This study shows a new cause of type 2 diabetes

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In a recent study published in Diabetes, researchers found a specific group of neurons in the brain may play a crucial role in the development of Type 2 diabetes.

The study is at Texas Tech University. One author is Andrew Shin.

In 2014, the team began studying how the human body regulates branched-chain amino acids (BCAAs).

These essential amino acids play important roles, producing energy from our food and creating neurotransmitters the brain needs to operate.

But recent studies have shown that having too much BCAAs in the blood might actually be bad news. People with obesity and Type 2 diabetes typically have higher levels of BCAAs in their blood.

In fact, their levels are consistently higher across all ages and ethnicity, meaning the amount of BCAAs in the blood can be used as an early marker for Type 2 diabetes risk.

Additionally, BCAA supplementation, which is common among athletes, can lead to insulin resistance and an abnormally high glucose level—in short, it creates the path to develop Type 2 diabetes.

Building upon earlier research, the team wanted to understand why BCAAs are elevated in blood and what underlying mechanisms make it so.

In this study, they found a specific group of neurons, called agouti-related protein neurons, in a specific area of the brain, the mediobasal hypothalamus, which are primarily responsible for controlling BCAA levels in the blood.

The findings explain why they may be higher and take part in raising blood glucose in people with obesity or Type 2 diabetes.

The team believes that if they can figure out how BCAAs are normally regulated in the body, that would allow them to pinpoint which part within the mechanistic pathway has gone wrong in people with obesity or Type 2 diabetes.

That would eventually help us develop dietary or pharmacological interventions to keep blood BCAA levels low.

The hope is that this would contribute to treating people who are susceptible to developing insulin resistance and Type 2 diabetes.

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