Fat linked to DNA methylation may help explain obesity-related diseases
New data have identified methylation changes in blood leukocyte DNA as a potential culprit behind obesity-related illnesses.
Researchers, to analyze a connection between obesity and immune dysfunction, performed a genome-wide methylation analysis involving seven obese and seven lean children aged 14 to 18 years. Participants all had BMIs at extreme ends of the obesity spectrum.
When compared with lean participants, obese children had higher methylation levels at one CpG site in the UBASH3A gene and lower levels at one CpG site in the TRIM3 gene. These results prompted the researchers to conduct a replication study examining six CpG sites in six genes among 46 obese and 46 lean participants aged 14 to 30 years.
Findings from this analysis further implicated methylation changes in the two genes in dysregulation of the immune system. If future studies confirm these data, it may explain why obese people are more vulnerable to certain health problems, such as diabetes and cardiovascular disease, the researchers said.
“You need to know disease pathways to find novel medications,” Xiaoling Wang, PhD, study researcher and genetic epidemiologist at the Georgia Prevention Institute, Medical College of Georgia, said in a press release. “We generally know [obese people] have a dysregulation of the immune function, but we didn’t know the specific site.”
In an accompanying editorial, Paul W. Franks, PhD, and Charlotte Ling, PhD, both of the Skane University Hospital, Lund University, in Malmo, Sweden, wrote, “Replication of these findings in independent settings will be necessary to ensure that these findings are true positives, and to fairly conclude that the relationships are causal will require appropriately designed experimental studies.”
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Disclosures: Drs. Wang, Franks and Ling report no relevant financial disclosures.
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