Influence of Ala54Thr polymorphism of fatty acid-binding protein 2 on histological alterations and insulin resistance of non alcoholic fatty liver disease.
A transition G to A at codon 54 of fatty acid binding protein type 2 (FABP2) produces an amino acid substitution (Ala 54 to Thr 54). This amino acid substitution was associated with modifications of insulin resistance, adipokines and insulin concentrations. The aim of this study was to evaluate the influence of Ala54Thr polymorphism in the FABP2 gene on the histological alterations of non-alcoholic fatty liver disease (NAFLD) and insulin resistance. Thirty subjects with the presence of biopsy-proven NAFLD were enrolled for this study. Glucose, Insulin, Insulin resistance (HOMA), total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, resistin, leptin, adiponectin, interleukin-6 and TNF-alfa serum levels were measured at basal time. A tetrapolar bioimpedance, BMI, waist circumference, waist to hip ratio, blood pressure and a prospective serial assessment of nutritional intake with 3 days written food records were examined. Genotype of Ala54Thr FABP2 gene polymorphism was studied. The mean age was 41.6 +/- 11 years and the mean BMI 29.2 +/- 6.6 with 24 males (80%) and 6 females (20%). Fifteen patients (50%) had the genotype Ala54/Ala54 (wild type group) and 15 (50%) patients Ala54/Thr54 (13 patients) or Thr54/Thr54 (2 patients) (mutant type group). Both genotype groups have the similar anthropometric parameters. Serum aspartate aminotransferase and alcaline phosfatase were higher in wild type group than mutant type group, with an unclear explanation. Dietary intake was similar in both groups. A non-statistical significant low levels of adiponectin in mutant group was observed. No differences were detected among other adipokines. There were no differences between genotypes in histological results of inflammation (portal or lobular inflammation) or grade of steatosis or fibrosis. In conclusion, the present study demonstrates that the polymorphism Ala54Thr of FABP in patients with NAFLD doesn't predict liver histological changes, nor both insulin resistance and serum adipokines variations.
Aller
R
R
Institute of Endocrinology and Nutrition, Medicine School and Unit of Investigation, Hospital Rio Hortega, Valladolid, Spain.
De Luis
D A
DA
Fernandez
L
L
Calle
F
F
Velayos
B
B
Izaola
O
O
Gonzalez Sagrado
M
M
Conde
R
R
Gonzalez
J M
JM
D054392:Adipokines / Q000097:blood / Q000235:genetics*; D000328:Adult; D000469:Alkaline Phosphatase / Q000097:blood / Q000235:genetics; D019943:Amino Acid Substitution / Q000235:genetics; D000886:Anthropometry; D001219:Aspartate Aminotransferases / Q000097:blood / Q000235:genetics; D050556:Fatty Acid-Binding Proteins / Q000235:genetics*; D005234:Fatty Liver / Q000235:genetics* / Q000503:physiopathology; D005260:Female; D005838:Genotype; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic
D054392:Adipokines; C493404:FABP2 protein, human; D050556:Fatty Acid-Binding Proteins; D001219:Aspartate Aminotransferases; D000469:Alkaline Phosphatase