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This version published online on March 23, 2006
Endocrinology, doi:10.1210/en.2006-0143
A more recent version of this article appeared on June 1, 2006
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*Compound via MeSH
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Medline Plus Health Information
*Diabetes
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*GLUCOSE

Submitted on February 6, 2006
Accepted on March 7, 2006

The brain as a molecular target for diabetic therapy

Elena Prodi and Silvana Obici*

Department of Psychiatry, Obesity Research Center, University of Cincinnati, College of Medicine, Cincinnati, Ohio

* To whom correspondence should be addressed. E-mail: silvana.obici{at}uc.edu.

Recent evidence highlights the important role of the brain in the control of glucose homeostasis. Hypothalamic centers sense the availability of peripheral nutrients via redundant and overlapping nutrient -induced peripheral signals such as leptin and insulin and via direct metabolic signaling. Responding to nutrient availability, these hypothalamic regions in turn exert a negative feed back not only on food intake, but also on endogenous glucose production. Disruptions in the mechanisms of CNS nutrient sensing alter these homeostatic responses and contribute to the pathophysiology of obesity and type 2 diabetes. In this review, we discuss the neural and molecular pathways so far identified as possible targets for therapeutic intervention.




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