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Endogenous Glucocorticoid Signaling in the Regulation of Bone and Marrow Adiposity: Lessons from Metabolism and Cross Talk in Other Tissues

  • Anuj K. Sharma
  • Xingming Shi
  • Carlos M. Isales
  • Meghan E. McGee-LawrenceEmail author
Bone Marrow and Adipose Tissue (G Duque and B Lecka-Czernik, Section Editors)
Part of the following topical collections:
  1. Topical Collection on Bone Marrow and Adipose Tissue

Abstract

Purpose of Review

The development of adiposity in the bone marrow, known as marrow adipose tissue (MAT), is often associated with musculoskeletal frailty. Glucocorticoids, which are a key component of the biological response to stress, affect both bone and MAT. These molecules signal through receptors such as the glucocorticoid receptor (GR), but the role of the GR in regulation of MAT is not yet clear from previous studies. The purpose of this review is to establish and determine the role of GR-mediated signaling in marrow adiposity by comparing and contrasting what is known against other energy-storing tissues like adipose tissue, liver, and muscle, to provide better insight into the regulation of MAT during times of metabolic stress (e.g., dietary challenges, aging).

Recent Findings

GR-mediated glucocorticoid signaling is critical for proper storage and utilization of lipids in cells such as adipocytes and hepatocytes and proteolysis in muscle, impacting whole-body composition, energy utilization, and homeostasis through a complex network of tissue cross talk between these systems. Loss of GR signaling in bone promotes increased MAT and decreased bone mass.

Summary

GR-mediated signaling in the liver, adipose tissue, and muscle is critical for whole-body energy and metabolic homeostasis, and both similarities and differences in GR-mediated GC signaling in MAT as compared with these tissues are readily apparent. It is clear that GC-induced pathways work together through these tissues to affect systemic biology, and understanding the role of bone in these patterns of tissue cross talk may lead to a better understanding of MAT-bone biology that improves treatment strategies for frailty-associated diseases.

Keywords

Glucocorticoid Cortisol Cortisone Corticosterone Adipocyte Osteoblast Bone marrow Aging 

Notes

Funding Information

The authors are supported by funding provided by the National Institute on Aging (NIA AG036675) and the American Diabetes Association (1-16-JDF-062).

Compliance with Ethical Standards

Conflict of Interest

Anuj K. Sharma, Xingming Shi, Carlos M. Isales, and Meghan E. McGee-Lawrence declare no conflict of interest.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  • Anuj K. Sharma
    • 1
  • Xingming Shi
    • 2
  • Carlos M. Isales
    • 2
    • 3
    • 4
  • Meghan E. McGee-Lawrence
    • 1
    • 3
    Email author
  1. 1.Department of Cellular Biology and Anatomy, Medical College of GeorgiaAugusta UniversityAugustaUSA
  2. 2.Department of Neuroscience and Regenerative MedicineAugusta UniversityAugustaUSA
  3. 3.Department of Orthopaedic SurgeryAugusta UniversityAugustaUSA
  4. 4.Department of Medicine, Division of Endocrinology, Diabetes and MetabolismAugusta UniversityAugustaUSA

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