Cited by 199Stress Responses and CortisolRegulation of Appetite and ObesityNeuropeptides and Animal Physiology

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Glucocorticoids, chronic stress, and obesity

Dallman, Mary F., Pecoraro, Norman C., La Fleur, Susanne E., Warne, James P., Ginsberg, Abigail B., Akana, Susan F., Laugero, Kevin C., Houshyar, Hani, Strack, Alison M., Bhatnagar, Seema, Bell, Mary E.·2006·Progress in Brain Research

DOI 10.1016/s0079-6123(06)53004-3

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Abstract

Glucocorticoids either inhibit or sensitize stress-induced activity in the hypothalamo-pituitary-adrenal (HPA) axis, depending on time after their administration, the concentration of the steroids, and whether there is a concurrent stressor input. When there are high glucocorticoids together with a chronic stressor, the steroids act in brain in a feed-forward fashion to recruit a stress-response network that biases ongoing autonomic, neuroendocrine, and behavioral outflow as well as responses to novel stressors. We review evidence for the role of glucocorticoids in activating the central stress-response network, and for mediation of this network by corticotropin-releasing factor (CRF). We briefly review the effects of CRF and its receptor antagonists on motor outflows in rodents, and examine the effects of glucocorticoids and CRF on monoaminergic neurons in brain. Corticosteroids stimulate behaviors that are mediated by dopaminergic mesolimbic "reward" pathways, and increase palatable feeding in rats. Moreover, in the absence of corticosteroids, the typical deficits in adrenalectomized rats are normalized by providing sucrose solutions to drink, suggesting that there is, in addition to the feed-forward action of glucocorticoids on brain, also a feedback action that is based on metabolic well being. Finally, we briefly discuss the problems with this network that normally serves to aid in responses to chronic stress, in our current overindulged, and underexercised society.

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Authors: Dallman, M. F., Pecoraro, N. C., La Fleur, S. E., Warne, J. P., Ginsberg, A. B., Akana, S. F., Laugero, K. C., Houshyar, H., Strack, A. M., Bhatnagar, S., & Bell, M. E.
Affiliations: University of California, San Francisco (US)
Corresponding author: Dallman, Mary F.
ORCID: Bhatnagar, Seema
Venue: Progress in Brain Research
Publisher: Elsevier
Published: 2006
Volume: 153
Pages: 75-105
ISSN: 0079-6123 (ISSN-L)
DOI: 10.1016/s0079-6123(06)53004-3
OpenAlex: W1553637564
Cited by: 198
References: 374
Citations by year: 2026: 2 · 2025: 2 · 2024: 6 · 2023: 11 · 2022: 4 · 2021: 9 · 2020: 4 · 2019: 9 · 2018: 8 · 2017: 5 · 2016: 12 · 2015: 12 · 2014: 16 · 2013: 14 · 2012: 12
FWCI: 33.08
Type: book chapter
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Progress in brain research (publishedVersion)
PubMed (publishedVersion)
Data Archiving and Networked Services (DANS) (submittedVersion)
Pure Amsterdam UMC (submittedVersion)
Funders: National Institute on Drug Abuse (DA-16944, R01DA016944)
National Institute of Diabetes and Digestive and Kidney Diseases (DK28172)
Topics: Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
Keywords: glucocorticoids, chronic stress, obesity, hypothalamic-pituitary-adrenal axis, corticotropin-releasing factor, CRF receptor antagonists, stress response networks, monoaminergic neurons, dopaminergic reward pathways, sucrose intake, adrenalectomy, metabolic feedback
MeSH terms: Animals, Chronic Disease, Glucocorticoids, Humans, Hypothalamo-Hypophyseal System, Obesity, Pituitary-Adrenal System, Stress, Physiological

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