Inflammation in the liver can play a key role in the development of fat accumulation in the arteries, cause blood clots as well as other cardiovascular conditions, researchers have found.
The study showed that the inflammatory processes in the liver can elevate cholesterol levels, which is associated with the increased risk of cardiovascular diseases. Elevated cholesterol is an important risk factor for atherosclerosis, which refers to build up of fat on the artery wall, circulatory disorders, which include diseased vessels, structural problems and blood clots, as well as other vascular complications.
Cardiovascular diseases, which play a key role among the long-term complications in people with diabetes, accounts for 75 % of all hospitalisation incidences, and are also responsible for 50 % of all deaths.
“Even if blood glucose levels are well controlled, some people with diabetes have a higher risk of long-term complications. We wanted to understand the underlying cause for this,” said Mauricio Berriel Diaz, Deputy Director at the Helmholtz Zentrum Munchen in Germany. For the study, published in the journal Cell Reports, the team focused on inflammatory processes that are known to occur in many metabolic disorders such as Type 2 diabetes and obesity and contribute significantly to long-term complications.
The scientists demonstrated that reactive oxygen species (ROS) in the liver inactivates the transcription factor complex GAbp (GA-binding protein). In experimental models, this loss in turn inhibited the protein AMPK - an energy sensor of the cell. As a result, excess cholesterol was produced, and typical atherosclerosis symptoms developed. “GAbp appears to be a molecular regulator at the interface between inflammation, cholesterol homeostasis and atherosclerosis. Without its protective effect, this leads to hypercholesterolemia and increased lipid deposition in the arteries,” said Katharina Niopek, researcher at the varsity.
{{/usCountry}}The scientists demonstrated that reactive oxygen species (ROS) in the liver inactivates the transcription factor complex GAbp (GA-binding protein). In experimental models, this loss in turn inhibited the protein AMPK - an energy sensor of the cell. As a result, excess cholesterol was produced, and typical atherosclerosis symptoms developed. “GAbp appears to be a molecular regulator at the interface between inflammation, cholesterol homeostasis and atherosclerosis. Without its protective effect, this leads to hypercholesterolemia and increased lipid deposition in the arteries,” said Katharina Niopek, researcher at the varsity.
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