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Verfasst von:Gao, Yuanqing [VerfasserIn]   i
 Fleming, Thomas [VerfasserIn]   i
 Nawroth, Peter Paul [VerfasserIn]   i
Titel:Dietary sugars, not lipids, drive hypothalamic inflammation
Verf.angabe:Yuanqing Gao, Maximilian Bielohuby, Thomas Fleming, Gernot F. Grabner, Ewout Foppen, Wagner Bernhard, Mara Guzmán-Ruiz, Clarita Layritz, Beata Legutko, Erwin Zinser, Cristina García-Cáceres, Ruud M. Buijs, Stephen C. Woods, Andries Kalsbeek, Randy J. Seeley, Peter P. Nawroth, Martin Bidlingmaier, Matthias H. Tschöp, Chun-Xia Yi
Umfang:12 S.
Fussnoten:Available online 20 June 2017 ; Gesehen am 19.06.2018
Titel Quelle:Enthalten in: Molecular metabolism
Jahr Quelle:2017
Band/Heft Quelle:6(2017), 8, S. 897-908
ISSN Quelle:2212-8778
Abstract:Objective: The hypothalamus of hypercaloric diet-induced obese animals is featured by a significant increase of microglial reactivity and its associated cytokine production. However, the role of dietary components, in particular fat and carbohydrate, with respect to the hypothalamic inflammatory response and the consequent impact on hypothalamic control of energy homeostasis is yet not clear. Methods: We dissected the different effects of high-carbohydrate high-fat (HCHF) diets and low-carbohydrate high-fat (LCHF) diets on hypothalamic inflammatory responses in neurons and non-neuronal cells and tested the hypothesis that HCHF diets induce hypothalamic inflammation via advanced glycation end-products (AGEs) using mice lacking advanced glycation end-products (AGEs) receptor (RAGE) and/or the activated leukocyte cell-adhesion molecule (ALCAM). Results: We found that consumption of HCHF diets, but not of LCHF diets, increases microgliosis as well as the presence of N(ε)-(Carboxymethyl)-Lysine (CML), a major AGE, in POMC and NPY neurons of the arcuate nucleus. Neuron-secreted CML binds to both RAGE and ALCAM, which are expressed on endothelial cells, microglia, and pericytes. On a HCHF diet, mice lacking the RAGE and ALCAM genes displayed less microglial reactivity and less neovasculature formation in the hypothalamic ARC, and this was associated with significant improvements of metabolic disorders induced by the HCHF diet. Conclusions: Combined overconsumption of fat and sugar, but not the overconsumption of fat per se, leads to excessive CML production in hypothalamic neurons, which, in turn, stimulates hypothalamic inflammatory responses such as microgliosis and eventually leads to neuronal dysfunction in the control of energy metabolism.
DOI:doi:10.1016/j.molmet.2017.06.008
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Kostenfrei: Verlag: http://dx.doi.org/10.1016/j.molmet.2017.06.008
 Kostenfrei: Verlag: http://www.sciencedirect.com/science/article/pii/S2212877817302399
 DOI: https://doi.org/10.1016/j.molmet.2017.06.008
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1576503526
Verknüpfungen:→ Zeitschrift

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