The GIPR is Predominantly Localized to Non-Adipocyte Cell Types Within White Adipose Tissue
Gastric inhibitory polypeptide
DOI:
10.2337/figshare.19184462
Publication Date:
2022-02-22T20:45:18Z
AUTHORS (11)
ABSTRACT
The incretin hormone glucose-dependent insulinotropic polypeptide (GIP) augments insulin secretion through its receptor expressed on islet b-cells. GIP also acts adipose tissue, yet paradoxically, both enhanced and reduced (GIPR) signaling reduce tissue mass attenuate weight gain in response to nutrient excess. Moreover, the precise cellular localization of GIPR expression within white (WAT) remains uncertain. Here, we used mouse genetics target <i>Gipr </i>expression adipocytes. Surprisingly, targeting Cre adipocytes using Adiponectin (<i>Adipoq</i>) promoter did not produce meaningful reduction WAT <i>Adipoq-Cre:Gipr</i><sup>flx/flx </sup>mice. In contrast, adenoviral <i>Cre</i> under control CMV promoter, or transgenic non-adipocyte-selective promoters (<i>Ap2</i>/<i>Fabp4</i> <i>Ubc</i>) markedly attenuated </i>expression. Analysis single nucleus RNA-seq data sets localized <i>Gipr</i>/<i>GIPR</i> predominantly pericytes mesothelial cells rather than Together, these observations reveal that are major GIPR+ cell type WAT, findings with mechanistic implications for understanding how GIP-based co-agonists biology.
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