ArticleInternational journal of obesity (2005)2017
Exploring the relationship between α-actinin-3 deficiency and obesity in mice and humans.
Article in International journal of obesity (2005), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Exploring protein relative relations in skeletal muscle proteomic analysis for insights into insulin resistance and type 2 diabetes.Scientific reports · 2024Article
- Association of theGenes · 2022Article
- ACTN3 Genotypes and Their Relationship with Muscle Mass and Function of Kosovan Adults.International journal of environmental research and public health · 2021Article
- Loss of α-actinin-3 during human evolution provides superior cold resilience and muscle heat generation.American journal of human genetics · 2021Article
- Combination of ACTN3 R577X and ACE I/D polymorphisms as a tool for prediction of obesity risk in children.International journal of obesity (2005) · 2021Article
- Relationships between the Expression of theJournal of human kinetics · 2019Article
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Authors and funding
10 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity is a worldwide health crisis, and the identification of genetic modifiers of weight gain is crucial in understanding this complex disorder. A common null polymorphism in the fast fiber-specific gene ACTN3 (R577X) is known to influence skeletal muscle function and metabolism. α-Actinin-3 deficiency occurs in an estimated 1.5 billion people worldwide, and results in reduced muscle strength and a shift towards a more efficient oxidative metabolism. The X-allele has undergone strong positive selection during recent human evolution, and in this study, we sought to determine whether ACTN3 genotype influences weight gain and obesity in mice and humans. An Actn3 KO mouse has been generated on two genetic backgrounds (129X1/SvJ and C57BL/6J) and fed a high-fat diet (HFD, 45% calories from fat). Anthropomorphic features (including body weight) were examined and show that Actn3 KO 129X1/SvJ mice gained less weight compared to WT. In addition, six independent human cohorts were genotyped for ACTN3 R577X (Rs1815739) and body mass index (BMI), waist-to-hip ratio-adjusted BMI (WHRadjBMI) and obesity-related traits were assessed. In humans, ACTN3 genotype alone does not contribute to alterations in BMI or obesity.
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