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Mechanism of the development of nonalcoholic steatohepatitis after pancreaticoduodenectomy
How nonalcoholic fatty liver inflammation develops after pancreas and duodenum surgery
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Abstract
The livers of post-pancreaticoduodenectomy (PD) NASH patients showed significant up-regulation of multiple genes associated with fat metabolism and inflammation.
- Gene expression related to fatty acid and triglyceride metabolism was markedly altered in post-PD NASH patients compared to healthy individuals and conventional NASH patients.
- Increased levels of genes encoding proteins involved in lipid uptake and storage were observed, indicating enhanced fat accumulation in liver cells.
- Despite lower serum levels of apolipoprotein B and triglycerides, there was a notable increase in mRNA levels related to their synthesis, suggesting impaired fat export from the liver.
- Elevated expression of immune response and oxidative stress-related genes points to significant activation of the body's immune response in post-PD NASH livers.
- These findings suggest that mechanisms like increased fat uptake, altered fat production, and disrupted fat export may contribute to NASH development after PD.
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