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Potential mechanism behind type 2 diabetes seen in study of twins
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Scientists have identified mechanisms that could play a role in type 2 diabetes and explain why only one of two identical twins would develop the chronic disease, according to research published in Diabetes.
Emma Nilsson, MD, PhD, of Lund University, Malmö, Sweden, and other researchers from Sweden and Denmark investigated DNA in 14 sets of monozygotic twins, in which one twin was healthy and one had type 2 diabetes.
“Twins are a good model for finding mechanisms, but the results are applicable to all,” Nilsson said in a press release.
The researchers used genome-wide expression and DNA methylation data in adipose tissue from monozygotic pairs to dissect molecular mechanisms; 480,000 points on the DNA were examined.
Adipose tissue of twins with diabetes showed decreased expression of genes involved in oxidative phosphorylation; carbohydrate, amino acid and lipid metabolism; and increased expression of genes involved in inflammation and glycan degradation.
“This means that they are not able to process fat as well, which leads to raised levels of fat in the blood and uptake of fat by other organs instead, such as the muscles, liver or pancreas,” Nilsson said in the release. “This causes insulin resistance, which leads to type 2 diabetes.”
The scientists repeated the analysis in adipose tissue from independent case-control cohorts; one compared 10 monozygotic and 10 dizygotic sets of twins. DNA methylation similarities were greater in monozygotic vs. dizygotic, according to the release.
“Non-identical twins generally share 50% of their DNA, and it is usually said that identical twins share 100% of theirs,” Nilsson said. “Despite this, we found 1,400 places on the identical twins’ DNA where there was a difference in DNA methylation between the diabetic and the non-diabetic. It is believed that these differences are due to differences in lifestyle and this confirms the theory that type 2 diabetes is strongly linked to lifestyle.”
The changes seen in DNA sequence were different in the twins with diabetes vs. those without; the duplicated or absent copies in the genetic code would lead to changes in gene properties, according to the release.
“We found six cases where one of the set of twins had more or fewer of these copies in his or her DNA, and we suspect that this could be another cause of the disease,” Nilsson said.
Disclosure: Please see study for full list of researchers’ financial disclosures.
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