Age-Related Epigenetic Changes May Lead to Development of Diabetes in Later Life

Epigenetic changes that cause increased methylation and partial or complete inactivation of genes during aging may contribute to the development of type II diabetes in older individuals.

Investigators at Lund University (Malmö, Sweden) examined whether age-related epigenetic changes affected human islet function and if blood-based epigenetic biomarkers reflected those changes and were linked to the future appearance of type II diabetes. To accomplish this task, they analyzed DNA methylation in the genomes of pancreatic islet cells obtained from 87 non-diabetic donors, aged 26–74 years.


They reported in the March 31, 2016, online edition of the journal Nature Communications that aging was associated with increased DNA methylation of 241 sites. These sites covered genetic loci previously associated with type II diabetes, for example, KLF14 (Krüppel-like factor 14). Blood-based epigenetic biomarkers reflected age-related methylation changes in 83 genes identified in human islets (for example, KLF14, FHL2 (Four and a half LIM domains 2), ZNF518B (Zinc finger protein 518B), and FAM123C (APC membrane recruitment protein 3). Some of these proteins were linked to insulin secretion and type II diabetes. Silencing these genes in beta-cells altered – often increasing – insulin secretion.

"Increased insulin secretion actually protects against type II diabetes. It could be the body's way of protecting itself when other tissue becomes resistant to insulin, which often happens as we get older", said senior author Dr. Charlotte Ling, professor of clinical science at Lund University. "You cannot change your genes and the risks that they entail, but epigenetics means that you can affect the DNA methylations, and thereby gene activity, through lifestyle choices."

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