gms | German Medical Science

60. Jahrestagung der Deutschen Gesellschaft für Neuropathologie und Neuroanatomie (DGNN)

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie

26. - 28.08.2015, Berlin

Characterization of glial reaction to high-fat diet in mouse and human hypothalamus

Meeting Abstract

  • corresponding author presenting/speaker Caroline Baufeld - Charite, Department of Neuropathology, Berlin, Germany
  • David Capper - Ruprecht-Karls Universität, Department of Neuropathology, Heidelberg, Germany
  • Andreas von Deimling - Ruprecht-Karls Universität, Department of Neuropathology, Heidelberg, Germany
  • Kelly Miller - Charite, Department of Neuropathology, Berlin, United States
  • Frank Heppner - Charite, Department of Neuropathology, Berlin, Germany

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. 60th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN). Berlin, 26.-28.08.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. Doc15dgnnP24

doi: 10.3205/15dgnn48, urn:nbn:de:0183-15dgnn487

Veröffentlicht: 25. August 2015

© 2015 Baufeld et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

Text

Diets high in fat are known to cause inflammation in the periphery as well as the central nervous system. In peripheral adipose tissue, it has been shown that inflammation is primarily mediated by macrophages that are recruited to the tissue. Similarly, a recent study demonstrated reactive microgliosis in the hypothalamus of mice fed a high-fat diet. We aimed to dissect the glial reaction to diets high in fat in a detailed manner by analyzing gene expression and cell number in the hypothalamus of mice fed HFD for 3 days or 8 weeks. We detected a significant increase in microglia cells and astrocyte reactivity in the hypothalamus after prolonged HFD feeding. However, this increase was not accompanied by an increase in pro-inflammatory markers, but rather by an anti-inflammatory reaction. Furthermore, we demonstrate that the detected increase in Iba1+ myeloid cells upon HFD is due to proliferation of endogenous microglia and not due to infiltrating macrophages. Histological analysis of post-mortem human brain tissue of obese versus non-obese individuals reveals that similar to the situation in the mouse brain, gliosis is also evident in the hypothalamus of obese individuals. Finally, to analyze whether this gliosis leads to profound changes in the hypothalamus area we conducted a region-specific genome-wide methylation analysis.