Data/hora: 10/06/2024 07:49:57

Provedor de dados: 	Brazilian Journal of Medical and Biological Research	
País: 	Brazil	
Título: 	Rimonabant improves metabolic parameters partially attributed to restoration of high voltage-activated Ca2+ channels in skeletal muscle in HFD-fed mice	
Autores: 	Chen,B.; Hu,N.	
Data: 	2017-01-01	
Ano: 	2017	
Palavras-chave: 	Cannabinoid receptor type 1; Obesity; Rimonabant; Skeletal Muscle; HVA calcium channel.	
Resumo: 	Cannabinoid type 1 receptor (CB1R) inhibition tends to be one of the promising strategies for the treatment of obesity and other related metabolic disorders. Although CB1R inhibition may cause adverse psychiatric effects including depression and anxiety, the investigation of the role of peripheral CB1R on weight loss and related metabolic parameters are urgently needed. We first explored the effect of rimonabant, a selective CB1R antagonist/inverse agonist, on some metabolic parameters in high fat-diet (HFD)-induced obesity in mice. Then, real-time PCR and electrophysiology were used to explore the contribution of high voltage-activated Ca2+ channels (HVACCs), especially Cav1.1, on rimonabant's effect in skeletal muscle (SM) in HFD-induced obesity. Five-week HFD feeding caused body weight gain, and decreased glucose/insulin tolerance in mice compared to those in the regular diet group (P&lt;0.05), which was restored by rimonabant treatment compared to the HFD group (P&lt;0.05). Interestingly, HVACCs and Cav1.1 were decreased in soleus muscle cells in the HFD group compared to the control group. Daily treatment with rimonabant for 5 weeks was shown to counter such decrease (P&lt;0.05). Collectively, our findings provided a novel understanding for peripheral CB1R's role in the modulation of body weight and glucose homeostasis and highlight peripheral CB1R as well as Cav1.1 in the SM as potential targets for obesity treatment.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2017000600602	
Editor: 	Associação Brasileira de Divulgação Científica	
Relação: 	10.1590/1414-431x20176141	
Formato: 	text/html	
Fonte: 	Brazilian Journal of Medical and Biological Research  v.50 n.6 2017	
Fonte: 	info:eu-repo/semantics/openAccess