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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Whole-Body ARHGAP21-Deficiency Improves Energetic Homeostasis in Lean and Obese Mice

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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]
Total Authors: 8
[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
Total Affiliations: 3
Document type: Journal article
Web of Science Citations: 0

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)

FAPESP's process: 12/14993-9 - Type 3 muscarinic receptor activation and association with ADP-rybosilation factor 1 and 6 on the pancreatic beta-cell function: downstream signalling pathways, islet arquitecture and insulin secretion
Grantee:Helena Cristina de Lima Barbosa Sampaio
Support type: Research Grants - Young Investigators Grants
FAPESP's process: 15/12611-0 - Molecular mechanisms involved in pancreatic beta cell disfunction and dead in diabetes mellitus: strategies for the inhibition of these processes and restoration of the insular mass
Grantee:Antonio Carlos Boschiero
Support type: Research Projects - Thematic Grants