What’s most interesting about it (the discovery) is that this links to one of the recently discovered genetic variants that make some people more likely to get diabetes than others.
A missing link in our current knowledge about type 2 diabetes has been discovered by New Zealand scientists. The research, led by University of Auckland’s professor Peter Shepherd, was published in The Journal of Biological Chemistry, notes how the team discovered a gene called TCF7L2 that binds directly to the beta-catenin protein, prompting a mechanism that manages blood sugar levels. TCF7L2 is a protein-coding gene that binds directly to the beta-catenin protein, initiating a mechanism that controls the release of insulin from the pancreas.
“This means that in the future we’ve got a better opportunity to develop new treatments or even preventative strategies for this disease,” Professor Peter Shepherd says. In cases of type 2 diabetes, either the body doesn’t produce enough insulin or the cells in the body don’t recognize the insulin that’s there, leading to high levels of glucose in the blood.
“What’s most interesting about it (the discovery) is that this links to one of the recently discovered genetic variants that make some people more likely to get diabetes than others.”
Scientists have created a large body of knowledge over the past 15 years about how hormones are released from cells in the body, but this is the first time this mechanism has been associated with the release of insulin. Shepherd said the mechanism works like a volume control on a TV, regulating, around the clock, how much insulin is available. He also noted that the findings would provide researchers with a better understanding why some people find themselves more at risk of diabetes, and provides new treatment possibilities. The research team believes that they have identified a much broader mechanism that affects multiple cell types, not just beta cells in the pancreas.
The hope is that new treatments for chronic diseases like diabetes will be more readily developed as an understanding of the biology behind the disease is better understood. Currently, between 50 to 60 percent of the population who are at risk of diabetes have genetic variants that put them at higher risk of developing the blood sugar disease. But the discovery of TCF7L2 opens up a plethora of drug options that could better manipulate beta catenin levels to help control the release of insulin.
