of dietary fat, and some recent studies have explored the cellular mechanisms of oro-sensory detection of dietary fatty acids. We further assessed the role of transient receptor potential canonical (TRPC) channels in oro-sensory perception of dietary lipids. Methods We determined by RT-qPCR and western blotting the expression of TRPC3/6/7 channels in mouse fungiform taste bud cells (mTBC). Immunocytochemistry was used to explore whether TRPC3 channels were co-expressed with fatty acid receptors. We employed wild-type (WT) mTBC, and those transfected with small interfering RNAs (siRNAs) against TRPC3 or STIM1. Ca(2+)signalling was studied in TBC fromTRPC3(-/-)mice and their WT littermates. Results We demonstrate that mouse fungiform taste bud cells (mTBC) express TRPC3, but not TRPC6 or TRPC7 channels, and their inactivation by siRNA or experiments on TBC fromTRPC3(-/-)mice brought about a decrease in fatty acid-induced gustatory Ca(2+)signalling, coupled with taste bud CD36 lipid sensor. TRPC3 channel activation was found to be under the control of STIM1 in lingual mTBC. Behavioural studies showed that spontaneous preference for a dietary long-chain fatty acid was abolished inTRPC3(-/-)mice, and in mice wherein lingual TRPC3 expression was silenced by employing siRNA. Conclusion We report that lingual TRPC3 channels are critically involved in fat taste perception.

Název v anglickém jazyce

Implication of TRPC3 channel in gustatory perception of dietary lipids

Popis výsledku anglicky

Aim The pathogenesis of obesity has been associated with high intake of dietary fat, and some recent studies have explored the cellular mechanisms of oro-sensory detection of dietary fatty acids. We further assessed the role of transient receptor potential canonical (TRPC) channels in oro-sensory perception of dietary lipids. Methods We determined by RT-qPCR and western blotting the expression of TRPC3/6/7 channels in mouse fungiform taste bud cells (mTBC). Immunocytochemistry was used to explore whether TRPC3 channels were co-expressed with fatty acid receptors. We employed wild-type (WT) mTBC, and those transfected with small interfering RNAs (siRNAs) against TRPC3 or STIM1. Ca(2+)signalling was studied in TBC fromTRPC3(-/-)mice and their WT littermates. Results We demonstrate that mouse fungiform taste bud cells (mTBC) express TRPC3, but not TRPC6 or TRPC7 channels, and their inactivation by siRNA or experiments on TBC fromTRPC3(-/-)mice brought about a decrease in fatty acid-induced gustatory Ca(2+)signalling, coupled with taste bud CD36 lipid sensor. TRPC3 channel activation was found to be under the control of STIM1 in lingual mTBC. Behavioural studies showed that spontaneous preference for a dietary long-chain fatty acid was abolished inTRPC3(-/-)mice, and in mice wherein lingual TRPC3 expression was silenced by employing siRNA. Conclusion We report that lingual TRPC3 channels are critically involved in fat taste perception.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30103 - Neurosciences (including psychophysiology)

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2021

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Acta Physiologica

ISSN

1748-1708

e-ISSN

1748-1716

Svazek periodika

231

Číslo periodika v rámci svazku

2

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

15

Strana od-do

e13554

Kód UT WoS článku

000568624500001

EID výsledku v databázi Scopus

2-s2.0-85090839841