Nonalcoholic steatohepatitis is a liver disease, causing fat to build up in the liver. The resulting inflammation may lead to liver cancer or cirrhosis (scarring) and possible liver failure. As reported in Archyde, currently the only available treatment consists of drugs to reduce the accumulation of fat or suppress inflammation.
A Protein to Treat Steatohepatitis
To date, an effective treatment has not been developed due to multiple symptoms and causes of the disease. Therefore, the patient’s response to treatment is also diverse.
A Korean medical team from Yonsei University joined SL Metagen Technologies to conduct an experiment using mouse models, with the goal of developing a protein to treat steatohepatitis.
Steatohepatitis differs from nonalcoholic fatty liver disease (NAFLD) which is characterized by a buildup of fat but without liver damage. Patients with nonalcoholic steatohepatitis (NASH) not only have a buildup of fat in the liver but also damage to the liver.
The first step in the experiment involved the linking of GLP-1 and GLP-2 hormones. These hormones are used to treat steatohepatitis symptoms.
GLP-1 lowers glucose by regulating insulin. It treats obesity and diabetes.
GLP-2 helps nutrient absorption by creating a gut environment.
The team treated nonalcoholic steatohepatitis-induced mouse models with the GLP 1, GLP 2, and the newly created dual GLP-1/2 experimental group over a four-week period.
The researchers created two targets:
Comparing GLP-1/2 Against GLP-1 and GLP-2, triglycerides and fibrosis (scarring) were lowest (22 and 46 percent respectively) in mice treated with GLP-1/2.
- Liver fibrosis improved 30 and 40 percent respectively
- Triglyceride and fibrosis levels were approximately 45 percent lower compared to mice that did not receive GLP-1/2.
The researchers also analyzed mouse feces to confirm the therapeutic effect of intestinal microbes on steatohepatitis. The researchers found a decrease in fibrosis and liver inflammation as well as a reduction in lipopolysaccharide leading to sepsis.
When comparing the GLP-1/2 group against GLP-1 plus GLP-2, lipopolysaccharide was reduced by 48 percent and 32 percent respectively. In addition, the gene that causes liver fibrosis also decreased 62 percent and 57 percent respectively.
Looking Forward
The success of the Korean team’s experiment will accelerate efforts to develop a treatment for nonalcoholic steatohepatitis.
