Cortisol as a factor contributing to the development of non-alcoholic fatty liver disease in severely obese patients: a single-center prospective study

Introduction Nonalcoholic fatty liver disease (NAFLD) is known to have high prevalence in obese patients, and has been found to be associated with the metabolic syndrome (MetS). This study aimed to investigate possible correlations of NAFLD with hypothalamic–pituitary–adrenal (HPA) axis activity and expression levels of hydroxysteroid (11-beta) dehydrogenase 1 (HSD11B1), nuclear receptor subfamily 3, group C, member 1 (glucocorticoid receptors) a (NR3C1a) and b (NR3C1b) in the liver, visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT). Material and methods In this single-center study, 34 severely obese patients (BMI > 40 kg/m2), scheduled to undergo bariatric surgery, were recruited and enrolled prospectively. Before the day of surgery, urinary free cortisol (UFC) and diurnal variation of serum and salivary cortisol were estimated. During surgery, biopsies of the liver, VAT, and SAT were obtained. Results The expression of the visceral adipose tissue HSD11B1 (VAT HSD11B1) was significantly higher in the groups of patients with NAFLD (NAFLD+) or NASH (NASH+), compared with those without (NAFLD-, NASH-). The expression of NR3C1a in the liver (LNR3C1a) was significantly lower in the NAFLD+ group compared with the NAFLD- group. In the NAFLD group, the expression of HSD11B1 in the liver (LHSD11B1) exhibited a negative correlation with LNR3C1a, whereas no association was found in the NAFLD+ group. Conclusions The activity of the HPA axis, and tissue and systemic cortisol levels, contribute to MetS development. There are similarities between MetS and NAFLD concerning their pathophysiological mechanisms.