Saudi Journal of Gastroenterology
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ORIGINAL ARTICLE
Year : 2006  |  Volume : 12  |  Issue : 2  |  Page : 68-72

The role of leptin in non-alcoholic fatty liver disease


1 Department of hepatology,gastroenterology and infectious disease, Faculty of medicine, Banha, Zagazig University, Egypt
2 Department of physiology,King Saud University., Saudi Arabia
3 Department of liver transplantation, King Faisal specialist hospital,Riyadh, Saudi Arabia
4 Division of gastroenterology, department of medicine, king saud University, Riyadh, Saudi Arabia

Correspondence Address:
Reda A Elbadawy
Department of hepatology, gastroenterology and infectious disease, Faculty of medicine, Banha, Zagazig University
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1319-3767.27848

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Background: The role of steatosis in the pathogenesis of chronic liver disease (CLD) is now believed to form part of a continuum in non-alcoholic fatty liver disease (NAFLD). One of the unconventional areas in which leptin is now receiving great attention is liver diseases. Several published studies indicate that circulating leptin is increased in patients with cirrhosis, chronic HCV, and non-alcoholic steatohepatitis (NASH). Aims: the present study aims to assess serum leptin levels in patients with NAFLD with and without HCV infection, and to correlate it with the biochemical markers and histopathology of liver diseases. Patients and Methods: the present study included 67 Saudi subjects divided into 3 age and sexmatched groups. Group A: 22 patients with DM (8 males and 14 females, mean age 44 12.9 years). Group B: 20 patients with chronic HCV infection (7 males and 13 females, mean age 48.9 14.1 years). Group C: 25 control healthy volunteers (15 males and 10 females, mean age 40.7 12.6 years). Serum leptin, C-peptide, and insulin levels were measured by radioimmunoassay. Liver biopsy was done for the HCV group only. Results: Patients with chronic HCV infection had significantly lower mean SD serum leptin levels (25.6 37.2 ng/mL) compared with the diabetic and control groups, 55.7 59.0 and 81.8 41.7 ng/mL (p = 0.002 and p = 0.046 respectively). However, in the HCV group, leptin levels did not differ significantly as regard steatosis grade, and fibrosis stage. Steatosis in the HCV group patients correlated with the body mass index and hyperglycemia, but not with leptin levels. Serum leptin correlated positively with serum insulin and C-peptide levels in both the HCV and diabetic groups, but not in the control group). Conclusion: Serum leptin can't be used as a non-invasive marker for the predication of steatosis and fibrosis in patients with NAFLD.


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