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Bravo-Sagua R, Mattar P, Díaz X, et al. Calcium Sensing Receptor as a Novel Mediator of Adipose Tissue Dysfunction: Mechanisms and Potential Clinical Implications. Front Physiol. 2016;7:395doi: 10.3389/fphys.2016.00395.
Bravo-Sagua, R., Mattar, P., Díaz, X., Lavandero, S., & Cifuentes, M. (2016). Calcium Sensing Receptor as a Novel Mediator of Adipose Tissue Dysfunction: Mechanisms and Potential Clinical Implications. Frontiers in physiology, 7395. https://doi.org/10.3389/fphys.2016.00395
Bravo-Sagua, Roberto, et al. "Calcium Sensing Receptor as a Novel Mediator of Adipose Tissue Dysfunction: Mechanisms and Potential Clinical Implications." Frontiers in physiology vol. 7 (2016): 395. doi: https://doi.org/10.3389/fphys.2016.00395
Bravo-Sagua R, Mattar P, Díaz X, Lavandero S, Cifuentes M. Calcium Sensing Receptor as a Novel Mediator of Adipose Tissue Dysfunction: Mechanisms and Potential Clinical Implications. Front Physiol. 2016 Sep 08;7:395. doi: 10.3389/fphys.2016.00395. eCollection 2016. PMID: 27660614; PMCID: PMC5014866.
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Front Physiol. 2016 Sep 08;7:395. doi: 10.3389/fphys.2016.00395. eCollection 2016.

Calcium Sensing Receptor as a Novel Mediator of Adipose Tissue Dysfunction: Mechanisms and Potential Clinical Implications.

Frontiers in physiology

Roberto Bravo-Sagua, Pamela Mattar, Ximena Díaz, Sergio Lavandero, Mariana Cifuentes

Affiliations

  1. Institute of Nutrition and Food Technology, University of ChileSantiago, Chile; Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine, Advanced Center for Chronic Diseases and Center for Molecular Studies of the Cell, University of ChileSantiago, Chile.
  2. Institute of Nutrition and Food Technology, University of Chile Santiago, Chile.
  3. Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine, Advanced Center for Chronic Diseases and Center for Molecular Studies of the Cell, University of ChileSantiago, Chile; Cardiology Division, Department of Internal Medicine, University of Texas Southwestern Medical CenterDallas, TX, USA.

PMID: 27660614 PMCID: PMC5014866 DOI: 10.3389/fphys.2016.00395

Abstract

Obesity is currently a serious worldwide public health problem, reaching pandemic levels. For decades, dietary and behavioral approaches have failed to prevent this disease from expanding, and health authorities are challenged by the elevated prevalence of co-morbid conditions. Understanding how obesity-associated diseases develop from a basic science approach is recognized as an urgent task to face this growing problem. White adipose tissue (WAT) is an active endocrine organ, with a crucial influence on whole-body homeostasis. WAT dysfunction plays a key role linking obesity with its associated diseases such as type 2 diabetes mellitus, cardiovascular disease, and some cancers. Among the regulators of WAT physiology, the calcium-sensing receptor (CaSR) has arisen as a potential mediator of WAT dysfunction. Expression of the receptor has been described in human preadipocytes, adipocytes, and the human adipose cell lines LS14 and SW872. The evidence suggests that CaSR activation in the visceral (i.e., unhealthy) WAT is associated with an increased proliferation of adipose progenitor cells and elevated adipocyte differentiation. In addition, exposure of adipose cells to CaSR activators in vitro elevates proinflammatory cytokine expression and secretion. An increased proinflammatory environment in WAT plays a key role in the development of WAT dysfunction that leads to peripheral organ fat deposition and insulin resistance, among other consequences. We propose that CaSR may be one relevant therapeutic target in the struggle to confront the health consequences of the current worldwide obesity pandemic.

Keywords: CaSR; adipocyte; adipose tissue dysfunction; inflammation; obesity; preadipocyte

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