The Type 2 “Missing Link”: What is Beta Catenin?

For the past decade, scientists have struggled to understand the connection between the development of type 2 diabetes and genetics. The scientific community first identified a variant on a gene called TCF7L2, which is now considered the largest contributing factor for a person's genetic presupposition to type 2 diabetes. But the big question – one that spawned years of research – was HOW.

And now, new research published earlier this month in the Journal of Biological Chemistry may have found that missing link.

What is Beta Catenin?

It was Professor Peter Shepherd and his team of researchers at the University of Auckland in New Zealand that made this breakthrough discovery. In their study of TCF7L2, they noticed that the gene bound to a particular protein in the body: a protein known as beta catenin.

“By observing this interaction,” Professor Shepherd explained, “[W]e found that beta catenin levels not only change in response to rising and falling nutrient levels, but that they also regulate how much insulin we have in our body and ensure that we have the right amount of insulin at the right time.”

Further research proved that beta catenin is incredibly instrumental in obesity (a risk factor that can lead to type 2 diabetes). This protein – and specifically, its binding process with TCF7L2 – controls our insulin levels, our metabolism of glucose, and even the release of hormones in our brains that control appetite and energy metabolism.

What Does This Mean For Diabetics?

Discussing his team's findings (and the $1.2 million grant they received from Health Research Council of New Zealand, otherwise known as HRC) Professor Shepherd was enthusiastic about the possibilites this discovery could yield for diabetic patients.

“It's hard work finding new mechanisms that contribute to disease,” he said. “This discovery potentially opens up a whole new drug discovery field to understand how we could manipulate beta catenin levels to control the release of insulin.”

Source: Phys.org

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