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Physiological Role of Cholecystokinin B/Gastrin Receptor in Leptin Secretion¹

INSERM, U-10, Institut Federatif de Recherche 2 (IFR2) Cellules Epithéliales, Hôpital Bichat (S.A., S.L., M.B., H.G., J.-P.L., L.M., J.M.M.L., A.B.), 75018 Paris; Department de Radiobiologie et de Radiopathologie-Centre d’Energie Atomique (DRR-CEA) (F.H.), 92265 Fontenay aux Roses Cedex; and INSERM EA99–11, Faculté de Médecine (Y.B.), 06107 Nice Cedex 02, France

Address all correspondence and requests for reprints to: Dr. Miguel J. M. Lewin, INSERM U-10, Hôpital Bichat, 170 boulevard Ney, 75018 Paris, France. E-mail: mjmlewin{at}bichat.inserm.fr

In the present study, we investigated whether cholecystokinin (CCK) or its structurally related peptide gastrin participates in long term regulation of adipocyte leptin secretion. The levels of circulating leptin observed after 2 and 6 h of refeeding in 18-h fast rats were significantly lowered by injection of the specific gastrin/CCK-B receptor antagonist YM022 at doses that did not affect feeding behavior. Moreover, in normally fed animals, circulating leptin was markedly decreased by chronic injection of YM022 (from 4 ± 0.6 to 2.1 ± 0.5 ng/ml). Consistent with these observations, YM022 treatment decreased leptin messenger RNA (mRNA) levels and increased the leptin content in rat epididymal fat tissue. Rat adipocytes exclusively contain gastrin/CCK-B receptor mRNA, but not CCK-A receptor mRNA. Furthermore, adipocyte membranes bound [¹²⁵I]CCK-8 in a saturable manner, with kinetics consistent with a single class of high affinity sites with a K_d of 0.2 nM. These data argue for a physiological role for the CCK-B/gastrin receptor in adipocyte leptin regulation. We therefore propose that gastrin is involved in long term regulation of leptin expression and secretion in rat fat tissues through activation of an adipocyte gastrin/CCK-B receptor.

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