Author/Authors :
Zamani Farhad نويسنده , Shidfar Farzad نويسنده School of Health, Tehran University of Medical Sciences, Tehran, IR Iran , Gholami Ali نويسنده , Hosseinzadeh Payam نويسنده Department of Nutrition & Biochemistry, School of Public Health, Tehran University of Medical Sciences, International campus , Amirkalali Bahareh نويسنده Gastrointestinal and Liver disease research Center
(GILDRC), Iran University of Medical Sciences, Tehran, IR
Iran , Sohrabi Masoud Reza نويسنده Gastrointestinal and Liver Disease Research Center
(GILDRC), Iran University of Medical Sciences, Tehran,
Iran
Abstract :
Background Studies on the association between visfatin and
nonalcoholic fatty liver disease (NAFLD) have contradictory results and
the role of this adipokine in NAFLD pathogenesis has remained unclear.
In vitro studies indicate that visfatin expression could be regulated by
sex hormones. Testosterone down-regulates visfatin expression in
pre-adipocytes and estrogen increases its expression in adipocytes.
Objectives This study aimed at exploring whether the association between
serum visfatin and markers of hepatic injury is the same for both
genders in patients with NAFLD. Methods In this cross-sectional study,
62 consecutive patients (32 males and 30 females) with NAFLD were
recruited. Fasting serum visfatin, caspase-cleaved cytokeratin 18
(cCK18), total soluble cytokeratin 18 (CK18), liver enzymes (AST and
ALT), insulin, and lipid-glucose profile was measured. Anthropometric
measurements, fibroscan and assessment of dietary intake and physical
activity level, were performed for each participant. Two independent
sample t tests, chi-square test, univariate, and multiple linear
regression (to adjust for confounding factors) were used to analyze the
data. Results In males, serum visfatin had a significant positive
association with serum Aspartate Aminotransferase (AST) (B = 0.47, P =
0.009), alanine aminotransferase (ALT) (B = 0.40, P = 0.035), CK18 (B =
0.50, P = 0.008), and cCK18 (B = 0.47, P = 0.012). In females, serum
visfatin only had a weak association with CK18 (B = 0.37, P = 0.045).
Instead, higher body mass index (BMI) was significantly associated with
increased serum CK18 (B = 0.44, P = 0.02), cCK18 (B = 0.42, P = 0.02),
controlled attenuation parameter (CAP) (B = 0.39, P = 0.049), and liver
stiffness measurement (LSM) (B = 0.40, P = 0.03) in females. Higher
waist to hip ratio was also significantly related to serum AST (B =
0.37, P = 0.04), ALT (B = 0.50, P = 0.02), CK18 (B = 0.41, P = 0.03),
cCK18 (B = 0.37, P = 0.04), and CAP (B = 0.39, P = 0.04) in this group.
In this study, females were significantly older (47.83 ± 81.10 vs 39.84
± 12.10, P = 0.008) and had higher BMI (32.31 ± 4.56 vs 29.42 ± 4.89, P
= 0.02) compared to males, thus the associations were adjusted for age,
BMI, and other confounders. Conclusions Interpretation of serum visfatin
level in relation to hepatic injury was probably gender-dependent in
NAFLD. While its increased serum level could be an indicator for more
hepatic injury in males, this was not the case in females. Body Mass
Index and waist to hip ratio were stronger predictors for hepatic injury
in females.