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The Calcium-sensing receptor is an important regulator of female visceral and perivascular adipocyte function.

E. Higgins, Z. Gonzalez-Galofre, J. McAbney, J. M. Leiper, L. B. Dowsett

Abstract

The Calcium-sensing receptor (CaSR) is a G protein-coupled receptor activated by fluctuations in extracellular calcium concentrations. Its importance in calcium homeostasis has long been established, though its role in other tissues is not well understood. Obesity is a major epidemic with both clinical and social consequences, therefore, understanding the full function and regulation of adipocytes is of critical importance. Adipocyte CaSR has previously been linked to lipolysis and inflammation in vitro. In this study, we set out to further our understanding of adipocyte CaSR in vivo via the generation of an adipocyte specific CaSR knockout mouse (CaSRAd-/-). We found female CaSRAd-/- mice weighed less than wildtype littermates with a significant reduction in visceral adipocyte size potentially due to increased expression of brown fat markers UCP-1 and Cidea. We also established that CaSR is expressed in perivascular adipose tissue (PVAT) and that its deletion protects female mice from PVAT driven hypercontractility. In contrast CaSR deletion had no effect on male body mass, adipocyte size or vascular reactivity. In conclusion, CaSR seems to be of importance in female but not male visceral and perivascular adipose tissue.

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