The new research findings were achieved through access to human insulin-producing cells from deceased donors and by not only studying one gene variant, but many genes. New methods were used to see how these genes influence the level of the gene in pancreatic islets and their effect on insulin secretion and glucose supply.
"With this approach, we can explain 25 percent of variations in blood sugar levels. Previously, the best studies have explained less than 3 percent," says Leif Groop from Lund University Diabetes Centre, the principal author of the study, published in the journal Cell Metabolism.
The results of the study provide greater insights into why, in cases of Type 2 diabetes, beta cells cease to perform their function of producing sufficient insulin to keep blood sugar levels under control.
"We have linked different gene variants to their effects on donated human beta cells and have compared cells from non-diabetic and diabetics," said Professor Groop.
The starting point for researchers was the 47 known gene variants that have a link to diabetes. "We used them as 'bait' to find new signal paths and chain of events where the 47 variants work together with other genes. We have to map patterns because a single gene rarely acts on its own," continued Groop.
To pick out the 20 strongest gene variants, criteria included a difference between beta cells from healthy individuals and diabetics and a link to insulin secretion and blood sugar levels. The goal of the study was to understand the relationship between gene variants and diabetes.
"By taking a new and more holistic approach, we have gone a step further than previous projects and succeeded in linking together gene variants and their signal paths in human beta cells that cause reduced insulin secretion. The next step is to look in more detail at the way in which the strongest genes affect insulin secretion," said Groop.
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