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Inhibition of glycine transporter-1 in the dorsal vagal complex improves metabolic homeostasis in diabetes and obesity

Author

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  • Jessica T. Y. Yue

    (UHN
    Present address: Department of Physiology, University of Alberta, Edmonton, Alberta, Canada T6G 2H7)

  • Mona A. Abraham

    (UHN
    Departments of Physiology)

  • Paige V. Bauer

    (UHN
    Departments of Physiology)

  • Mary P. LaPierre

    (UHN
    Departments of Physiology)

  • Peili Wang

    (Section of Endocrinology, Yale University School of Medicine)

  • Frank A. Duca

    (UHN)

  • Beatrice M. Filippi

    (UHN)

  • Owen Chan

    (Section of Endocrinology, Yale University School of Medicine)

  • Tony K. T. Lam

    (UHN
    Departments of Physiology
    University of Toronto
    Banting and Best Diabetes Centre, University of Toronto)

Abstract

Impaired glucose homeostasis and energy balance are integral to the pathophysiology of diabetes and obesity. Here we show that administration of a glycine transporter 1 (GlyT1) inhibitor, or molecular GlyT1 knockdown, in the dorsal vagal complex (DVC) suppresses glucose production, increases glucose tolerance and reduces food intake and body weight gain in healthy, obese and diabetic rats. These findings provide proof of concept that GlyT1 inhibition in the brain improves glucose and energy homeostasis. Considering the clinical safety and efficacy of GlyT1 inhibitors in raising glycine levels in clinical trials for schizophrenia, we propose that GlyT1 inhibitors have the potential to be repurposed as a treatment of both obesity and diabetes.

Suggested Citation

  • Jessica T. Y. Yue & Mona A. Abraham & Paige V. Bauer & Mary P. LaPierre & Peili Wang & Frank A. Duca & Beatrice M. Filippi & Owen Chan & Tony K. T. Lam, 2016. "Inhibition of glycine transporter-1 in the dorsal vagal complex improves metabolic homeostasis in diabetes and obesity," Nature Communications, Nature, vol. 7(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms13501
    DOI: 10.1038/ncomms13501
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