Activity and expression of semicarbazide-sensitive benzylamine oxidase in a rodent model of diabetes: Interactive effects with methylamine and alpha-aminoguanidine

被引：13

作者：

Cioni, L ^{[1
]}

De Siena, G ^{[1
]}

Ghelardini, C ^{[1
]}

Sernissi, O ^{[1
]}

Alfarano, C ^{[1
]}

Pirisino, R ^{[1
]}

Raimondi, L ^{[1
]}

机构：

[1] Univ Florence, Dept Pharmacol, I-50121 Florence, Italy

来源：

EUROPEAN JOURNAL OF PHARMACOLOGY | 2006年 / 529卷 / 1-3期

关键词：

diabetes; methylamine; alpha-aminoguandine; hyperphagia; K(v)1.6 potassium channel; semicarbazide-sensitive benzylamine oxidase activity;

D O I：

10.1016/j.ejphar.2005.10.052

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Previous data indicate that methylamine injection in fasted healthy mice produced a hypophagic effect dependent of neuronal K(v)1.6 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 11 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 mu g, i.c.v.) showed similar hypophagic effects in obese and lean mice consistently with the levels of neuronal K(v)1.6 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. (c) 2005 Elsevier BY. All rights reserved.

引用

页码：179 / 187

页数：9

共 35 条

[21] Methylamine and benzylamine induced hypophagia in mice: Modulation by semicarbazide-sensitive benzylamine oxidase inhibitors and aODN towards Kv1.1 channels [J].