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Am J Physiol Regul Integr Comp Physiol (September 12, 2002). doi:10.1152/ajpregu.00275.2002
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Articles in PresS, published online ahead of print September 12, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00275.2002
Submitted on May 15, 2002
Accepted on September 6, 2002

DIFFERENTIAL SUPPRESSION OF HYPERGLYCEMIC, FEEDING, AND NEUROENDOCRINE RESPONSES IN ANOREXIA

Dawna Salter1 and Alan G Watts1*

1 Department of Biological Sciences, University of Southern California, Los Angeles, CA, USA

* To whom correspondence should be addressed. E-mail: watts{at}rcf.usc.edu.

We have used the anorexia shown by rats provided with hypertonic saline to drink to investigate central mechanisms that can inhibit feeding. Rats dehydrated (DE) in this manner for 3 or 5 days showed a severe attenuation of the compensatory feeding seen after an overnight fast, compared to control euhydrated (EU) rats or rats whose food was restricted to match the intake of anorexic rats. Food intake following injections of 2-deoxy-D-glucose (2DG) was also significantly decreased in DE animals compared to that eaten following a 2DG injection given before DE. However, all the DE animals demonstrated a robust eating response after water was returned, irrespective of whether they had received injection of 2DG or vehicle. Despite a profound reduction in 2DG-induced feeding, other glucoregulatory responses to 2DG remained intact in DE animals. After 2DG injection, both corticosterone secretion and blood glucose were significantly elevated from pre-injection values regardless of whether or not animals were DE. Thus, the mechanisms responsible for anorexia in DE-animals specifically target stimulatory feeding pathways but leave intact other counter-regulatory glucometabolic motor events.




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