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The hypothalamic neural-glial network and the metabolic syndrome.

Best Pract. Res. Clin. Endocrinol. Metab. 28, 661-671 (2014)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Despite numerous educational interventions and biomedical research efforts, modern society continues to suffer from obesity and its associated metabolic diseases, such as type 2 diabetes mellitus, and these diseases show little sign of abating. One reason for this is an incomplete understanding of the pathology of the metabolic syndrome, which obstructs the development of effective therapeutic strategies. While hypothalamic neuropathy is a potential candidate that may contribute to the pathogenesis of the metabolic syndrome, the specific causes of hypothalamic neuropathy remain largely unknown. During different stages of high-calorie diet-induced metabolic syndrome, the hypothalamus undergoes gliosis and angiogenesis, both of which potentially reflect ongoing inflammatory processes. This overview discusses current data suggesting a role for hypothalamic inflammation-like processes in diet-induced metabolic diseases and provides a perspective on how to unravel molecular mechanisms of “hypothalamic inflammation” in order to develop anti-obesity therapeutic strategies.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Blood Brain Barrier ; Cytokines ; Diabetes ; Leptin Resistance ; Mitochondria ; Neurogenesis; Diet-induced Obesity; Blood-brain-barrier; Leptin Resistance; Energy-balance; Feeding-behavior; Neuropeptide-y; Knockout Mice; Body-weight; Fatty-acids; Paraventricular Nucleus
Sprache englisch
Veröffentlichungsjahr 2014
HGF-Berichtsjahr 2014
ISSN (print) / ISBN 1521-690X
e-ISSN 1532-1908
Quellenangaben Band: 28, Heft: 5, Seiten: 661-671 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort Oxford
Begutachtungsstatus Peer reviewed
POF Topic(s) 30201 - Metabolic Health
90000 - German Center for Diabetes Research
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502200-001
G-501900-221
PubMed ID 25256762
Erfassungsdatum 2014-03-28