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1 Psychology, Barnard College, Columbia University, New York, NY, USA
2 St. Luke's-Roosevelt Hospital Center, New York Obesity Research Center, New York, NY, USA
* To whom correspondence should be addressed. E-mail: pjc37{at}columbia.edu.
Ghrelin is a 28 amino acid acylated peptide and is the endogenous ligand for the growth hormone secretagogue receptor (GHS-R). The GHS-R is expressed in hypothalamic nuclei including the arcuate nucleus where it is colocalized with NPY neurons. In the present study we examined the effects of ghrelin on feeding and energy substrate utilization (respiratory quotient; RQ) following direct injections into either the arcuate (Arc) or the paraventricular (PVN) nucleus of the hypothalamus. Ghrelin was administered at the beginning of the dark cycle at doses of 15-60 pmol to male and female rats. In feeding studies, food intake was measured 2 and 4 h postinjection. Separate groups of rats were injected with ghrelin and RQ (VCO2/VO2) was measured using an open circuit calorimeter over a 4 h period. Both Arc and PVN injections of ghrelin increased food intake in male and female rats. Ghrelin also increased RQ reflecting a shift in energy substrate utilization in favor of carbohydrate oxidation. Because these effects are similar to those observed after PVN injection of NPY, we then assessed the impact of co-injecting ghrelin with NPY into the PVN. When rats were pretreated with very low doses of ghrelin (2.5-10 pmol), NPY's (50 pmol) effects on eating and RQ were potentiated. Overall, these data are in agreement with evidence suggesting that ghrelin functions as a gut-brain endocrine hormone implicated in the regulation of food intake and energy metabolism. Our findings are also consistent with a possible interactive role of hypothalamic ghrelin and NPY systems.
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