Previous data indicate that methylamine injection in fasted healthy mice produced a hypophagic effect dependent of neuronal Kv1.6 channels expression and increased by alpha-aminoguanidine, an inhibitor of semicarbazide-sensitive benzylamine oxidase enzymes mainly involved in amine degradation. In the present work we have investigated: 1) the level of expression and activity of the semicarbazide-sensitive benzylamine oxidase; 2) the effect of methylamine alone and in the presence of alpha-aminoguanidine on food intake of genetic obese and type II diabetes mice (the db/db mice). Db/db mice showed higher levels of semicarbazide-sensitive benzylamine oxidase activities in adipose tissue and in plasma than their lean counterpart (db/db+ mice). Methylamine (30–75 μg, i.c.v.) showed similar hypophagic effects in obese and lean mice consistently with the levels of neuronal Kv1.6 found in both animal strains. Alpha-aminoguandine (50 mg/kg, i.p.) increased methylamine (i.c.v.) hypophagia in both obese and lean mice and only in obese mice when methylamine was given i.p. These results suggest a crucial role of semicarbazide-sensitive benzylamine oxidase activity in controlling methylamine hypophagia in hyperphagic diabetic mice.
Activity and expression of semicarbazide-sensitive benzylamine oxidase in a rodent model of diabetes: interactive effects with methylamine and alpha-aminoguanidine / L. Cioni; G. De Siena; C. Ghelardini; O. Sernissi; C. Alfarano; R. Pirisino; L. Raimondi. - In: EUROPEAN JOURNAL OF PHARMACOLOGY. - ISSN 0014-2999. - ELETTRONICO. - 529:(2006), pp. 179-187. [10.1016/j.ejphar.2005.10.052]
Activity and expression of semicarbazide-sensitive benzylamine oxidase in a rodent model of diabetes: interactive effects with methylamine and alpha-aminoguanidine.
DE SIENA, GAETANO;GHELARDINI, CARLA;PIRISINO, RENATO GIOVANNI PAOLO;RAIMONDI, LAURA
2006
Abstract
Previous data indicate that methylamine injection in fasted healthy mice produced a hypophagic effect dependent of neuronal Kv1.6 channels expression and increased by alpha-aminoguanidine, an inhibitor of semicarbazide-sensitive benzylamine oxidase enzymes mainly involved in amine degradation. In the present work we have investigated: 1) the level of expression and activity of the semicarbazide-sensitive benzylamine oxidase; 2) the effect of methylamine alone and in the presence of alpha-aminoguanidine on food intake of genetic obese and type II diabetes mice (the db/db mice). Db/db mice showed higher levels of semicarbazide-sensitive benzylamine oxidase activities in adipose tissue and in plasma than their lean counterpart (db/db+ mice). Methylamine (30–75 μg, i.c.v.) showed similar hypophagic effects in obese and lean mice consistently with the levels of neuronal Kv1.6 found in both animal strains. Alpha-aminoguandine (50 mg/kg, i.p.) increased methylamine (i.c.v.) hypophagia in both obese and lean mice and only in obese mice when methylamine was given i.p. These results suggest a crucial role of semicarbazide-sensitive benzylamine oxidase activity in controlling methylamine hypophagia in hyperphagic diabetic mice.File | Dimensione | Formato | |
---|---|---|---|
EJP2006.pdf
Accesso chiuso
Tipologia:
Versione finale referata (Postprint, Accepted manuscript)
Licenza:
Tutti i diritti riservati
Dimensione
334.57 kB
Formato
Adobe PDF
|
334.57 kB | Adobe PDF | Richiedi una copia |
I documenti in FLORE sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.