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Submitted on July 10, 2006
Accepted on September 14, 2006
Department of Pharmacology, German Institute of Human Nutrition Potsdam-Rehbruecke, D-14558, Germany; Department of Psychiatry, University of Cincinnati Genome Research Institute, Cincinnati, OH 45237, USA; Department of Physiology, University of Santiago de Compostela, Santiago de Compostela 15781, Spain; Physiology and Animal Husbandry, Institute of Animal Sciences, ETH Zurich, Schwerzenbach 8603, Switzerland; Energy Balance and Obesity Division, Rowett Research Institute, Aberdeen AB21 9SB, UK, Department of Chemistry, Indiana University, Bloomington, IN 47405, USA
* To whom correspondence should be addressed. E-mail: fscadigo{at}usc.es.
Ghrelin stimulates food intake and adiposity and thereby increases body weight in rodents after central as well as peripheral administration. Recently, it was discovered that the gene precursor of ghrelin encoded another secreted and bioactive peptide named obestatin. First reports appeared to demonstrate that this peptide requires an amidation for its biological activity and acts through the orphan receptor, GPR-39. Obestatin was shown to have actions opposite to ghrelin on food intake, body weight and gastric emptying. In the present study we failed to observe any effect of obestatin on food intake, body weight, body composition, energy expenditure, locomotor activity, respiratory quotient or hypothalamic neuropeptides involved in energy balance regulation. In agreement with the first report, we were unable to find any effect of obestatin on growth hormone secretion in vivo. Moreover, we were unable to find mRNA expression of GPR-39, the putative obestatin receptor, in the hypothalamus of rats. Therefore, the results presented here do not support a role of the obestatin/GPR-39 system in the regulation of energy balance.
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