ArticleFrontiers in endocrinology2019
Whole-Body ARHGAP21-Deficiency Improves Energetic Homeostasis in Lean and Obese Mice.
Article in Frontiers in endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Novel polymorphism atAnimal biotechnology · 2025Article
- Impact of Sleeve Gastrectomy on Body Weight and Food Intake Regulation in Diet-Induced Obese Mice.Current issues in molecular biology · 2024Article
- The bile acid TUDCA reduces age-related hyperinsulinemia in mice.Scientific reports · 2022Article
- Resistance Training Improves Beta Cell Glucose Sensing and Survival in Diabetic Models.International journal of molecular sciences · 2022Article
- Energy homeostasis deregulation is attenuated by TUDCA treatment in streptozotocin-induced Alzheimer's disease mice model.Scientific reports · 2021Article
- Resistance exercise training improves glucose homeostasis by enhancing insulin secretion in C57BL/6 mice.Scientific reports · 2021Article
- ARHGAP21 Acts as an Inhibitor of the Glucose-Stimulated Insulin Secretion Process.Frontiers in endocrinology · 2020Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
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.
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