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.hese 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 amine oxidase in a rodent model of diabetes: interactive effects with methylamine and alpha-amino guanidine / Cioni L, De Siena G, Ghelardini C, Sernissi O, Alfarano C, Pirisino R, Raimondi L.. - In: EUROPEAN JOURNAL OF PHARMACOLOGY. - ISSN 0014-2999. - ELETTRONICO. - 4:(2005), pp. 179-187.

Activity and expression of semicarbazide-sensitive amine oxidase in a rodent model of diabetes: interactive effects with methylamine and alpha-amino guanidine

Cioni L;De Siena G;Ghelardini C;Alfarano C;Pirisino R;Raimondi L.
2005

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.hese results suggest a crucial role of semicarbazide-sensitive benzylamine oxidase activity in controlling methylamine hypophagia in hyperphagic diabetic mice.
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179
187
Cioni L, De Siena G, Ghelardini C, Sernissi O, Alfarano C, Pirisino R, Raimondi L.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2158/221729
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