CALHM1 Deletion in Mice Affects Glossopharyngeal Taste Responses, Food Intake, Body Weight, and Life Span.

Citation data:

Chemical senses, ISSN: 1464-3553, Vol: 40, Issue: 6, Page: 373-9

Publication Year:
2015
Captures 10
Readers 10
Citations 7
Citation Indexes 7
PMID:
25855639
DOI:
10.1093/chemse/bjv009
PMCID:
PMC4542651
Author(s):
Hellekant, Göran, Schmolling, Jared, Marambaud, Philippe, Rose-Hellekant, Teresa A
Publisher(s):
Oxford University Press (OUP)
Tags:
Biochemistry, Genetics and Molecular Biology, Neuroscience, Medicine
article description
Stimulation of Type II taste receptor cells (TRCs) with T1R taste receptors causes sweet or umami taste, whereas T2Rs elicit bitter taste. Type II TRCs contain the calcium channel, calcium homeostasis modulator protein 1 (CALHM1), which releases adenosine triphosphate (ATP) transmitter to taste fibers. We have previously demonstrated with chorda tympani nerve recordings and two-bottle preference (TBP) tests that mice with genetically deleted Calhm1 (knockout [KO]) have severely impaired perception of sweet, bitter, and umami compounds, whereas their sour and salty tasting ability is unaltered. Here, we present data from KO mice of effects on glossopharyngeal (NG) nerve responses, TBP, food intake, body weight, and life span. KO mice have no NG response to sweet and a suppressed response to bitter compared with control (wild-type [WT]) mice. KO mice showed some NG response to umami, suggesting that umami taste involves both CALHM1- and non-CALHM1-modulated signals. NG responses to sour and salty were not significantly different between KO and WT mice. Behavioral data conformed in general with the NG data. Adult KO mice consumed less food, weighed significantly less, and lived almost a year longer than WT mice. Taken together, these data demonstrate that sweet taste majorly influences food intake, body weight, and life span.

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