The link between diet and epigenetics in humans is notoriously difficult to study since people are, unsurprisingly, resistant to being fed a strictly controlled diet. Researchers at the Karolinska Institute have, however, shown that exposure to fatty acids can cause epigenetic modifications in muscle cells from healthy individuals that are the same as changes seen in people with type II diabetes.
Both hereditary and environmental factors are believed to play a role in the development of type II diabetes which is characterised by reduced sensitivity to insulin and a reduced ability to consume energy in the form of glucose. The team had previously shown that, in skeletal muscle cells from individuals with early-onset diabetes, the gene for PGC-1α (peroxisome proliferator-activated receptor-gamma coactivator 1α) is hypermethylated and shows reduced expression levels. PGC-1α is a promiscuous co-activator that plays a key role in regulating mitochondrial function and metabolism. In the present study, the team showed that DNA methylation occurs rapidly when cells from healthy individuals are exposed to factors linked to diabetes such as the fatty acid, palmitic acid, and the cytokine, TNF-α. It remains to be seen whether dietary factors substantially influence methylation of the gene for PGC-1α but the study suggests a mechanism whereby over-consumption of fatty foods could promote the development of type II diabetes. Since some epigenetic modifications are known to be inheritable, the study also raises the interesting question of whether the consequences of dietary excess can be visited on future generations.
The study is published in the journal Cell Metabolism.
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