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García-Cáceres, C.* ; Fuente-Martin, E.* ; Díaz, F.* ; Granado, M.* ; Argente-Arizon, P.* ; Frago, L.M.* ; Freire-Regatillo, A.* ; Barrios, V.* ; Argente, J.* ; Chowen, J.A.*

The opposing effects of ghrelin on hypothalamic and systemic inflammatory processes are modulated by its acylation status and food intake in male rats.

Endocrinology 155, 2868-2880 (2014)
DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Ghrelin is an endogenous hormone that stimulates appetite and adipose tissue accrual. Both the acylated (AG) and non-acylated (DAG) isoforms of this hormone are also reported to exert antiinflammatory and protective effects systemically and in the central nervous system. As inflammatory processes have been implicated in obesity-associated secondary complications, we hypothesized that this natural appetite stimulator may protect against negative consequences resulting from excessive food intake. Adult male Wistar rats were treated icv (5 μg/day) with AG, DAG, the ghrelin mimetic GH-releasing peptide (GHRP)-6, AG, and pair-fed with controls (AG-pf) or saline for 14 days. Regardless of food intake AG increased visceral adipose tissue (VAT) and decreased circulating cytokine levels. However, AG reduced cytokine production in VAT only in rats fed ad libitum. Hypothalamic cytokine production was increased in AG-treated rats fed ad libitum and by DAG, but intracellular inflammatory signaling pathways associated with insulin and leptin resistance were unaffected. Gliosis was not observed in response to any treatment as glial markers were either reduced or unaffected. AG, DAG, and GHRP-6 stimulated production of hypothalamic insulin like-growth factor I that is involved in cell protective mechanisms. In hypothalamic astrocyte cell cultures AG decreased tumor necrosis factorα and DAG decreased interleukin-1β mRNA levels, suggesting direct anti-inflammatory effects on astrocytes. Thus, whereas ghrelin stimulates food intake and weight gain, it may also induce mechanisms of cell protection that help to detour or delay systemic inflammatory responses and hypothalamic gliosis due to excess weight gain, as well as its associated pathologies.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Sprache englisch
Veröffentlichungsjahr 2014
HGF-Berichtsjahr 0
ISSN (print) / ISBN 0013-7227
e-ISSN 1945-7170
Zeitschrift Endocrinology
Quellenangaben Band: 155, Heft: 8, Seiten: 2868-2880 Artikelnummer: , Supplement: ,
Verlag Endocrine Society
Verlagsort Chevy Chase, Md.
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)
POF Topic(s) 30502 - Diabetes: Pathophysiology, Prevention and Therapy
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502200-010
DOI 10.1210/en.2014-1074
Scopus ID 84905018799
Erfassungsdatum 2014-08-10
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