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Adiponectin: A Differential Marker Between Steatosis and Steatohepatitis.
Abstract
Background: Nonalcoholic fatty liver disease (NAFLD) becoming a world - wide public health problem.It represents a spectrum of disease ranging from simple steatosis to steatohepatitis (NASH). Adipocytokines refer to adipocyte-derived biologically active molecules TNF-α, leptin and adiponectin, all been implicated in development of hepatic inflammation and fibrosis in NAFLD patients. This new hormone differ from its predecssors in important feature, production and concentration acutully decrease in obesity, and all adipose-derived hormone are increased. It is possible that adiponectin expression is activated during adipogenesis, a feed back inhibition on its production may occur during the development of obesity. Adiponectin may exert a hepatic protective effect.
Objective: Was to evaluate adiponectin level as a differential marker between steatosis and Steatohepatitis.
Methods: Twenty NAFLD patients, twenty biopsy proved NASH and twenty control subjects, matched for age,sex and BMI.All the subjects were subjected to an abdominal ultrasonography, routine biochemical evaluation: liver function ALT& AST, lipid profile (cholesterol, triglycerides, HDL-C), CRP& Adipocytokines (TNF-α, IL-6, LEPTIN, & Adiponectin).
Results: Plasma adiponectin levels were significantly lower in NAFLD patients than control gp (6.15± 1.39ng/ml vs12.03±3.46ng/ml). Adiponctin was significantly lower in NASH than NAFLD (1.80 0±0.96 ng/ml vs 6.15±1.39 ng/ml). leptin level was significantly higher in NAFLD than NASHgp (69.50±18.70ng/ml vs 43.20±6.93ng/ml). adiponectin ROC curve showed an AUROC curve in NAFLD gp (o.945 p=0.049) while inNASH was(0.995 p=0.007).TNF-α & IL-6 was significantly higher in NASH than NAFLD gp (79.25±13.89 pg/ml vs41.25±17.53 pg/ml)and (110.20±55.34 pg/ml vs 43.85±16.13). Plasma adiponectin level in NAFLD gp was inversely correlated with T.G (r=-0.368 p=0.111). GOT (r=-0.037 p=0.878) & GPT (r=-0.022 p=0.926) while it was +ve correlated in NASH gp with Cholesterol (r=0.317 p=0.174) & T.G (r=0.042 p=0.861).
Conclusion: This data support a role for low circulating adiponectin in the pathogenisis of NAFLD and hypoadiponectinemia found to be a feature of NASH. ADIPONECTIN found to be a non –invasive differential marker between NAFLD & NASH.
Objective: Was to evaluate adiponectin level as a differential marker between steatosis and Steatohepatitis.
Methods: Twenty NAFLD patients, twenty biopsy proved NASH and twenty control subjects, matched for age,sex and BMI.All the subjects were subjected to an abdominal ultrasonography, routine biochemical evaluation: liver function ALT& AST, lipid profile (cholesterol, triglycerides, HDL-C), CRP& Adipocytokines (TNF-α, IL-6, LEPTIN, & Adiponectin).
Results: Plasma adiponectin levels were significantly lower in NAFLD patients than control gp (6.15± 1.39ng/ml vs12.03±3.46ng/ml). Adiponctin was significantly lower in NASH than NAFLD (1.80 0±0.96 ng/ml vs 6.15±1.39 ng/ml). leptin level was significantly higher in NAFLD than NASHgp (69.50±18.70ng/ml vs 43.20±6.93ng/ml). adiponectin ROC curve showed an AUROC curve in NAFLD gp (o.945 p=0.049) while inNASH was(0.995 p=0.007).TNF-α & IL-6 was significantly higher in NASH than NAFLD gp (79.25±13.89 pg/ml vs41.25±17.53 pg/ml)and (110.20±55.34 pg/ml vs 43.85±16.13). Plasma adiponectin level in NAFLD gp was inversely correlated with T.G (r=-0.368 p=0.111). GOT (r=-0.037 p=0.878) & GPT (r=-0.022 p=0.926) while it was +ve correlated in NASH gp with Cholesterol (r=0.317 p=0.174) & T.G (r=0.042 p=0.861).
Conclusion: This data support a role for low circulating adiponectin in the pathogenisis of NAFLD and hypoadiponectinemia found to be a feature of NASH. ADIPONECTIN found to be a non –invasive differential marker between NAFLD & NASH.
