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@ARTICLE{Sartorius:136511,
      author       = {Sartorius, Tina and Lutz, Stefan Z and Hoene, Miriam and
                      Waak, Jens and Peter, Andreas and Weigert, Cora and
                      Rammensee, Hans-Georg and Kahle, Philipp J and Häring,
                      Hans-Ulrich and Hennige, Anita M},
      title        = {{T}oll-like receptors 2 and 4 impair insulin-mediated brain
                      activity by interleukin-6 and osteopontin and alter sleep
                      architecture.},
      journal      = {The FASEB journal},
      volume       = {26},
      number       = {5},
      issn         = {0892-6638},
      address      = {Bethesda, Md.},
      publisher    = {FASEB},
      reportid     = {DZNE-2020-02833},
      pages        = {1799-1809},
      year         = {2012},
      abstract     = {Impaired insulin action in the brain represents an early
                      step in the progression toward type 2 diabetes, and elevated
                      levels of saturated free fatty acids are known to impair
                      insulin action in prediabetic subjects. One potential
                      mediator that links fatty acids to inflammation and insulin
                      resistance is the Toll-like receptor (TLR) family.
                      Therefore, C3H/HeJ/TLR2-KO (TLR2/4-deficient) mice were fed
                      a high-fat diet (HFD), and insulin action in the brain as
                      well as cortical and locomotor activity was analyzed by
                      using telemetric implants. TLR2/4-deficient mice were
                      protected from HFD-induced glucose intolerance and insulin
                      resistance in the brain and displayed an improvement in
                      cortical and locomotor activity that was not observed in
                      C3H/HeJ mice. Sleep recordings revealed a $42\%$ increase in
                      rapid eye movement sleep in the deficient mice during
                      daytime, and these mice spent $41\%$ more time awake during
                      the night period. Treatment of control mice with a
                      neutralizing IL-6 antibody improved insulin action in the
                      brain as well as cortical activity and diminished
                      osteopontin protein to levels of the TLR2/4-deficient mice.
                      Together, our data suggest that the lack of functional
                      TLR2/4 protects mice from a fat-mediated impairment in
                      insulin action, brain activity, locomotion, and sleep
                      architecture by an IL-6/osteopontin-dependent mechanism.},
      keywords     = {Animals / Astrocytes: metabolism / Brain: physiology /
                      Cells, Cultured / Electroencephalography / Glucose Tolerance
                      Test / Insulin: physiology / Insulin Resistance /
                      Interleukin-6: immunology / Interleukin-6: physiology /
                      Locomotion / Mice / Mice, Inbred C3H / Mice, Knockout /
                      Osteopontin: physiology / Phosphorylation / Proto-Oncogene
                      Proteins c-akt: metabolism / Real-Time Polymerase Chain
                      Reaction / Sleep / Toll-Like Receptor 2: genetics /
                      Toll-Like Receptor 2: physiology / Toll-Like Receptor 4:
                      genetics / Toll-Like Receptor 4: physiology / Insulin (NLM
                      Chemicals) / Interleukin-6 (NLM Chemicals) / Tlr2 protein,
                      mouse (NLM Chemicals) / Tlr4 protein, mouse (NLM Chemicals)
                      / Toll-Like Receptor 2 (NLM Chemicals) / Toll-Like Receptor
                      4 (NLM Chemicals) / Osteopontin (NLM Chemicals) /
                      Proto-Oncogene Proteins c-akt (NLM Chemicals)},
      cin          = {AG Kahle 2},
      ddc          = {570},
      cid          = {I:(DE-2719)1210000-4},
      pnm          = {345 - Population Studies and Genetics (POF3-345)},
      pid          = {G:(DE-HGF)POF3-345},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:22278939},
      doi          = {10.1096/fj.11-191023},
      url          = {https://pub.dzne.de/record/136511},
}