For years, type 2 diabetes has largely been framed around one key problem: insulin.
When the body becomes resistant to insulin, blood sugar rises, increasing the risk of long-term complications. But new research suggests another hormone may be playing a bigger early role than many people realize.
In a study published in Diabetes Care, researchers found that adults within the first year of a type 2 diabetes diagnosis had post-meal glucagon levels about 75% higher than people with normal blood sugar regulation. More notably, those elevated glucagon levels were closely tied to fat accumulation in the liver, also known as Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), rather than to insulin resistance alone.
The findings suggest that fatty liver may be more deeply involved in the earliest stages of type 2 diabetes than previously understood.
Glucagon is often overshadowed by insulin, but it plays a critical role in blood sugar balance. While insulin helps lower blood sugar, glucagon signals the liver to release stored glucose into the bloodstream. In healthy metabolism, those hormones work in balance. When that balance breaks down, blood sugar regulation may become increasingly unstable.
Researchers analyzed metabolic data from 50 adults with newly diagnosed type 2 diabetes and compared them with 50 adults with normal glucose metabolism. They found that higher glucagon levels after meals were strongly associated with liver fat content, supporting the possibility of “hepatic glucagon resistance,” a state in which the liver may become less responsive to glucagon, potentially prompting the body to release more of it.
In other words, fatty liver may not simply be a consequence of metabolic disease. It could also be actively shaping hormone dysfunction earlier in the process.
That distinction matters because MASLD, commonly called fatty liver disease, is increasingly common and often develops silently alongside obesity, insulin resistance and poor metabolic health.
The study does not prove fatty liver directly causes type 2 diabetes, nor does it show that lowering liver fat will automatically prevent it. But it adds to growing evidence that liver health may be a major early player in blood sugar dysfunction.
As newer therapies increasingly target multiple metabolic pathways, understanding the liver’s role could help reshape future approaches to diabetes and fatty liver disease alike.
This study was primarily funded by the German Diabetes Center, the German Center for Diabetes Research, the German Federal Ministry of Health, the German Federal Ministry of Education and Research, the German Research Foundation and nonprofit foundation support, including the Schmutzler Foundation. No obvious commercial industry funding was disclosed.