Abstract
Commentary: FTO obesity variant circuitry and adipocyte browning in humans.
Highlights
Reviewed by: Helene Choquet, University of California, San Francisco, USA Eusebio Chiefari, Magna Græcia University of Specialty section: This article was submitted to Genomic Endocrinology, a section of the journal Frontiers in Genetics
Their study, published in the New England Journal of Medicine, provides evidence for the rs1421085 T to C single-nucleotide alteration to result in a cellular phenotype consistent with obesity in primary human adipocytes, including decreased mitochondrial energy generation and increased triglyceride accumulation (Claussnitzer et al, 2015)
Many Genome-wide association studies (GWAS) regions are enriched for histone modifications (The ENCODE Project Consortium, 2012), suggesting they may play a role in gene regulation
Summary
Reviewed by: Helene Choquet, University of California, San Francisco, USA Eusebio Chiefari, Magna Græcia University of Specialty section: This article was submitted to Genomic Endocrinology, a section of the journal Frontiers in Genetics. Genome-wide association studies (GWAS) identified >90 loci containing genetic variants, many in intronic regions, associated with human obesity. The strongest genetic association with risk to polygenic obesity are single-nucleotide variants in intron 1 and 2 of the FTO (fat mass and obesity associated) gene (Yang et al, 2012; Locke et al, 2015).
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