Abstract
BackgroundThe FTO gene, located on chromosome 16q12.2, and the MAF gene, located on chromosome 16q22-23, were identified as genes harboring common variants with an impact on obesity predisposition. We studied the association of common variants with birth weight, gain of body weight, body mass index (BMI), Ponderal index and relevant neonatal outcomes in a large German cohort of infants with a birth weight below 1500 grams.MethodsThe single nucleotide polymorphisms rs9939609 (FTO gene) and rs1424233 (MAF gene) were genotyped using allelic discrimination assays in a prospective multicenter cohort study conducted in 15 neonatal intensive care units in Germany from September 2003 until January 2008. DNA samples were extracted from buccal swabs according to standard protocols.Results1946 infants were successfully genotyped at FTO and 2149 infants at MAF. Allele frequencies were not significantly different from other European cohorts. The polymorphisms were in Hardy-Weinberg equilibrium. The polymorphisms did not show associations with birth weight, BMI and Ponderal Index at discharge, and weight gain, neither testing for a dominant, additive nor for a recessive model.DiscussionSince an association of the polymorphisms with weight gain has been demonstrated in multiple populations, the lack of association in a population of preterm infants with regular tube feeding after birth and highly controlled feeding volumes provides evidence for the hypothesis that these polymorphisms affect food intake behavior and hunger rather than metabolism and energy consumption.
Highlights
Obesity is a major cause of morbidity and mortality, associated with an increased risk of type 2 diabetes mellitus, heart disease, metabolic syndrome, hypertension, stroke and certain forms of cancer [1]
We could neither find an association of the rs9939609 or rs1424233 with birth weight nor weight gain in Very low birth weight (VLBW)-infants
These findings support the hypothesis that the polymorphisms have no impact on energy consumption and metabolism but rather on food uptake behavior
Summary
Obesity is a major cause of morbidity and mortality, associated with an increased risk of type 2 diabetes mellitus, heart disease, metabolic syndrome, hypertension, stroke and certain forms of cancer [1]. Twin and adoption studies [2] have suggested that BMI is highly heritable, progress in identifying specific variants involved in regulating body weight has largely been confined to rare mutations causing severe, monogenic early-onset forms of obesity [3]. Genome-wide association studies (GWAs) have identified polymorphisms in or close to the FTO and MAF gene to be associated with obesity [4,5,6]. The FTO gene is located on chromosome 16q12.2 It is harboring common variants with an impact on obesity predisposition and fat mass at a population level [4,5,6,7]. The FTO gene, located on chromosome 16q12.2, and the MAF gene, located on chromosome 16q22-23, were identified as genes harboring common variants with an impact on obesity predisposition. We studied the association of common variants with birth weight, gain of body weight, body mass index (BMI), Ponderal index and relevant neonatal outcomes in a large German cohort of infants with a birth weight below 1500 grams
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