Eur J Endocrinol
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DOI: 10.1530/eje.1.01821
European Journal of Endocrinology, Vol 152, Issue 1, 113-118
Copyright © 2005 by European Society of Endocrinology
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CLINICAL STUDY

Plasma adiponectin is decreased in nonalcoholic fatty liver disease

Claudio Pagano, Giorgio Soardo, Walter Esposito, Francesco Fallo, Lorenza Basan, Debora Donnini, Giovanni Federspil, Leonardo A Sechi and Roberto Vettor

Endocrine-Metabolic Laboratory, Department of Medical and Surgical Sciences, University of Padova, Padova, Italy and Liver Unit, Internal Medicine, Department of Pathology and Experimental and Clinical Medicine, University of Udine, Udine, Italy

(Correspondence should be addressed to Claudio Pagano, Department of Medical and Surgical Sciences, University of Padova, Via ospedale 105, 35100 Padova, Italy; Email: claudio.pagano{at}unipd.it)

Objectives: Nonalcoholic fatty liver disease (NAFLD) is a major cause of liver-related morbidity and is frequently associated with obesity and metabolic syndrome. The recently discovered hormone adiponectin is produced by adipose tissue, and low plasma adiponectin is considered a key factor in the development of the insulin resistance underlying metabolic syndrome. Animal studies suggest that adiponectin may protect against non-alcoholic steatohepatitis, but direct evidence in humans is lacking. We therefore conducted this study to assess the relationship between plasma adiponectin and nonalcoholic fatty liver disease to explore its role in the pathogenesis of this disease.

Design and methods: We measured plasma adiponectin and anthropometric, biochemical, hormonal and metabolic correlates in a group of 17 NAFLD patients with diagnosis confirmed by biopsy, and 20 controls with comparable age, body-mass index and sex. Furthermore we compared plasma adiponectin in patients with simple steatosis and steatohepatitis.

Results: Plasma adiponectin was significantly lower in NAFLD patients than controls (5.93±0.45 vs 15.67±1.60 ng/ml). Moreover, NAFLD patients were significantly more insulin resistant while having similar serum leptin. Adiponectin was similar in simple steatosis and in steatohepatitis (6.16±0.78 vs 5.69±0.49 ng/ml). An inverse correlation was observed between adiponectin and homeostatic model assessment (HOMA) of insulin resistance (P = 0.008), while adiponectin did not correlate with serum transaminases and lipid values.

Conclusions: These data support a role for low circulating adiponectin in the pathogenesis of NAFLD and confirm the strict association between reduced adiponectin production by adipose tissue, NAFLD and insulin resistance.




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