Abstract
Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease characterized by excessive lipid deposition. Lipid metabolism disturbances are possibly associated with hepatocyte inflammation development and oxidative balance impairment. The aim of our experiment was to examine the first moment when changes in plasma and liver arachidonic acid (AA) levels as a pro-inflammatory precursor may occur during high-fat diet (HFD)-induced NAFLD development. Wistar rats were fed a diet rich in fat for five weeks, and after each week, inflammation and redox balance parameters were evaluated in the liver. The AA contents in lipid fractions were assessed by gas–liquid chromatography (GLC). Protein expression relevant to inflammatory and lipogenesis pathways was determined by immunoblotting. The oxidative system indicators were determined with assay kits. Our results revealed that a high-fat diet promoted an increase in AA levels, especially in the phospholipid (PL) fraction. Importantly, rapid inflammation development via increased inflammatory enzyme expression, elevated lipid peroxidation product content and oxidative system impairment was caused by the HFD as early as the first week of the experiment. Based on these results, we may postulate that changes in AA content may be an early indicator of inflammation and irreversible changes in NAFLD progression.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases in Western societies [1,2]
We observed significantly increased arachidonic acid content in the DAG fraction at Ineatchhewlieveekr,inwteheobhsigehrv-featdfseiegdninifig cgarnotulpy (ifnircsrtewaseeedk:a+r1a0c7h.2i%do; nseiccoancdidwceoenk:te+n94t .i9n%t;htehiDrdAwGeefkr:action at each+7w7.5e%ek; foinurtthhewheiegkh: +-5fa9t.8f%ee; fdifitnhgwgereok:u+p12(3fi.8r%st;wp
In our previous study on a 5-week animal model, an increase in the total DAG, TAG and free fatty acids (FFAs) concentrations occurred that correlated with the observed changes in the liver histology. These results suggested a relationship between an excessive accumulation in the cytoplasm of hepatocytes, mainly as triacylglycerols, and the development of NAFLD [13]
Summary
Non-alcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases in Western societies [1,2]. It is estimated that nearly 25% of the global population might be suffering from NAFLD [1,3,4] This condition is characterized by histological changes resulting from excessive lipid deposition in more than 5% of the liver cell volume without the inordinate consumption of alcohol [1,5,6]. In the sera of obese patients with coexisting fatty liver, there are significant changes in the levels of adiponectin, leptin and resistin. These molecules, together with pro-inflammatory cytokines, released from the adipose tissue can be involved in hepatic steatosis development [8]
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