ESPE Abstracts

Background: Obesity results from interactions between environmental and genetic factors. Despite a relatively high heritability of common, non-syndromic obesity (40–70%), the search for genetic variants contributing to susceptibility has been a challenging task. To date, more than 40 genetic variants have been associated with obesity and fat distribution. However, since these variants do not fully explain the heritability of obesity, other forms of variation, such as epigenetics marks, must be considered.DNA methylation is one of the best-understood epigenetic mechanisms and an important programming mechanism of the genome, in which cells and tissues can adapt to past and present environmental exposures. The methylation of the leptin gene promoter suppresses its expression and decrease in leptin production is highly associated with obesity.

Aim: The study aimed to study the leptin gene methylation status in a six-month-old cohort of Egyptian infants.

Patients and Methods: The study was carried on 50 infants aged 6-month-old, attending the outpatient clinic of Alexandria University Children's Hospital. All infants joined the study were subjected to full history taking, thorough clinical examination stressing on anthropometric measurement. Peripheral blood samples were taken for genetic analysis to study the methylation status of leptin gene promoter by methylation-specific polymerase chain reaction (MS-PCR) at 31 nt at 51 nt loci

Results: Out of 50 infants 25 were exclusively breastfed and 25 were artificially fed. A significantly higher percentage of formula-fed infants were methylated in leptin gene promoter at 31 nt locus compared with breastfed infants. Also, at 51nt locus infants with methylated leptin gene had significantly higher weight for length standard deviation score compared to infants with methylated gene

Conclusion: Leptin gene is unmethylated in breastfed infants compared to formula-fed infants. So epigenetics mechanisms could play a role in the development of obesity.