
Variants in the FTO gene have been strongly associated with obesity in a very large sample (38,759) of diabetic and control subjects. To replicate these findings, the previously reported SNP in the FTO gene (rs9939609, T/A) was genotyped in 5,607 subjects from five different Utah studies. The studies included a random sample of the Utah population, families selected for aggregation of extreme thinness, families selected for severe obesity, a series of unrelated severe obesity subjects, and families participating in a 25‐year longitudinal study of cardiovascular disease and aging. Results show a strong significant increase in the rs9939609 A allele frequency with increasing BMI (P < 0.0001). In the longitudinal study, FTO genotypes were significantly associated with BMI at a baseline exam, a 2½‐year follow‐up exam and a 25‐year follow‐up exam using an additive genetic model. The mean genotype difference in BMI ranged from 1.3 to 2.1 kg/m2 across exams. The genotype difference in BMI means was established in youth, and at‐risk subjects under age 20 at baseline had a significantly larger 25‐year BMI increase (10.0 for A/A; 9.7 for A/T, and 8.5 kg/m2 for T/T, P = 0.05). We conclude that the BMI increases associated with FTO genotypes begin in youth and are maintained throughout adulthood.
Adult, Aged, 80 and over, Male, Aging, Adolescent, Genotype, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Middle Aged, Body Mass Index, Pedigree, Gene Frequency, Cardiovascular Diseases, Child, Preschool, Humans, Female, Genetic Predisposition to Disease, Obesity, Child, Aged, Follow-Up Studies
Adult, Aged, 80 and over, Male, Aging, Adolescent, Genotype, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Middle Aged, Body Mass Index, Pedigree, Gene Frequency, Cardiovascular Diseases, Child, Preschool, Humans, Female, Genetic Predisposition to Disease, Obesity, Child, Aged, Follow-Up Studies
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