Macrophage migration inhibitory factor expression and MIF gene −173 G/C polymorphism in nonalcoholic fatty liver disease
Adult
Male
Genotype
Biopsy
Polymerase Chain Reaction
Severity of Illness Index
03 medical and health sciences
Gene Frequency
Nonalcoholic fatty liver disease
Humans
Macrophage Migration-Inhibitory Factors
Macrophage migration inhibitory factor
0303 health sciences
Polymorphism, Genetic
Gene polymorphism
Middle Aged
Immunohistochemistry
Up-Regulation
3. Good health
Fatty Liver
Intramolecular Oxidoreductases
Phenotype
Liver
Case-Control Studies
Female
DOI:
10.1097/meg.0b013e328331a596
Publication Date:
2010-01-08T08:46:01Z
AUTHORS (12)
ABSTRACT
To investigate the macrophage migration inhibitory factor (MIF) expression and -173 G/C polymorphism of the MIF gene in nonalcoholic fatty liver disease (NAFLD).Ninety-one patients with diagnosis of NAFLD and 104 healthy controls were included in the study. MIF -173 G/C polymorphism was detected using the PCR-restriction fragment length polymorphism based method. NAFLD was stratified as nonalcoholic steatohepatitis (NASH), probable NASH and steatosis, respectively in groups 1, 2 and 3, according to NAFLD Activity Score. MIF expression was detected by immunohistochemistry staining.Mean age of the patients was 50.1+/-9.6 years, and 54 of them were male. Serum alanine aminotransferase and aspartate aminotransferase were 50/83, 42/63 and 31/32, respectively in groups 1, 2 and 3, (P<0.05). Both the MIF expression of hepatocytes and mononuclear cells were more prominent in groups 1 and 2 than group 3. There was no correlation between MIF expression of hepatocytes and fibrosis stage. However, MIF expression of mononuclear cells significantly increased according to fibrosis stage (P<0.05, R : 0.2). There was no significant correlation between MIF genotype and MIF expression in the liver.MIF expression is significantly increased especially by mononuclear cells in liver tissue of patients with NASH secondary to inflammation. Thus, it should be considered as a consequence not a causal factor.
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CITATIONS (20)
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