For many years, scientists studying type 2 diabetes have mainly focused on one hormone: insulin. Insulin is produced by the pancreas and helps move sugar from the blood into the body’s cells, where it can be used for energy.
In people with type 2 diabetes, the body slowly becomes less sensitive to insulin, a condition known as insulin resistance. As a result, sugar builds up in the bloodstream over time, leading to high blood glucose levels.
But now, researchers from the German Diabetes Center have discovered that another hormone may play a much bigger role in type 2 diabetes than previously thought.
Their new study suggests that glucagon, a hormone that works in the opposite way to insulin, becomes abnormally high very early in the disease process. The findings were published in the medical journal Diabetes Care.
The discovery may help scientists better understand why type 2 diabetes develops and why it is so closely connected to fatty liver disease. It may also open the door to future treatments that target not only insulin but also glucagon and liver health.
Glucagon is a hormone produced by the pancreas, just like insulin. However, the two hormones have opposite jobs. While insulin lowers blood sugar by helping cells absorb glucose, glucagon raises blood sugar by telling the liver to release stored glucose into the bloodstream.
In healthy people, insulin and glucagon work together in a carefully balanced system. After a meal, insulin levels rise to lower blood sugar, while glucagon levels usually fall. Between meals, glucagon helps maintain stable blood sugar levels by signaling the liver to release glucose when needed.
Scientists have known for years that many people with type 2 diabetes have unusually high glucagon levels. However, it was not fully clear when this problem begins or what exactly causes it.
To investigate, the researchers studied 50 adults who had recently been diagnosed with type 2 diabetes and compared them with 50 adults who had normal blood sugar control. The participants were part of the German Diabetes Study, which is the largest ongoing study of newly diagnosed diabetes in adults in Europe.
The researchers examined blood samples and several metabolic measurements to better understand how glucagon behaves early in diabetes.
The results were striking.
Within the first year after diagnosis, people with type 2 diabetes had glucagon levels after meals that were about 75% higher than those of people without diabetes.
Surprisingly, these high glucagon levels were strongly linked to fat buildup in the liver, also known as metabolic dysfunction-associated steatotic liver disease, or MASLD. This condition was previously called fatty liver disease.
Fatty liver disease happens when too much fat collects inside liver cells. It has become extremely common around the world, especially in people who are overweight, obese, or living with type 2 diabetes.
In many cases, people may not even realize they have it because symptoms are often mild or absent during the early stages.
The liver plays a central role in metabolism. It helps control blood sugar, stores nutrients, removes toxins, and processes fats. When excess fat builds up inside the liver, these functions may become disrupted.
The researchers found that the increased glucagon levels were closely connected to liver fat rather than to insulin resistance itself. This finding challenges the traditional idea that insulin resistance alone explains most of the metabolic problems in type 2 diabetes.
Professor Michael Roden, Scientific Director of the German Diabetes Center, explained that type 2 diabetes should no longer be viewed only as a problem involving insulin. According to the researchers, the liver and glucagon regulation appear to be extremely important parts of the disease as well.
The findings also support an idea called hepatic glucagon resistance. This means the liver may become less sensitive to glucagon. As a result, the body may release even more glucagon in an attempt to force the liver to respond.
This process may create a harmful cycle. The liver becomes less responsive, glucagon levels rise further, and blood sugar regulation becomes increasingly disturbed.
The discovery is especially important because several new diabetes drugs currently being tested in clinical trials are designed to target the glucagon system. Some of these treatments aim not only to improve blood sugar control but also to treat fatty liver disease itself.
The researchers believe their findings suggest that treating fatty liver disease early could potentially lower the risk of developing type 2 diabetes later on.
Lead author Maximilian Huttasch explained that early screening for fatty liver disease may become increasingly important, especially for people at high risk of diabetes. Detecting liver fat early could allow doctors to recommend lifestyle changes or treatments before severe metabolic problems develop.
The study also highlights how closely connected different organs are in controlling metabolism. Type 2 diabetes is not simply a disease of blood sugar or the pancreas alone. The liver, hormones, fat storage, and the body’s overall metabolic system all appear to interact in complex ways.
Even though the findings are promising, the researchers say more studies are still needed. Scientists must better understand exactly how glucagon resistance develops in the liver and whether it can safely be targeted with medications.
Still, the research represents an important step forward in understanding type 2 diabetes. It suggests that future treatments may focus not only on insulin but also on restoring the balance between glucagon, the liver, and blood sugar regulation.
As rates of diabetes and fatty liver disease continue rising around the world, discoveries like this may help scientists develop more effective ways to prevent and treat these common metabolic disorders.
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Source: German Diabetes Center.
