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Submitted on July 30, 2007
Accepted on November 12, 2007
Department of Pediatrics, University of Virginia, Charlottesville, VA 22908; Center for the Study of Weight Regulation and Department of Pediatrics, Oregon Health & Science University, Portland, OR 97239; Department of Behavioral Medicine, Kagoshima University Graduate School of Medical & Dental Sciences, 8–35-1 Sakuragaoka, Kagoshima, 890-8520 JAPAN; Nephrology Division, Department of Medicine, Baylor College of Medicine, Houston, TX 77030; IPSEN, Milford, MA, 01757
* To whom correspondence should be addressed. E-mail: marksd{at}ohsu.edu.
Chronic kidney disease (CKD) is associated with an increase in inflammatory cytokines and can result in cachexia with loss of muscle and fat stores. We previously demonstrated efficacy of treating a model of cancer cachexia with ghrelin and a ghrelin receptor agonist. Currently, we examine a surgical model of CKD in rats, resulting in uremia and decreased accrual of lean body mass. Treatment with ghrelin and two ghrelin receptor agonists (BIM-28125 and BIM-28131) resulted in increased food intake and an improvement in lean body mass accrual that was related in part to a decrease in muscle protein degradation as assessed by muscle levels of the 14 kD actin fragment resulting from cleaved actomyosin. Additionally there was a decrease in circulating inflammatory cytokines in nephrectomized animals treated with ghrelin relative to saline treatment. Ghrelin-treated animals also had a decrease in the expression of IL-1 receptor in the brainstem and a decrease in expression of pro-hormone convertase-2 (PC-2), an enzyme involved in the processing of pro-opiomelanocortin (POMC) to the anorexigenic peptide 
-MSH. We conclude that ghrelin treatment in uremia results in improved lean mass accrual in part due to suppressed muscle proteolysis and possibly related to anti-inflammatory effects.
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