BBA clinicalDec 18, 2015

How nonalcoholic fatty liver inflammation develops after pancreas and duodenum surgery

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Apr 4, 2026

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.

Simplified

BACKGROUND AND AIM: It is recognized that nonalcoholic fatty liver disease (NAFLD), including nonalcoholic steatohepatitis (NASH), may develop after pancreaticoduodenectomy (PD). However, the mechanism of NASH development remains unclear. This study aimed to examine the changes in gene expression associated with NASH occurrence following PD.

METHODS: The expression of genes related to fatty acid/triglyceride (FA/TG) metabolism and inflammatory signaling was examined using liver samples obtained from 7 post-PD NASH patients and compared with 6 healthy individuals and 32 conventional NASH patients.

RESULTS: The livers of post-PD NASH patients demonstrated significant up-regulation of the genes encoding CD36, FA-binding proteins 1 and 4, acetyl-coenzyme A carboxylase α, diacylglycerol acyltransferase 2, and peroxisome proliferator-activated receptor (PPAR) γ compared with normal and conventional NASH livers. Although serum apolipoprotein B (ApoB) and TG were decreased in post-PD NASH patients, the mRNAs of ApoB and microsomal TG transfer protein were robustly increased, indicating impaired TG export from the liver as very-low-density lipoprotein (VLDL). Additionally, elevated mRNA levels of myeloid differentiation primary response 88 and superoxide dismutases in post-PD NASH livers suggested significant activation of innate immune response and augmentation of oxidative stress generation.

CONCLUSIONS: Enhanced FA uptake into hepatocytes and lipogenesis, up-regulation of PPARγ, and disruption of VLDL excretion into the circulation are possible mechanisms of steatogenesis after PD.

GENERAL SIGNIFICANCE: These results provide a basis for understanding the pathogenesis of NAFLD/NASH following PD.

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How nonalcoholic fatty liver inflammation develops after pancreas and duodenum surgery

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