Titre
Targeted gene disruption reveals a leptin-independent role for the mouse beta3-adrenoceptor in the regulation of body composition.
Type
article
Institution
Externe
Périodique
Auteur(s)
Revelli, J.P.
Auteure/Auteur
Preitner, F.
Auteure/Auteur
Samec, S.
Auteure/Auteur
Muniesa, P.
Auteure/Auteur
Kuehne, F.
Auteure/Auteur
Boss, O.
Auteure/Auteur
Vassalli, J.D.
Auteure/Auteur
Dulloo, A.
Auteure/Auteur
Seydoux, J.
Auteure/Auteur
Giacobino, J.P.
Auteure/Auteur
Huarte, J.
Auteure/Auteur
Ody, C.
Auteure/Auteur
Liens vers les personnes
ISSN
0021-9738
Statut éditorial
Publié
Date de publication
1997
Volume
100
Numéro
5
Première page
1098
Dernière page/numéro d’article
1106
Langue
anglais
Résumé
Targeted disruption of mouse beta3-adrenoceptor was generated by homologous recombination, and validated by an acute in vivo study showing a complete lack of effect of the beta3-adrenoceptor agonist CL 316,243 on the metabolic rate of homozygous null (-/-) mice. In brown adipose tissue, beta3-adrenoceptor disruption induced a 66% decrease (P < 0.005) in beta1-adrenoceptor mRNA level, whereas leptin mRNA remained unchanged. Chronic energy balance studies in chow-fed mice showed that in -/- mice, body fat accumulation was favored (+41%, P < 0.01), with a slight increase in food intake (+6%, NS). These effects were accentuated by high fat feeding: -/- mice showed increased total body fat (+56%, P < 0.025) and food intake (+12%, P < 0.01), and a decrease in the fat-free dry mass (-10%, P < 0.05), which reflects a reduction in body protein content. Circulating leptin levels were not different in -/- and control mice regardless of diet. The significant shift to the right in the positive correlation between circulating leptin and percentage of body fat in high fat-fed -/- mice suggests that the threshold of body fat content inducing leptin secretion is higher in -/- than in control mice. Taken together, these studies demonstrate that beta3-adrenoceptor disruption creates conditions which predispose to the development of obesity.
Sujets
PID Serval
serval:BIB_40CED56E402D
PMID
Open Access
Oui
Date de création
2012-12-18T14:50:09.855Z
Date de création dans IRIS
2025-05-20T19:53:18Z