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Interaction of glucose sensing and leptin action in the brain

Authors
  • Li, Rosa J.W.1, 2
  • Zhang, Song-Yang1, 2
  • Lam, Tony K.T.1, 2, 3, 4
  • 1 Department of Physiology, University of Toronto, Toronto, ON, M5S 1A8, Canada
  • 2 Toronto General Hospital Research Institute, UHN, Toronto, ON, M5G 1L7, Canada
  • 3 Department of Medicine, University of Toronto, Toronto, ON, M5S 1A8, Canada
  • 4 Banting and Best Diabetes Centre, University of Toronto, Toronto, ON, M5G 2C4, Canada
Type
Published Article
Journal
Molecular Metabolism
Publisher
Elsevier BV
Publication Date
May 13, 2020
Volume
39
Identifiers
DOI: 10.1016/j.molmet.2020.101011
PMID: 32416314
PMCID: PMC7267726
Source
PubMed Central
Keywords
License
Unknown

Abstract

Background In response to energy abundant or deprived conditions, nutrients and hormones activate hypothalamic pathways to maintain energy and glucose homeostasis. The underlying CNS mechanisms, however, remain elusive in rodents and humans. Scope of review Here, we first discuss brain glucose sensing mechanisms in the presence of a rise or fall of plasma glucose levels, and highlight defects in hypothalamic glucose sensing disrupt in vivo glucose homeostasis in high-fat fed, obese, and/or diabetic conditions. Second, we discuss brain leptin signalling pathways that impact glucose homeostasis in glucose-deprived and excessed conditions, and propose that leptin enhances hypothalamic glucose sensing and restores glucose homeostasis in short-term high-fat fed and/or uncontrolled diabetic conditions. Major conclusions In conclusion, we believe basic studies that investigate the interaction of glucose sensing and leptin action in the brain will address the translational impact of hypothalamic glucose sensing in diabetes and obesity.

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