Macrophage-mediated Inflammation in White Adipose Tissue and Non-alcoholic Fatty Liver Disease.

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NAFLD is a huge health burden and can lead to liver damage,scarring and cancer, therefore gaining a further understanding of the mechanisms involved in causing liver damage is particularly important to identify drug targets that could reverse this process. White adipose tissue (WAT) or fat fails to ...

NAFLD is a huge health burden and can lead to liver damage,scarring and cancer, therefore gaining a further understanding of the mechanisms involved in causing liver damage is particularly important to identify drug targets that could reverse this process. White adipose tissue (WAT) or fat fails to respond normally in obesity which leads to fat deposition in other organs, particularly the liver, and the fat tissue becomes inflamed. The inflammation in the fat is lead by specific immune cells called macrophages. This inflammatory state in the fat tissue is thought to be a precursor to liver inflammation and liver damage. This has been demonstrated in mouse models where the fat inflammatory cells contributed to liver inflammation and worsened liver damage, emphasising the importance of the relationship between fat tissue and the liver in NAFLD. Liver damage or liver fibrosis is also the result of activation of these inflammatory cells, the macrophages, in the liver which drive scarring through cells called fibroblasts that lay down collagen. Therefore, understanding the interaction between the cells involved in inflammation (macrophages) and scarring (fibroblasts) in both the fat and the liver is key to identifying potential drug targets for reversal of this process. Our lab demonstrated, using an obese animal model, that the release of pro-fibrotic compounds called prostagladins from the fat macrophages is linked to NAFLD and liver inflammation. Based on these results the investigators aim to deepen the understanding of the link between fat and liver inflammation and damage specifically looking at cell interactions (the macrophage and fibroblast) by using genetic tests on liver and fat samples in obese patients.

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