Mayo Clinic Researchers Pinpoint Cause of Fatty Liver Disease from Excessive Alcohol Consumption

Mayo Clinic researchers have identified a key enzyme called valosin-containing protein (VCP) that plays a crucial role in recycling damaged proteins in the liver. When exposed to excessive alcohol, VCP becomes nearly completely removed from the lipid droplet surface, allowing a specific protein called HSD17b13 to accumulate, leading to fatty liver disease. This condition affects more than one in three people in the U.S. and can lead to type 2 diabetes and liver cancer. The researchers' findings suggest that HSD17b13 is a potential target for new therapies to prevent or treat fatty liver disease.

Key Takeaways:

  • Excessive alcohol consumption contributes to fatty liver disease by altering the valosin-containing protein (VCP) that recycles damaged proteins in the liver.
  • VCP is responsible for removing a specific protein called HSD17b13 from the surface of lipid droplets, preventing them from over-accumulating in liver cells and contributing to fatty liver disease.
  • When exposed to excessive alcohol, VCP is nearly completely removed from the lipid droplet surface, allowing HSD17b13 to accumulate and leading to fatty liver disease.
  • Fatty liver disease, also known as Metabolic Dysfunction Associated Steatotic Liver Disease (MAFLD), affects more than one in three people in the U.S.
  • The condition can lead to type 2 diabetes and liver cancer if left untreated.
  • The researchers' findings suggest that HSD17b13 is a potential target for new therapies to prevent or treat fatty liver disease.
  • The study is part of a larger effort at Mayo Clinic called the Precure initiative, which aims to develop tools that empower clinicians to predict and intercept biological processes before they evolve into disease or progress into complex, hard-to-treat conditions.

Statistics:

  • More than one in three people in the U.S. are affected by fatty liver disease (MAFLD).
  • Fatty liver disease can lead to type 2 diabetes and liver cancer if left untreated.
  • The study found that exposure to excessive alcohol removes VCP almost completely from the lipid droplet surface, allowing HSD17b13 to accumulate.
  • The researchers witnessed and captured the elaborate recycling mechanism of VCP working with a chaperone protein to deliver damaged proteins to a lysosome, which then breaks apart the unwanted proteins.

Sources:

  • Journal of Cell Biology.
  • Mayo Clinic.
  • NewsRx LLC.
  • VerticalNews Health & Science.