Treatment could prevent more severe liver damage such as cirrhosis from developing.
Researchers in Germany have discovered a new therapy to treat non-alcoholic fatty liver disease.
There are currently no treatment options available for non-alcoholic fatty liver disease, which is common among people with type 2 diabetes, and can go on to develop more severe liver damage such as cirrhosis and hepatocellular carcinoma.
The results of a study recently published in Nature Metabolism, researchers from the Institute for Diabetes and Cancer at Helmholtz Zentrum München, in Munich, reported they had discovered a potential novel therapeutic target for treating non-alcoholic fatty liver disease.
The treatment, called Rab24, is a small Rab GTPase, which was found to be a novel regulator of mitochondrial (double-membrane-bound organelle) activity and plasticity.
The group of researchers showed that it is highly unregulated in the liver of obese patients with non-alcoholic fatty liver disease.
In follow-up tests they were able to demonstrate that by reducing Rab24 liver steatosis and glucose tolerance are strongly improved in models of diet induced obesity. This indicated a general improvement of liver and systemic health.
In conclusion they said Rab24 is therefore a potential novel therapeutic target for treating non-alcoholic fatty liver disease.
Liver mitochondria under the microscope © Anja Zeigerer, Institute for Diabetes and Cancer (IDC), Helmholtz Zentrum München
Anja Zeigerer, diabetes researcher who lead the research team, said: “The incidence of type 2 diabetes and its comorbidities, such as non-alcoholic fatty liver disease, is increasing tremendously.
“Non-alcoholic fatty liver disease is affecting 1.8 billion people worldwide, with no approved treatment options on the market. Thus, finding novel intracellular targets such as Rab24 for possible therapeutic options is very much needed.”
The researchers found that Rab24 interferes with the machinery that is responsible for mitochondrial fission (cells dividing) and that by decreasing Rab24, mitochondria are more connected and therefore more functional. Importantly, they saw that Rab24 was highly upregulated in the liver of obese patients with non-alcoholic fatty liver disease.
Susanne Seitz, lead study author, said: “In a next step, we want to explore Rab24 as a potential therapeutic target for non-alcoholic fatty liver disease in more detail. We will investigate inhibitors of Rab24’s effect on mitochondrial fission and test whether such inhibitors could mimic the observed improvements of this study.”