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JCI online early table of contents: July 1, 2010
Date:7/1/2010

ffects each brain region mediates has not been clearly determined. However, Lori Zeltser and Laurence Ring have now generated mice in which leptin signaling is disrupted in only the hypothalamic region of the brain and shown that leptin signals in the hypothalamus are required to prevent the development of obesity up to 8 weeks of age. After 8 weeks of age, leptin signals in regions of the brain other than the hypothalamus were able to control further development of obesity, although they could not reverse obesity established prior to 8 weeks of age. The authors suggest that these data might have implications for combating childhood obesity.

TITLE: Disruption of hypothalamic leptin signaling in mice leads to early-onset obesity, but physiological adaptations in mature animals stabilize adiposity levels

AUTHOR CONTACT:
Lori M. Zeltser
Columbia University, New York, New York, USA.
Phone: 212.851.5314; Fax: 212.851.5306; E-mail: lz146@columbia.edu.

View this article at: http://www.jci.org/articles/view/41985?key=ee928b6505cbee5baee5


METABOLIC DISEASE: A tale of tribbles 3: understanding its role in type 2 diabetes

Type 2 diabetes is characterized by insufficient secretion of the hormone insulin, which controls glucose levels in the blood, and reduced mass of insulin-secreting pancreatic beta-cells. A team of researchers, led by Rohit Kulkarni, at Harvard Medical School, Boston, has now confirmed recent data indicating that a genetic variant of the tribbles 3 (TRB3) gene is associated with increased risk of developing type 2 diabetes and determined the reasons underlying this. Specifically, the protein generated by the genetic variant was shown to impair the release of insulin from mouse and human pancreatic beta-cells in which it was expressed and to reduce the mass of pancre
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Contact: Karen Honey
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Journal of Clinical Investigation
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