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Deletion of Proteinase Activated Receptor 2 (PAR2) Does Not Ameliorate Age‐Related Obesity
Author(s) -
Reynolds Thomas,
Ives Stephen
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.02036
Subject(s) - medicine , endocrinology , adipose tissue , receptor , obesity , insulin resistance , chemistry , white adipose tissue , lean body mass , body weight , biology
The purpose of this study was to determine if proteinase activated receptor 2 (PAR2) plays a role in the development of age‐related obesity and insulin resistance. Body composition and insulin action were assessed in 18‐month old male PAR2 knockout (PAR2‐KO) mice, age‐matched male C57BL6 mice (AG), and young male C57BL6 mice (YG, 6 months old). Body composition was assessed by magnetic resonance spectroscopy (Bruker LF50 BCA Mini‐Spec) and insulin action was assessed by glucose tolerance (GT), insulin tolerance (IT) and AICAR tolerance (AT) testing. Body mass was significantly higher in PAR2‐KO and AG mice when compared to YG mice (P ≤.0001). Surprisingly, PAR2‐KO mice weighed significantly more than AG mice (P=.042). Similar to body mass, epididymal white adipose tissue (EWAT) mass was significantly higher in PAR2‐KO and AG mice when compared to YG mice (P ≤.0001). No significant differences in EWAT mass existed between PAR2‐KO and AG mice (P=.95). Body composition analysis revealed that PAR2‐KO and AG mice had significantly greater fat mass and higher body fat percentage than YG mice. Further, fat mass was significantly greater in PAR2‐KO mice compared to AG mice (P=.045); however, only a trend for differences in body fat percentage was observed between PAR2‐KO and AG mice (P=.09). No differences existed in lean body mass among the PAR2‐KO, AG, and YG mice (P=.58). With regards to insulin action, area under the curve (AUC) for GT was significantly lower in PAR2‐KO compared to AG mice (P =.0003) and YG mice (P=.001); however, no differences existed for the AUC for IT or AT indicating that PAR2‐KO mice have greater insulin secretion rather than enhanced insulin sensitivity. In summary, age‐related obesity does not appear to be dependent on PAR2 expression; in fact, an absence of PAR2 may increase adiposity with advancing age.