We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Therapeutic Effect of Prolyl Endopeptidase Inhibitor in High-fat Diet-induced Metabolic Dysfunction-associated Fatty Liver Disease
Summary
Studies in a high-fat diet mouse model of metabolic fatty liver disease found that increased prolyl endopeptidase activity during disease progression may drive the transition from simple steatosis to steatohepatitis, and that the PREP inhibitor KYP-2047 showed therapeutic potential.
These findings suggest that increased PREP activity/expression during MAFLD development might be a key factor in the transition from simple steatosis to steatohepatitis, and KYP-2047 might possess therapeutic potential for MAFLD treatment.
Sign in to start a discussion.
More Papers Like This
Adipose tissue as target of environmental toxicants: focus on mitochondrial dysfunction and oxidative inflammation in metabolic dysfunction-associated steatotic liver disease
This review examines how environmental toxicants, including micro and nanoplastics, target fat tissue and contribute to metabolic diseases like obesity, diabetes, and fatty liver disease. These pollutants disrupt mitochondria (the energy-producing parts of cells) and trigger a cycle of oxidative stress and inflammation that damages both fat tissue and the liver. The findings suggest that microplastic exposure could be one of several environmental factors contributing to the rising rates of metabolic disease worldwide.
Chronic Nanoplastic Exposure Promotes the Development and Progression of Metabolic Dysfunction‐Associated Steatotic Liver Disease
This study found that chronic exposure to nanoplastics promotes the development and worsening of metabolic dysfunction-associated steatotic liver disease (formerly known as fatty liver disease). Nanoplastics appear to increase vulnerability to liver disease progression. The finding is concerning because fatty liver disease is already widespread, and everyday nanoplastic exposure through food and water could be making it worse.
Disruption of hepatic metabolism in Lep KO mice.
Researchers found that polystyrene microplastics administered orally for nine weeks accumulated in liver tissue of leptin-knockout obese mice and induced histopathological liver alterations, including disruption of hepatic lipid, glucose, and amino acid metabolism.
Microplastics in metabolic dysfunction-associated steatotic liver disease: An emerging threat to liver health
This review examined emerging evidence linking microplastic exposure to the development and progression of metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD). The authors found that microplastics detected in liver tissue can exacerbate hepatic inflammation, lipid accumulation, and oxidative stress through multiple mechanisms, adding a novel environmental risk factor to MASLD pathogenesis.
Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice
Researchers found that polystyrene nanoplastics worsened liver damage in mice fed a high-fat diet by increasing oxidative stress, inflammation, and the infiltration of immune cells in liver tissue. The nanoplastic exposure accelerated the progression from fatty liver to hepatic fibrosis in the diet-induced model. The study suggests that nanoplastic exposure may compound the health risks associated with metabolic conditions affecting the liver.