GDF15 in appetite and exercise: Essential player or coincidental bystander?

Research output: Contribution to journalReviewpeer-review

Standard

GDF15 in appetite and exercise: Essential player or coincidental bystander? / Klein, Anders Bue; Kleinert, Maximilian; Richter, Erik A.; Clemmensen, Christoffer.

In: Endocrinology, Vol. 163, No. 1, 2022, p. 1-10.

Research output: Contribution to journalReviewpeer-review

Harvard

Klein, AB, Kleinert, M, Richter, EA & Clemmensen, C 2022, 'GDF15 in appetite and exercise: Essential player or coincidental bystander?', Endocrinology, vol. 163, no. 1, pp. 1-10. https://doi.org/10.1210/endocr/bqab242

APA

Klein, A. B., Kleinert, M., Richter, E. A., & Clemmensen, C. (2022). GDF15 in appetite and exercise: Essential player or coincidental bystander? Endocrinology, 163(1), 1-10. https://doi.org/10.1210/endocr/bqab242

Vancouver

Klein AB, Kleinert M, Richter EA, Clemmensen C. GDF15 in appetite and exercise: Essential player or coincidental bystander? Endocrinology. 2022;163(1):1-10. https://doi.org/10.1210/endocr/bqab242

Author

Klein, Anders Bue ; Kleinert, Maximilian ; Richter, Erik A. ; Clemmensen, Christoffer. / GDF15 in appetite and exercise: Essential player or coincidental bystander?. In: Endocrinology. 2022 ; Vol. 163, No. 1. pp. 1-10.

Bibtex

@article{4eb8458a4ed24d299e9da2ac3ffb61c2,
title = "GDF15 in appetite and exercise: Essential player or coincidental bystander?",
abstract = "Growth differentiation factor 15 (GDF15) has recently moved to the forefront of metabolism research. When administered pharmacologically, GDF15 reduces food intake and lowers body weight via the hindbrain-situated receptor GFRAL (glial cell-derived neurotrophic factor family receptor alpha like). Endogenous GDF15 is a ubiquitous cellular stress signal that can be produced and secreted by a variety of cell types. Circulating levels are elevated in a series of disease states, but also in response to exogenous agents such as metformin, colchicine, AICAR and cisplatin. Recently, exercise has emerged as a relevant intervention to interrogate GDF15 physiology. Prolonged endurance exercise increases circulating GDF15 to levels otherwise associated with certain pathological states and in response to metformin treatment. Yet, the jury is still out as to whether GDF15 is a functional 'exerkine' mediating organ-to-brain cross-talk or whether it is a coincidental bystander. In this review, we discuss the putative physiological implication of exercise-induced GDF15, focusing on the potential impact on appetite and metabolism.",
keywords = "Faculty of Science, Exercise, GDF15, Growth differentiation factor 15, Appetite, Energy balance, Exerkine",
author = "Klein, {Anders Bue} and Maximilian Kleinert and Richter, {Erik A.} and Christoffer Clemmensen",
note = "{\textcopyright} The Author(s) 2021. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.",
year = "2022",
doi = "10.1210/endocr/bqab242",
language = "English",
volume = "163",
pages = "1--10",
journal = "Journal of Clinical Endocrinology and Metabolism",
issn = "0013-7227",
publisher = "Oxford University Press",
number = "1",

}

RIS

TY - JOUR

T1 - GDF15 in appetite and exercise: Essential player or coincidental bystander?

AU - Klein, Anders Bue

AU - Kleinert, Maximilian

AU - Richter, Erik A.

AU - Clemmensen, Christoffer

N1 - © The Author(s) 2021. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

PY - 2022

Y1 - 2022

N2 - Growth differentiation factor 15 (GDF15) has recently moved to the forefront of metabolism research. When administered pharmacologically, GDF15 reduces food intake and lowers body weight via the hindbrain-situated receptor GFRAL (glial cell-derived neurotrophic factor family receptor alpha like). Endogenous GDF15 is a ubiquitous cellular stress signal that can be produced and secreted by a variety of cell types. Circulating levels are elevated in a series of disease states, but also in response to exogenous agents such as metformin, colchicine, AICAR and cisplatin. Recently, exercise has emerged as a relevant intervention to interrogate GDF15 physiology. Prolonged endurance exercise increases circulating GDF15 to levels otherwise associated with certain pathological states and in response to metformin treatment. Yet, the jury is still out as to whether GDF15 is a functional 'exerkine' mediating organ-to-brain cross-talk or whether it is a coincidental bystander. In this review, we discuss the putative physiological implication of exercise-induced GDF15, focusing on the potential impact on appetite and metabolism.

AB - Growth differentiation factor 15 (GDF15) has recently moved to the forefront of metabolism research. When administered pharmacologically, GDF15 reduces food intake and lowers body weight via the hindbrain-situated receptor GFRAL (glial cell-derived neurotrophic factor family receptor alpha like). Endogenous GDF15 is a ubiquitous cellular stress signal that can be produced and secreted by a variety of cell types. Circulating levels are elevated in a series of disease states, but also in response to exogenous agents such as metformin, colchicine, AICAR and cisplatin. Recently, exercise has emerged as a relevant intervention to interrogate GDF15 physiology. Prolonged endurance exercise increases circulating GDF15 to levels otherwise associated with certain pathological states and in response to metformin treatment. Yet, the jury is still out as to whether GDF15 is a functional 'exerkine' mediating organ-to-brain cross-talk or whether it is a coincidental bystander. In this review, we discuss the putative physiological implication of exercise-induced GDF15, focusing on the potential impact on appetite and metabolism.

KW - Faculty of Science

KW - Exercise

KW - GDF15

KW - Growth differentiation factor 15

KW - Appetite

KW - Energy balance

KW - Exerkine

U2 - 10.1210/endocr/bqab242

DO - 10.1210/endocr/bqab242

M3 - Review

C2 - 34849709

VL - 163

SP - 1

EP - 10

JO - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

SN - 0013-7227

IS - 1

ER -

ID: 286422671