The “transcription factors” FOXA2 and HNF1A activate a pancreatic enzyme that in healthy people prevents diabetes developing. When the proteins stop working, the enzyme is shut down, which in turn upsets the ability of insulin-secreting beta cells in the pancreas to monitor blood sugar levels.
Without this glucose sugar-sensing mechanism, blood sugar cannot be regulated properly. The discovery, published in the journal Nature Medicine, helps explain why Type 2 diabetes is so often linked to obesity and it could also lead to a potential cure for the condition, the researchers said.
Study leader Dr Jamey Marth said: “Now that we know more fully how states of over-nutrition can lead to Type 2 diabetes, we can see more clearly how to intervene. “The identification of the molecular players in this pathway to diabetes suggests new therapeutic targets and approaches towards developing an effective preventative or perhaps curative treatment.
“This may be accomplished by beta cell gene therapy or by drugs that interfere with this pathway in order to maintain normal beta cell function.” Experiments in mice showed that preserving the function of the enzyme affected by FOXA2 and HNF1A blocked the onset of diabetes, even in obese animals.
Diminished glucose sensing by beta cells was an important factor in both the development and severity of the disease. Dr Marth and his team are now looking at ways to augment the enzyme’s activity in humans.
More than two million people in the UK have Type 2 diabetes, the most common form of the disease. Insulin-dependent or Type 1 diabetes is a quite different condition caused by an autoimmune disorder.
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