| Texto completo | |
| Autor(es): |
Soares, Gabriela Moreira
[1, 2]
;
Zangerolamo, Lucas
[1, 2]
;
Costa-Junior, Jose Maria
[1, 2]
;
Vettorazzi, Jean Franciesco
[1, 2]
;
Carneiro, Everardo Magalhaes
[1, 2]
;
Saad, Sara Teresinha
[3]
;
Boschero, Antonio Carlos
[1, 2]
;
Barbosa-Sampaio, Helena Cristina
[1, 2]
Número total de Autores: 8
|
| Afiliação do(s) autor(es): | [1] Univ Estadual Campinas, Inst Biol, Dept Struct & Funct Biol, UNICAMP, Campinas, SP - Brazil
[2] Univ Estadual Campinas, Inst Biol, Obes & Comorbid Res Ctr, UNICAMP, Campinas, SP - Brazil
[3] Univ Estadual Campinas, Hematol & Hemotherapy Ctr, HEMOCTR, UNICAMP, Campinas, SP - Brazil
Número total de Afiliações: 3
|
| Tipo de documento: | Artigo Científico |
| Fonte: | FRONTIERS IN ENDOCRINOLOGY; v. 10, MAY 29 2019. |
| Citações Web of Science: | 0 |
| Resumo | |
Inhibition of Rab-GAP TBC1 domain family member 1 (TBC1D1) reduces body weight and increases energy expenditure in mice. Here, we assessed the possible involvement of GTPase activating protein 21 (ARHGAP21), a Rho-GAP protein, in energy homeostasis. Wild-type and whole-body ARHGAP21-haplodeficient mice were fed either chow or high-fat diet for 10 weeks. These mice were analyzed for body weight, food intake, voluntary physical activity, and energy expenditure by indirect calorimetry. Real-time PCR was performed to determine changes in the expression of hypothalamic-anorexic genes. Whole-body ARHGAP21-haplodeficient mice showed lower body weight and food intake associated with increased energy expenditure. These mice also showed higher expression of hypothalamic-anorexic genes such as POMC and CART. Our data suggest that the reduction in body weight of ARHGAP21-haplodeficient mice was related to alterations in the central nervous system. This suggests a new role for ARHGAP21 in energetic metabolism and prompts us to consider GAP protein members as possible targets for the prevention and treatment of obesity and related diseases. (AU) | |
| Processo FAPESP: | 12/14993-9 - Ativação do receptor muscarínico tipo 3 e associação com fatores de ribosilação do ADP 1 e 6 na função da célula-beta pancreática: vias de sinalização downstream, arquitetura da ilhota e secreção de insulina |
| Beneficiário: | Helena Cristina de Lima Barbosa |
| Modalidade de apoio: | Auxílio à Pesquisa - Jovens Pesquisadores |
| Processo FAPESP: | 15/12611-0 - Mecanismos moleculares envolvidos na disfunção e morte de células beta pancreáticas no Diabetes mellitus: estratégias para a inibição desses processos e para a recuperação da massa insular |
| Beneficiário: | Antonio Carlos Boschiero |
| Modalidade de apoio: | Auxílio à Pesquisa - Temático |