Serum leptin levels in patients with viral chronic hepatitis or liver cirrhosis

Citation
R. Testa et al., Serum leptin levels in patients with viral chronic hepatitis or liver cirrhosis, J HEPATOL, 33(1), 2000, pp. 33-37
Citations number
28
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
JOURNAL OF HEPATOLOGY
ISSN journal
01688278 → ACNP
Volume
33
Issue
1
Year of publication
2000
Pages
33 - 37
Database
ISI
SICI code
0168-8278(200007)33:1<33:SLLIPW>2.0.ZU;2-Y
Abstract
Background/Aim: Serum levels of leptin, the adipocyte-derived hormone regul ating food intake and energy expenditure in mammals, have been found to be increased in cirrhotic patients. The aim of the present study was to invest igate leptin serum level in relation to anthropometric features and liver f unction in patients with viral chronic hepatitis or liver cirrhosis. Methods: Serum leptin levels were determined by radioimmunoassay in 30 male and 10 female patients with chronic hepatitis, in 42 male and 10 female pa tients with liver cirrhosis, and in four respective control groups. Liver f unction was evaluated by the monoethylglycinexylidide formation test. Body mass index and body fat mass were estimated by weight, height and skinfold thickness measurements. Results: Compared with controls, absolute serum leptin levels were signific antly (p<0.01) lower in chronic hepatitis patients and similar in cirrhotic patients. Leptin serum levels were significantly (p<0.05) higher in cirrho tic than in chronic hepatitis patients. When expressed in relation to body fat mass, the above differences persisted; however, cirrhotic females showe d significantly (p<0.05) higher serum leptin values than controls. Serum le ptin values correlated negatively (p<0.01) with monoethylglycinexylidide se rum values in all groups of patients. Conclusions: In patients with chronic viral liver disease, serum leptin lev els tend to increase as liver function worsens. This may reflect a decline in the ability to downregulate energy expenditure as an adaptation to anore xia and/or to defective substrate utilisation due to liver disease and may negatively influence body weight homeostasis in these patients.