Role of Some Adipokines in Nonalcoholic Fatty Liver Diseases

Document Type : Original Article

Authors

1 Department of Medical Biochemistry, Faculty of Medicine, Tanta University, Egypt

2 Department of Tropical Medicine , Faculty of Medicine, Tanta University, Egypt

Abstract

Background: The prevalence of non-alcoholic fatty liver disease (NAFLD) is
increasing dramatically. It is unclear why some patients develop steatohepatitis,
fibrosis and cirrhosis from steatosis, while others do not. A role for adipokines has
been claimed. Aim of the Study: Evaluation of serum levels of leptin, soluble leptin
receptor (sOB-R), TNF-, adiponectin and insulin resistance (IR) in cases of NAFLD,
and to clarify their potential role in disease progression. Subjects and Methods: The
study included 60 individuals, who were divided into three equal groups; group I:
Normal healthy volunteers (control subjects) with BMI (Kg/m2) of 25.2 ±2.6; group
II: Obese individuals with fatty infiltration of the liver and having normal liver
functions and BMI of 31.8±1.1. Group III: Obese individuals with elevated liver
functions and BMI of 32.7 ± 1.4. All groups were subjected to estimation of liver
function tests, lipid profile, fasting blood glucose level, HBsAg, HCVAb and
evaluation of body mass index (BMI). Serum levels of insulin, leptin, soluble leptin
receptor (sOB-R), TNF -, and adiponectin were measured in all groups using ELISA
technique. IR was estimated by homeostasis model assessment index ratio (HOMAIR).
Results: Serum triglycerides, insulin and HOMA-IR were significantly increased
in the patients’ groups, when compared to the control group. Serum levels of ALT,
AST, leptin and TNF- were significantly increased, while sOB-R and serum
adiponectin levels were significantly decreased in group III compared to groups I and
II. Serum leptin and TNF- levels were positively correlated with BMI and HOMA-IR
in groups II & III and with serum ALT and AST enzyme activity in group III, while,
sOB-R levels were negatively correlated with serum leptin, TNF-, BMI and HOMAIR
in both patients’ groups and with ALT and AST enzyme activity in group III. On
the contrary, serum adiponectin levels were negatively correlated with BMI and
HOMA-IR, serum leptin and TNF- levels in groups II & III and with both ALT and
AST enzyme activity in group III. Conclusion: Measurement of serum TNF-, serum
leptin and/or adiponectin may be helpful biochemical markers of NAFLD,
particularly when serum AST and ALT are within normal limits.

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