Peer Reviewed

1

Document Type

Contribution to Book

Publication Date

25-9-2019

Keywords

adipose tissue, autophagy, browning, insulin resistance, obesity

Comments

The original book chapter is available at https://www.intechopen.com/

Abstract

In addition to the well-documented role in the kidney, the mineralocorticoid receptor (MR) has been recently identified in different “non-classical” target tissues, such as the brain, the heart, vasculature, macrophages/monocytes, and adipose tissue. In this context, the MR is involved in adipocyte fundamental processes such as differentiation, autophagy, and adipokine secretion. Excessive activation of the MR contributes to metabolic derangements occurring in mice with obesity and metabolic syndrome. Interestingly, MR pharmacological blockade in murine models of obesity has led to protection from weight gain and adipocyte dysfunctions. Unfortunately, there is still a lack of knowledge on the metabolic effects of MR antagonists, and larger clinical studies are deemed necessary to clarify the metabolic role of MR blockade in humans. This review discusses the role of MR in adipose tissue, focusing on regulation by MR of key cellular processes occurring in the adipocyte. The molecular pathways affected by MR activation or blockade in adipose tissue have been investigated only in part. Hence, more studies are necessary to get more insights in the role of aldosterone/MR in this “non-classical” target tissue and to better understand its potential implications in obesity and metabolic syndrome.

Disciplines

Medical Molecular Biology | Medical Sciences

Citation

Armani A, Marzolla V, Feraco A, Gorini S, Mammi C, Infante M, Caprio M. Mineralocorticoid Receptor in Novel Target Tissues: A Closer Look at the Adipocyte. In: Harvey B, Jaisser F, editors. Aldosterone-Mineralocorticoid Receptor - Cell Biology to Translational Medicine: InTechOpen; 2019.

DOI Link

10.5772/intechopen.87231

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial 4.0 License

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