Mediation of inflammation, obesity and fatty liver disease by advanced glycation endoproducts.

Abstract:

OBJECTIVE:Fatty liver may induce various complications including chronic hepatitis or liver cirrhosis, and is frequently occurred in obesity individuals. Advanced glycosylation end products (AGEs) were known to play a critical role in multiple liver diseases. This study, therefore, aimed to study the effect of AGEs on obesity, related liver cirrhosis and inflammation, on an obesity fatty liver rat model. MATERIALS AND METHODS:A total of 60 Sprague Dawley (SD) rats were randomly divided into control, model and AGEs inhibitor groups (n=20 each). AGEs level, body weight and liver function were examined in each animal, followed by hematoxylin-eosin (HE) staining to detect the pathological change of liver. Further Real-time PCR and enzyme-linked immunosorbent assay (ELISA) were employed to detect inflammatory cytokine levels including tumor necrosis factor (TNF)-α and interleukin (IL)-6. RESULTS:AGEs level was significantly elevated in obesity fatty liver model rats, which also had higher total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL-C) and high-density lipoprotein (HDL-C) levels, along with deteriorated liver function and higher TNF-α and IL-6 levels. The application of AGEs inhibitor aminoguanidine significantly improved liver functions and lower TNF-α or IL-6 levels when compared to the model group (p<0.05 in all cases). CONCLUSIONS:Obesity fatty liver can promote AGEs level, further causing pathological changes and increased secretion of inflammatory cytokines. The inhibition of AGEs can improve the metabolism of fatty acids, decrease inflammatory cytokines and benefit the treatment of obesity fatty liver.

authors

Xiong DD,Zhang M,Li N,Gai JF,Mao L,Li M

doi

10.26355/eurrev_201711_13835

subject

Has Abstract

pub_date

2017-11-01 00:00:00

pages

5172-5178

issue

22

eissn

1128-3602

issn

2284-0729

journal_volume

21

pub_type

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