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Heppner, K.M.* ; Piechowski, C.L.* ; Müller, A.* ; Ottaway, N.* ; Sisley, S.* ; Smiley, D.L.* ; Habegger, K.M.* ; Pfluger, P.T. ; DiMarchi, R.* ; Biebermann, H.* ; Tschöp, M.H. ; Sandoval, D.A.* ; Perez-Tilve, D.*

Both acyl and des-acyl ghrelin regulate adiposity and glucose metabolism via CNS ghrelin receptors.

Diabetes 63, 122-131 (2014)

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Ghrelin receptors (GHSRs) in the central nervous system (CNS) mediate hyperphagia and adiposity induced by acyl ghrelin (AG). Evidence suggests that des-acyl ghrelin (dAG) has biological activity through GHSR independent mechanisms. We combined in vitro and in vivo approaches to test possible GHSR-mediated biological activity of dAG. Both AG (100nM) and dAG (100nM) significantly increased IP3 formation in HEK-293 cells transfected with human GHSR. As expected, intracerebroventricular (icv) infusion of AG in mice increased fat mass (FM), in comparison with the saline-infused controls. Icv-dAG also increased FM at the highest dose tested (5 nmol/day). Chronic icv infusion of AG or dAG increased glucose-stimulated insulin secretion (GSIS). Subcutaneously infused AG regulated FM and GSIS in comparison to saline-infused control mice, whereas dAG failed to regulate these parameters even with doses that were efficacious when delivered icv. Furthermore, icv-dAG failed to regulate FM and induce hyperinsulinemia in GHSR deficient (Ghsr-/-) mice. In addition, a hyperinsulinemic-euglycemic clamp suggests that icv-dAG impairs glucose clearance without affecting endogenous glucose production. Taken together, these data demonstrate that dAG is an agonist of GHSR and regulates body adiposity and peripheral glucose metabolism through a CNS GHSR-dependent mechanism.

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