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      Ketogenic diet leads to O-GlcNAc modification in the BTBR(T+tf/j) mouse model of autism.

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          Abstract

          Protein O-linked-β-N-acetyl glucosamine (O-GlcNAc) is a post-translational modification to Ser/Thr residues that integrates energy supply with demand. Abnormal O-GlcNAc patterning is evident in several neurological disease states including epilepsy, Alzheimer's disease and autism spectrum disorder (ASD). A potential treatment option for these disorders includes the high-fat, low-carbohydrate, ketogenic diet (KD). The goal of this study was to determine whether the KD induces changes in O-GlcNAc in the BTBR(T+tf/j) (BTBR) mouse model of ASD.

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          Author and article information

          Journal
          Biochim. Biophys. Acta
          Biochimica et biophysica acta
          Elsevier BV
          0006-3002
          0006-3002
          May 11 2017
          Affiliations
          [1 ] Faculty of Kinesiology, University of Calgary, Calgary, AB, Canada; Department of Medical Science, University of Calgary Cumming School of Medicine, Calgary, AB, Canada. Electronic address: cnewell@ucalgary.ca.
          [2 ] Faculty of Kinesiology, University of Calgary, Calgary, AB, Canada.
          [3 ] Alberta Children's Hospital Research Institute, University of Calgary Cumming School of Medicine, Alberta Children's Hospital, AB, Canada.
          [4 ] Department of Medical Science, University of Calgary Cumming School of Medicine, Calgary, AB, Canada.
          [5 ] Alberta Children's Hospital Research Institute, University of Calgary Cumming School of Medicine, Alberta Children's Hospital, AB, Canada; Department of Medical Genetics and Pediatrics, University of Calgary Cumming School of Medicine, Alberta Children's Hospital, AB, Canada.
          [6 ] Alberta Children's Hospital Research Institute, University of Calgary Cumming School of Medicine, Alberta Children's Hospital, AB, Canada; Department of Paediatrics, University of Calgary Cumming School of Medicine, Alberta Children's Hospital, Calgary, AB, Canada; Department of Clinical Neurosciences, University of Calgary Cumming School of Medicine, Alberta Children's Hospital, Calgary, AB, Canada; Department of Physiology & Pharmacology, University of Calgary Cumming School of Medicine, Alberta Children's Hospital, Calgary, AB, Canada.
          [7 ] Faculty of Kinesiology, University of Calgary, Calgary, AB, Canada; Department of Medical Science, University of Calgary Cumming School of Medicine, Calgary, AB, Canada; Alberta Children's Hospital Research Institute, University of Calgary Cumming School of Medicine, Alberta Children's Hospital, AB, Canada.
          Article
          S0925-4439(17)30150-3
          10.1016/j.bbadis.2017.05.013
          28502704

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