Children who are breastfed have a lower risk of obesity, which might be because of fewer specific genetic changes in the LEP gene — the gene coding for the leptin hormone, which controls appetite and energy expenditure, according to a new study.
The research, “Leptin Gene Methylation Status In Egyptian Infants,” was presented at the 58th Annual European Society for Paediatric Endocrinology Meeting, recently held in Vienna.
Although 40–70% of obesity cases are thought to have a genetic component, none of the over 40 variants associated with obesity and fat distribution can fully explain the heritability of obesity. Epigenetic changes — alterations in gene expression but not in the gene itself that respond to environmental exposures — may be an explanation as they affect how genes are inherited.
Leptin is involved in energy balance. A specific type of epigenetic change in the LEP gene, called methylation — the addition of a methyl chemical group — leads to lower leptin levels and is associated with obesity.
A team with the Alexandria University Children’s Hospital, in Egypt, assessed whether the reported lower risk of obesity among breastfed children is associated with epigenetic regulation of the LEP gene.
The study included 50 infants, all 6 months old. Half were breastfed and half were artificially fed with milk formula. All underwent a thorough clinical examination and genetic analysis of blood samples.
The results revealed that the percentage of infants with methylation in a specific spot of the LEP gene was higher in the formula-fed group. Also, methylation of the other tested gene spot was associated with increased weight among non-breastfed infants.
“These findings suggest that epigenetic mechanisms may play a role in the development of obesity,” Omneya Magdy Omar, MD, the study’s lead author, said in a press release.
“Although preliminary,” she added, “we have shown a possible link between breastfeeding and reduced risk of obesity, and added to the growing body of evidence that breastfeeding is recommended whenever possible,”
According to Omar, having a limited number of participants from a restricted geographical area is a limitation of the study, as are the lack of quantification of leptin levels and of a long-term follow-up period.
To address these gaps, the team is planning multi-center studies to assess long-term effects on epigenetic regulation of leptin, and to explore possible treatments to prevent and treat childhood obesity.
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