For decades, scientists studying type 2 diabetes have focused mainly on insulin. Insulin is the hormone that helps move sugar out of the blood and into the body’s cells so it can be used for energy.
When the body stops responding properly to insulin, blood sugar levels slowly rise, leading to type 2 diabetes.
But a new study from the German Diabetes Center suggests that insulin may only be part of the story. Researchers have discovered that another hormone, called glucagon, becomes unusually high very early in type 2 diabetes.
The findings may change how scientists understand the disease and could lead to new treatments in the future.
The study was published in the journal Diabetes Care.
Glucagon is produced by the pancreas, just like insulin, but it has the opposite job. While insulin lowers blood sugar, glucagon raises it. It does this by signaling the liver to release stored sugar into the bloodstream when the body needs energy.
In healthy people, insulin and glucagon work together in balance. After eating, insulin rises and glucagon falls so that blood sugar stays stable. But when this balance is disturbed, blood sugar control becomes more difficult.
Scientists have known for many years that glucagon levels are often high in people with type 2 diabetes. However, researchers did not fully understand when this problem begins or why it happens.
To explore this question, scientists at the German Diabetes Center studied 50 adults who had recently been diagnosed with type 2 diabetes and compared them with 50 adults who had normal blood sugar levels. The researchers analyzed blood samples and several metabolic measurements to better understand the role of glucagon early in the disease.
The participants came from the German Diabetes Study, which is the largest long-term study of newly diagnosed diabetes patients in Europe.
The researchers found that people with type 2 diabetes had glucagon levels after meals that were around 75% higher than those of people without diabetes. Surprisingly, the increase was strongly linked to fatty liver disease rather than insulin resistance itself.
Fatty liver disease, now often called metabolic dysfunction-associated steatotic liver disease or MASLD, happens when fat builds up inside liver cells. It has become extremely common around the world, especially in people who are overweight or have diabetes.
The liver plays a major role in controlling blood sugar and metabolism. It stores nutrients, processes fats, and helps regulate the body’s energy supply. When fat builds up inside the liver, these important functions may stop working normally.
The scientists believe the liver may become less sensitive to glucagon, a problem known as hepatic glucagon resistance. Because the liver does not respond properly, the body may produce even more glucagon in an attempt to force the liver to release glucose.
This may create a harmful cycle where glucagon levels continue rising while blood sugar control worsens.
Professor Michael Roden, Scientific Director of the German Diabetes Center, said the findings show that type 2 diabetes should not only be viewed as a disease involving insulin. According to the researchers, the liver and glucagon system also play very important roles.
The discovery may have major importance for future treatments. Several newer drugs currently being tested in clinical trials are designed to affect the glucagon system. Some of these medicines may help improve blood sugar levels while also reducing fatty liver disease.
The findings also highlight the importance of liver health. Many people with fatty liver disease may not realize they are at higher risk of developing type 2 diabetes later on.
Lead researcher Maximilian Huttasch explained that early screening for fatty liver disease could help doctors identify high-risk patients sooner. If liver fat is detected early, lifestyle changes such as weight loss, healthier eating, and exercise may help reduce the risk of diabetes.
The study also reminds scientists that metabolism is extremely complex. Type 2 diabetes does not involve only one hormone or one organ. Instead, the pancreas, liver, fat tissue, hormones, and blood sugar systems all interact with each other.
Even though the findings are exciting, more research is still needed. Scientists must better understand how glucagon resistance develops in the liver and whether new treatments can safely target this process.
Still, the research represents an important step forward in diabetes science. It suggests that future therapies may focus not only on insulin but also on restoring healthy communication between the liver and glucagon.
Overall, the study provides a new way of thinking about type 2 diabetes and highlights how closely liver disease and blood sugar problems are connected.
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Source: German Diabetes Center.
