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JCI online early table of contents: April 11, 2011
Date:4/12/2011

ibit glucagon action are known to improve blood sugar levels in diabetic mouse models. When glucagon signaling is absent in mice, they are resistant to developing diabetes, but the interpretation of this model is complicated because the mice also have increased levels of a glucagon-related peptide called GLP-1, which itself is known to have similar physiological effects.

In order to better understand the roles of glucagon and GLP-1, Daniel Drucker and colleagues, from the University of Toronto, in Canada, generated mice in which the receptors for both had been deleted. Remarkably, the absence of GLP-1 signaling did not alter the improved glucose tolerance of mice lacking glucagon signaling. These mice had pancreatic islets that were more sensitive to other molecules that promote insulin release because they upregulate receptors for those alternative signals. The authors believe that their results demonstrate a plasticity of the many pathways that control insulin secretion.

TITLE: Dual elimination of the glucagon and GLP-1 receptors in mice reveals plasticity in the incretin axis

AUTHOR CONTACT:
Daniel J. Drucker
Toronto General Hospital, Toronto, Ontario, CAN
Phone: 416/340-4125; Fax: 416-978-4108; E-mail: d.drucker@utoronto.ca
View this article at: http://www.jci.org/articles/view/43615?key=226988cd0e7c660f01da


ENDOCRINOLOGY Insight into a common disorder of the critically ill

Critically ill patients often display characteristic changes in levels of thyroid hormones, a condition called non-thyroidal illness syndrome (NTIS). One of the initial signs of NTIS is a low level of the active hormone triiodothyronine (also called T3), and lower T3 levels correlate with poor prognosis and survival. Therefore, understanding how hormone metabolism goes awry in patients without p
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Contact: Kathryn Claiborn
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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