diture and increased their food intake after fasting. By contrast, mice lacking AMPK function in AgRP neurons showed age-dependent decrease in body weight. Surprisingly, these effects were mediated by an inability of the neurons to respond to changes in glucose levels and not caused by impaired responses to the hormone regulators of energy balance leptin and insulin. These latter observations, that AMPK is only required for the response of POMC and AgRP neurons to some signals that regulate energy balance led the authors to conclude that AMPK is "not a general sensor and integrator of energy homeostasis in the hypothalamus."
The surprising nature of the results is discussed further in an accompanying commentary by Joel Elmquist from the University of Texas Southwestern. Elmquist notes that it is complex studies such as these that uncover unexpected results that are "needed to combat the growing problems that are obesity and diabetes."
TITLE: AMPK is essential for energy homeostasis regulation and glucose sensing by POMC and AgRP neurons
AUTHOR CONTACT:
Dominic J. Withers
University College London, London, United Kingdom.
Phone: 44-20-7679-6586; Fax: 44-20-7679-6583; E-mail: d.withers@ucl.ac.uk.
View the PDF of this article at: https://www.the-jci.org/article.php?id=31516
ACCOMPANYING COMMENTARY
TITLE: "AMPing up" our understanding of the hypothalamic control of energy balance
AUTHOR CONTACT:
Joel K. Elmquist,
University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Phone: (214) 648-2911; Fax: (214) 648-5612; E-mail: joel.elmquist@utsouthwestern.edu.
View the PDF of this article at: https://www.the-jci.org/article.php?id=32975
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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
1-Aug-2007
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