Abstract
To the Editor: In an exome-sequencing study involving 2548 children who presented with severe obesity, Mendes de Oliveira et al. (Oct. 21 issue)1 reported 19 different GNAS variants in 22 patients with severe childhood-onset obesity without features of pseudohypoparathyroidism. The majority of these variants (16 of 19) were missense variants that were functionally characterized for their effects on signaling by the Gαs subunit–coupled melanocortin 4 receptor. The authors suggest that children with severe childhood-onset obesity should be screened for GNAS variants in accordance with the diagnostic approach favored by Mantovani et al.2 to enable early diagnosis and treatment. However, interpreting .
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