Background: The Taste receptor, type 1 (TAS1R) family of heterotrimeric G protein-coupled receptors participates in monitoring energy and nutrient needs. TAS1R member 3 (TAS1R3) either recognizes amino acids such as glycine and L-glutamate or sweet molecules such as sucrose and fructose when dimerized with TAS1R member 1 (TAS1R1) or TAS1R member 2 (TAS1R2), respectively. Loss of TAS1R3 expression can cause impaired mTORC1 signaling and increased autophagy, indicating that signaling through this receptor is critical for assessing nutrient needs. Recently, it was reported that global deletion of TAS1R3 expression in Tas1R3 mutant mice leads to increased cortical bone mass and trabecular remodeling but the underlying cellular mechanism leading to this phenotype remains unclear. Results: To address this open question, we quantified bone turnover markers in serum from 20-week-old wild type and Tas1R3 mutant mice and found that levels of the resorption marker Collagen Type I C-telopeptide (CTx) were reduced on average by >60% in the absence of TAS1R3 expression. Levels of the bone formation marker Procollagen Type I N-terminal Propeptide (P1NP) tend to be higher in Tas1R3 mutant mice but this finding did not reach statistical significance (p

Creator

• Eaton, Michael

• Newby, Jordan

Language

• English

Keyword

• TAS1R3

• autophagy

• bone resorption

• Taste receptor type 1 (TAS1R)

Date created

• 1/1/2015

Resource type

• poster

Source

• mucom_rd_13

Rights statement

• http://rightsstatements.org/vocab/InC/1.0/