Insulin Signaling in Bone Marrow Adipocytes

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Insulin Signaling in Bone Marrow Adipocytes. / Tencerova, Michaela; Okla, Meshail; Kassem, Moustapha.

In: Current Osteoporosis Reports, Vol. 17, No. 6, 2019, p. 446-454.

Research output: Contribution to journalReviewResearchpeer-review

Harvard

Tencerova, M, Okla, M & Kassem, M 2019, 'Insulin Signaling in Bone Marrow Adipocytes', Current Osteoporosis Reports, vol. 17, no. 6, pp. 446-454. https://doi.org/10.1007/s11914-019-00552-8

APA

Tencerova, M., Okla, M., & Kassem, M. (2019). Insulin Signaling in Bone Marrow Adipocytes. Current Osteoporosis Reports, 17(6), 446-454. https://doi.org/10.1007/s11914-019-00552-8

Vancouver

Tencerova M, Okla M, Kassem M. Insulin Signaling in Bone Marrow Adipocytes. Current Osteoporosis Reports. 2019;17(6):446-454. https://doi.org/10.1007/s11914-019-00552-8

Author

Tencerova, Michaela ; Okla, Meshail ; Kassem, Moustapha. / Insulin Signaling in Bone Marrow Adipocytes. In: Current Osteoporosis Reports. 2019 ; Vol. 17, No. 6. pp. 446-454.

Bibtex

@article{22ad963f6a7640e9bf864ca9a84aeb99,
title = "Insulin Signaling in Bone Marrow Adipocytes",
abstract = "Purpose of Review: The goal of this review is to discuss the role of insulin signaling in bone marrow adipocyte formation, metabolic function, and its contribution to cellular senescence in relation to metabolic bone diseases. Recent Findings: Insulin signaling is an evolutionally conserved signaling pathway that plays a critical role in the regulation of metabolism and longevity. Bone is an insulin-responsive organ that plays a role in whole body energy metabolism. Metabolic disturbances associated with obesity and type 2 diabetes increase a risk of fragility fractures along with increased bone marrow adiposity. In obesity, there is impaired insulin signaling in peripheral tissues leading to insulin resistance. However, insulin signaling is maintained in bone marrow microenvironment leading to hypermetabolic state of bone marrow stromal (skeletal) stem cells associated with accelerated senescence and accumulation of bone marrow adipocytes in obesity. Summary: This review summarizes current findings on insulin signaling in bone marrow adipocytes and bone marrow stromal (skeletal) stem cells and its importance for bone and fat metabolism. Moreover, it points out to the existence of differences between bone marrow and peripheral fat metabolism which may be relevant for developing therapeutic strategies for treatment of metabolic bone diseases.",
keywords = "Bone marrow adipose tissue, Bone marrow mesenchymal stem cells, Insulin signaling, Marrow adiposity",
author = "Michaela Tencerova and Meshail Okla and Moustapha Kassem",
year = "2019",
doi = "10.1007/s11914-019-00552-8",
language = "English",
volume = "17",
pages = "446--454",
journal = "Current Osteoporosis Reports",
issn = "1544-1873",
publisher = "Current Science, Inc.",
number = "6",

}

RIS

TY - JOUR

T1 - Insulin Signaling in Bone Marrow Adipocytes

AU - Tencerova, Michaela

AU - Okla, Meshail

AU - Kassem, Moustapha

PY - 2019

Y1 - 2019

N2 - Purpose of Review: The goal of this review is to discuss the role of insulin signaling in bone marrow adipocyte formation, metabolic function, and its contribution to cellular senescence in relation to metabolic bone diseases. Recent Findings: Insulin signaling is an evolutionally conserved signaling pathway that plays a critical role in the regulation of metabolism and longevity. Bone is an insulin-responsive organ that plays a role in whole body energy metabolism. Metabolic disturbances associated with obesity and type 2 diabetes increase a risk of fragility fractures along with increased bone marrow adiposity. In obesity, there is impaired insulin signaling in peripheral tissues leading to insulin resistance. However, insulin signaling is maintained in bone marrow microenvironment leading to hypermetabolic state of bone marrow stromal (skeletal) stem cells associated with accelerated senescence and accumulation of bone marrow adipocytes in obesity. Summary: This review summarizes current findings on insulin signaling in bone marrow adipocytes and bone marrow stromal (skeletal) stem cells and its importance for bone and fat metabolism. Moreover, it points out to the existence of differences between bone marrow and peripheral fat metabolism which may be relevant for developing therapeutic strategies for treatment of metabolic bone diseases.

AB - Purpose of Review: The goal of this review is to discuss the role of insulin signaling in bone marrow adipocyte formation, metabolic function, and its contribution to cellular senescence in relation to metabolic bone diseases. Recent Findings: Insulin signaling is an evolutionally conserved signaling pathway that plays a critical role in the regulation of metabolism and longevity. Bone is an insulin-responsive organ that plays a role in whole body energy metabolism. Metabolic disturbances associated with obesity and type 2 diabetes increase a risk of fragility fractures along with increased bone marrow adiposity. In obesity, there is impaired insulin signaling in peripheral tissues leading to insulin resistance. However, insulin signaling is maintained in bone marrow microenvironment leading to hypermetabolic state of bone marrow stromal (skeletal) stem cells associated with accelerated senescence and accumulation of bone marrow adipocytes in obesity. Summary: This review summarizes current findings on insulin signaling in bone marrow adipocytes and bone marrow stromal (skeletal) stem cells and its importance for bone and fat metabolism. Moreover, it points out to the existence of differences between bone marrow and peripheral fat metabolism which may be relevant for developing therapeutic strategies for treatment of metabolic bone diseases.

KW - Bone marrow adipose tissue

KW - Bone marrow mesenchymal stem cells

KW - Insulin signaling

KW - Marrow adiposity

U2 - 10.1007/s11914-019-00552-8

DO - 10.1007/s11914-019-00552-8

M3 - Review

C2 - 31749085

AN - SCOPUS:85075362215

VL - 17

SP - 446

EP - 454

JO - Current Osteoporosis Reports

JF - Current Osteoporosis Reports

SN - 1544-1873

IS - 6

ER -

ID: 234638312