Ghrelin in non-alcoholic fatty liver disease

Background and Aim: Non-alcoholic fatty liver disease (NAFLD) has been associated with insulin resistance. The mechanism(s) of progression from NAFLD to non-alcoholic steatohepatitis (NASH) remains uncertain. Ghrelin (GHR) promotes GH, ACTH, cortisol and epinephrine release, increases food intake, leading to energy spare and increased body weight. Materials and Methods: We measured GHR in 76 consecutive NAFLD patients (M/F: 69/7, median age 38 years (range 19-74)). 20 patients had normal body weight (BMIs25 kg/m2), 45 were overweight (BMI between 25 and 29.9), 11 obese (BMIr30). Results: Median GHR was 237 pmol/I_ (95% CI 158-419), higher in fe- males (357 vs. 258 pmol/L; P=O.161). Compared with the first quartile, increasing GHR was not associated with changes in BMI or fasting glu- cose, insulin, degree of insulin resistance (HOMA-R), glucose tolerance (120.min glucose during OGTT) and elevated transaminases (ALT). Fi- nally GHR was not associated with the presence of more severe liver dis- ease (NASH, 233&80 pmol/I_ (n=36) vs. pm-e fatty liver, 240&77). Conclusion: GHR is high in NAFLD patients, mainly in patients with normal body weight, but is not associated with insulin resistance and/or disease activity.