Kinin B1 receptor gene ablation affects hypothalamic CART production

Kinin B1 receptor gene ablation affects hypothalamic CART production

Author Torres, Hugo A. M. Autor UNIFESP Google Scholar
Motta, Fabiana Louise Autor UNIFESP Google Scholar
Sales, Vicencia Micheline Autor UNIFESP Google Scholar
Batista, Carolina Autor UNIFESP Google Scholar
Silva, Joelcimar M. da Google Scholar
Vignoli, Thiago Autor UNIFESP Google Scholar
Barnabe, Gabriela F. Autor UNIFESP Google Scholar
Goeldner, Francine O. Autor UNIFESP Google Scholar
D'Almeida, Vania Autor UNIFESP Google Scholar
Bittencourt, Jackson C. Google Scholar
Sinigaglia-Coimbra, Rita Autor UNIFESP Google Scholar
Bader, Michael Google Scholar
Mello, Luiz Eugenio A. M. Autor UNIFESP Google Scholar
Pesquero, Joao Bosco Autor UNIFESP Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Max Delbruck Ctr Mol Med MDC
Abstract A role for the kinin B1 receptor in energy-homeostatic processes was implicated in previous studies; notably, the studies where kinin B1 receptor knockout mice (B1(-/-)) were shown to have impaired adiposity, impaired leptin and insulin production, lower feed efficiency, protection from liver steatosis and diet-induced obesity when fed a high fat diet (HFD). in particular, in a model where the B1 receptor is expressed exclusively in the adipose tissue, it rescues the plasma insulin concentration and the weight gain seen in wild type mice. Taking into consideration that leptin participates in the formation of hypothalamic nuclei, which modulate energy expenditure, and feeding behavior, we hypothesized that these brain regions could also be altered in B1(-/-) mice. We observed for the first time a difference in the gene expression pattern of cocaine and amphetamine related transcript (CART) in the (lateral hypothalamic area (LHA) resulting from the deletion of the kinin B1 receptor gene. the correlation between CART expression in the LHA and the thwarting of diet-induced obesity corroborates independent correlations between CART and obesity. Furthermore, it seems to indicate that the mechanism underlying the 'lean' phenotype of B1(-/-) mice does not stem solely from changes in peripheral tissues but may also receive contributions from changes in the hypothalamic machinery involved in energy homeostasis processes.
Keywords hypothalamus
kinin B1 receptor
knockout mice
lateral hypothalamic area
Language English
Sponsor Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Associacao Beneficente de Coleta de Sangue/Universidade Federal de São Paulo (COLSAN-UNIFESP) fellowship
Grant number CNPq: 134730/2006-2
FAPESP: (2008)/06676-8
FAPESP: (2004)/13849-5
Date 2013-07-01
Published in Biological Chemistry. Berlin: Walter de Gruyter Gmbh, v. 394, n. 7, p. 901-908, 2013.
ISSN 1431-6730 (Sherpa/Romeo, impact factor)
Publisher Walter de Gruyter Gmbh
Extent 901-908
Origin http://dx.doi.org/10.1515/hsz-2012-0302
Access rights Closed access
Type Article
Web of Science ID WOS:000319913000010
URI http://repositorio.unifesp.br/handle/11600/36528

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