Why the study?
While CaSR has an established role in calcium homeostasis, its in vivo function in adipocytes remains poorly understood despite in vitro links to lipolysis and inflammation.
Does adipocyte-specific deletion of CaSR affect body mass, adipocyte size, and vascular reactivity in mice?
Does adipocyte-specific deletion of CaSR affect body mass, adipocyte size, and vascular reactivity in mice?
Adipocyte CaSR plays a sex-specific role in regulating visceral adiposity and perivascular adipose tissue-driven vascular hypercontractility in females.
Adipocyte CaSR deletion attenuates visceral adiposity and vascular hypercontractility in female mice only; leaves open sex-specific human translation.
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 (CaSR Ad-/- ). We found female CaSR Ad-/- 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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Higgins et al. (2023) studied this question.
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