Journal
CELL METABOLISM
Volume 15, Issue 5, Pages 646-655Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2012.01.013
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Funding
- Canadian Diabetes Association [OG-3-10-3048]
- Canadian Institute of Health Research [MOP-86554, MOP-82701]
- Canada Research Chair in Obesity
- John Kitson Mclvor Endowed Chair in Diabetes Research
- Ontario ministry of Research and Innovation [ER08-05-141]
- Banting and Best Diabetes Centre/University Health Network
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Lipid sensing and insulin signaling in the brain independently triggers a negative feedback system to lower glucose production and food intake. Here, we discuss the underlying molecular and neuronal mechanisms of lipid sensing and insulin signaling in the hypothalamus and how these mechanisms are affected in response to high-fat feeding. We propose that high-fat feeding concurrently disrupts hypothalamic insulin-signaling and lipid-sensing mechanisms and that experiments aimed to restore both insulin action and lipid sensing in the brain could effectively lower glucose production and food intake to restore metabolic homeostasis in type 2 diabetes and obesity.
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