Abstract
Non-alcoholic fatty liver (NAFLD) is a progressive liver disease that varies from fat accumulation to severe liver damage. The development of liver inflammation is an important step in the course of NAFLD, because it causes liver damage and increases the risk of arteriosclerosis. In this thesis, the two possible causes of liver inflammation and arteriosclerosis were analyzed: fatty tissue macrophages and saccharified proteins (AGEs) via their receptor, RAGE.
The conclusions of this thesis are:
-Fat tissue macrophages increase the number of immune cells in the blood by releasing inflammatory factors.
- Fatty tissue macrophages influence the degree of liver inflammation, but not atherosclerosis in the model used.
- Fatty liver and liver inflammation, yet also absorption from food contribute to AGE accumulation in the liver.
-AGEs can cause liver inflammation, but RAGE does not seem to play a role in liver inflammation or arteriosclerosis.
The conclusions of this thesis are:
-Fat tissue macrophages increase the number of immune cells in the blood by releasing inflammatory factors.
- Fatty tissue macrophages influence the degree of liver inflammation, but not atherosclerosis in the model used.
- Fatty liver and liver inflammation, yet also absorption from food contribute to AGE accumulation in the liver.
-AGEs can cause liver inflammation, but RAGE does not seem to play a role in liver inflammation or arteriosclerosis.
Original language | English |
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Award date | 22 Feb 2019 |
Place of Publication | Maastricht |
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Print ISBNs | 9789463234894 |
DOIs | |
Publication status | Published - 2019 |