A recent study published in the Journal of Clinical Investigation suggests that effectively treating type 2 diabetes might require a new approach—focusing on certain neurons in the brain instead of just targeting obesity or insulin resistance.
This discovery, led by researchers at UW Medicine, challenges the long-standing belief that type 2 diabetes is mainly driven by weight gain and poor diet.
For years, scientists have known that a group of neurons in the brain’s hypothalamus, called AgRP neurons, tend to be hyperactive in mice with diabetes. These neurons are known for their role in regulating appetite and energy balance, but researchers began to suspect they might also be contributing to high blood sugar levels, a defining feature of type 2 diabetes.
To test this theory, the research team used a genetic method to block communication from these neurons. They achieved this by making the neurons express tetanus toxin, which essentially silenced their ability to send signals to other parts of the brain.
Surprisingly, this intervention caused blood sugar levels in diabetic mice to return to normal—and the effect lasted for months. Even more surprising was that this happened without any changes in body weight or food intake. The mice remained the same size, ate the same amount of food, but their blood sugar stayed in a healthy range.
This finding goes against the traditional understanding of type 2 diabetes, which has always focused on problems like obesity, lack of exercise, and poor diet.
These factors are thought to lead to insulin resistance, where the body’s cells no longer respond to insulin properly, or to low insulin production by the pancreas. Until now, the role of the brain in managing blood sugar has largely been ignored.
Dr. Michael Schwartz, the lead author of the study and an endocrinologist at UW Medicine, explained that these findings represent a major shift in how we understand diabetes.
He described it as a “departure from the conventional wisdom of what causes diabetes.” According to Schwartz, the evidence shows that AgRP neurons are playing a much bigger role in high blood sugar than anyone previously realized.
This new research also connects with earlier studies by the same team. In those studies, scientists found that injecting a peptide called FGF1 directly into the brain of diabetic mice could cause their diabetes to go into remission.
They later discovered that this effect was linked to the inhibition of AgRP neurons. This means that shutting down these neurons not only lowers blood sugar but might even reverse the disease, at least in mice.
Interestingly, while blocking AgRP neuron activity helped control diabetes, it did not seem to affect obesity. The diabetic mice in the study maintained their body weight even after their blood sugar normalized.
This suggests that these brain cells are more closely linked to blood sugar regulation than to weight control. For doctors and researchers, this is an important clue—it means that therapies aimed at these neurons could treat diabetes without necessarily affecting a person’s weight.
Dr. Schwartz pointed out that this could lead to a whole new way of thinking about diabetes treatment. Currently, many diabetes medications, including newer ones like Ozempic, are believed to work in part by affecting AgRP neurons, although the exact impact is not fully understood.
Schwartz believes that studying how these drugs interact with AgRP neurons could open up new possibilities for managing the disease.
He also highlighted the need for more research to answer some important questions: Why do these neurons become hyperactive in people with diabetes? How can their activity be regulated safely?
If these questions are answered, it might be possible to develop drugs that target AgRP neurons directly, potentially offering a new form of treatment for diabetes that focuses on the brain rather than just the body’s metabolism.
If this brain-based approach proves successful, it could mark a shift in how doctors understand and treat type 2 diabetes. Rather than focusing only on reducing weight or managing diet, doctors might begin to look at how the brain influences blood sugar levels. This could lead to more effective treatments and better outcomes for people living with the disease.
This study is still in its early stages, and much more work is needed before these findings can be applied to humans. However, the idea that diabetes might be controlled by targeting specific brain cells is a promising new direction. If scientists can find a way to safely regulate AgRP neuron activity in people, it could change how we think about and manage type 2 diabetes for good.
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The research findings can be found in Journal of Clinical Investigation.
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