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Kinin B1 receptor gene ablation affects hypothalamic CART production

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Item Type:Article
Title:Kinin B1 receptor gene ablation affects hypothalamic CART production
Creators Name:Torres, H.A.M. and Motta, F.L. and Sales, V.M. and Batista, C. and da Silva, J.M. and Vignoli, T. and Barnabé, G.F. and Goeldner, F.O. and D'Almeida, V. and Bittencourt, J.C. and Sinigaglia-Coimbra, R. and Bader, M. and Mello, L.E.A.M. and Pesquero, J.B.
Abstract:A role for the kinin B1 receptor in energy-homeostatic processes was implicated by previous works. Notably the studies where kinin B1 receptor knockout mice (B1-/-) are observed 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). More particularly, 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 CART (cocaine-and-amphetamine related transcript) in the LHA (lateral hypothalamic area) 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. Further it seems to indicate that the mechanism underlying the 'lean' phenotype of B1-/- mice is not solely stemming 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, Lateral Hypothalamic Area, Animals, Mice
Source:Biological Chemistry
Publisher:de Gruyter
Page Range:901-908
Date:July 2013
Additional Information:The final publication is available at www.degruyter.com.
Official Publication:https://doi.org/10.1515/hsz-2012-0302
PubMed:View item in PubMed

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