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

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 sy...

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Veröffentlicht in:Scientific reports 2021-05, Vol.11 (1), p.10409-10409, Article 10409
Hauptverfasser: Sundararaman, Sai Sahana, Peters, Linsey J. F., Jansen, Yvonne, Gencer, Selin, Yan, Yi, Nazir, Sumra, Bonnin Marquez, Andrea, Kahles, Florian, Lehrke, Michael, Biessen, Erik A. L., Jankowski, Joachim, Weber, Christian, Döring, Yvonne, van der Vorst, Emiel P. C.
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Sprache:eng
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Zusammenfassung: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
2045-2322
DOI:10.1038/s41598-021-89893-y