Adipocyte calcium sensing receptor is not involved in visceral adipose tissue inflammation or atherosclerosis development in hyperlipidemic Apoe −/− mice

Abstract The calcium sensing receptor (CaSR) is a G-protein coupled receptor that especially plays an important role in the sensing of extracellular calcium to maintain its homeostasis. Several in-vitro studies demonstrated that CaSR plays a role in adipose tissue metabolism and inflammation, result...

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Main Authors: Sai Sahana Sundararaman, Linsey J. F. Peters, Yvonne Jansen, Selin Gencer, Yi Yan, Sumra Nazir, Andrea Bonnin Marquez, Florian Kahles, Michael Lehrke, Erik A. L. Biessen, Joachim Jankowski, Christian Weber, Yvonne Döring, Emiel P. C. van der Vorst
Format: Article
Language:English
Published: Nature Portfolio 2021-05-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-021-89893-y
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Summary:Abstract The calcium sensing receptor (CaSR) is a G-protein coupled receptor that especially plays an important role in the sensing of extracellular calcium to maintain its homeostasis. Several in-vitro studies demonstrated that CaSR plays a role in adipose tissue metabolism and inflammation, resulting in systemic inflammation and contributing to atherosclerosis development. The aim of this study was to investigate whether adipocyte CaSR plays a role in adipose tissue inflammation in-vivo and atherosclerosis development. By using a newly established conditional mature adipocyte specific CaSR deficient mouse on a hyperlipidemic and atherosclerosis prone Apoe −/− background it could be shown that CaSR deficiency in adipocytes does neither contribute to initiation nor to progression of atherosclerotic plaques as judged by the unchanged lesion size or composition. Additionally, CaSR deficiency did not influence gonadal visceral adipose tissue (vAT) inflammation in-vivo, although a small decrease in gonadal visceral adipose cholesterol content could be observed. In conclusion, adipocyte CaSR seems not to be involved in vAT inflammation in-vivo and does not influence atherosclerosis development in hyperlipidemic Apoe−/− mice.
ISSN:2045-2322