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Adipocyte glucocorticoid receptors mediate fat-to-brain signaling

Authors
de Kloet, Annette D.Krause, Eric G.Solomon, Matia B.Flak, Jonathan N.Scott, Karen A.Kim, Dong-HoonMyers, BrentUlrich-Lai, Yvonne M.Woods, Stephen C.Seeley, Randy J.Herman, James P.
Issue Date
6월-2015
Publisher
PERGAMON-ELSEVIER SCIENCE LTD
Keywords
Hypothalamic-pituitary-adrenal axis; Corticosterone; Adipose; Obesity; Stress
Citation
PSYCHONEUROENDOCRINOLOGY, v.56, pp.110 - 119
Indexed
SCIE
SCOPUS
Journal Title
PSYCHONEUROENDOCRINOLOGY
Volume
56
Start Page
110
End Page
119
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/93324
DOI
10.1016/j.psyneuen.2015.03.008
ISSN
0306-4530
Abstract
Stress-related (e.g., depression) and metabolic pathologies (e.g., obesity) are important and often co-morbid public health concerns. Here we identify a connection between peripheral glucocorticoid receptor (GR) signaling originating in fat with the brain control of both stress and metabolism. Mice with reduced adipocyte GR hypersecrete glucocorticoids following acute psychogenic stress and are resistant to diet-induced obesity. This hypersecretion gives rise to deficits in responsiveness to exogenous glucocorticoids, consistent with reduced negative feedback via adipocytes. Increased stress reactivity occurs in the context of elevated hypothalamic expression of hypothalamic-pituitary-adrenal (HPA) axis-excitatory neuropeptides and in the absence of altered adrenal sensitivity, consistent with a central cite of action. Our results identify a novel mechanism whereby activation of the adipocyte GR promotes peripheral energy storage while inhibiting the HPA axis, and provide functional evidence for a fat-to-brain regulatory feedback network that serves to regulate not just homeostatic energy balance but also responses to psychogenic stimuli. (C) 2015 Elsevier Ltd. All rights reserved.
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