ABSTRACT
Abstract: 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 disease. Several published studies indicate that circulating leptin is increased in cirrhosis, HCV and NASH. The aim of this study was to investigate the role of leptin in NAFLD, by measuring the serum leptin level and correlating it with biochemical markers of liver disease and the result of liver biopsy in chronic hepatitis C [CHC] patients
Patients and Methods: Sixty seven Saudi subjects were included. They were divided into 3 groups. Group A [n = 22, 8 males and 14 females] patients had diabetes mellitus [DM]; their mean age was 44 +/- 12.9 years. Group B [n = 20, 7 males and 13 females] patients had CHC as diagnosed by HCV Ab and HCV RNA; their mean age was 48.9 +/- 14.1 years and group C the control healthy volunteers [n = 25, 15 males and 10 females with a mean age of 40.68 +/- 12.6 years]. All the groups matched for age and sex. Serum leptin, C peptide and insulin were measured by radio immununoassay for all subjects. Liver biopsy was done for the HCV group only
Results: showed no correlation between leptin levels, C-peptide and serum insulin. There was a statistically significant difference in serum leptin level between groups A and B and B and C but no statistical difference between groups A and C. The HCV group patients had hypoleptinaemia in comparison to other studied groups. Serum leptin levels for the studied groups [for DM, HCV and control group] were respectively 55.65+/- 59.02 ng /ml, 25.62 +/- 37.2 ng/ml and 82.78 +/- 49.73 ng/ml. There was no correlation between the leptin level and the histopathology of the liver as regards the steatosis grade, inflammatory grading in HCV group and the fibrosis stage. The steatosis in the HCV group patients was related to body mass index [BMI] and hyperglycemia not to the leptin level. HCV appears to be a prediabetic condition
In Conclusion: Serum leptin can not be used as a non invasive marker for the prediction of steatosis, necrosis nor fibrosis in NAFLD
ABSTRACT
Leptin is a cytokine l6kd peptide hormone. Its crucial role is regulation of appetite and the body fat mass mainly through action on the hypothalamus. It is produced mainly in adipocytes of white fat, as well as from other tissues e.g. placenta, skeletal muscles, fundus of the stomach and activated hepatic stellate cell [HSC] and recently reported that leptin is produced from B cell of islands of the pancreas. The gene responsible for production is present on chromosome 7 called obse gene [ob/gene]. Leptin receptors [OB-R] were present in two forms short [OB-Ra or OB-RS] and long one [OB-Rb or OB-RI]. The main action of leptin depends on long form [OB-Rl], where very little evidence is available implicating a role for the short form in the action of leptin. One of the unconventional areas in which leptin is now receiving great attention is liver diseases as several published studies indicate that circulating leptin level are increased in cirrhosis, hepatitis C virus [HCV] and non-alcoholic steatohepatitis [NASH]