Stergios A Polyzos1, Jannis Kountouras2, Athanasios D Anastasilakis3, Georgios Α Triantafyllou4, Christos S Mantzoros4. 1. Department of Medicine, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece. Electronic address: stergios@endo.gr. 2. Department of Medicine, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece. 3. Department of Endocrinology, 424 General Military Hospital, Thessaloniki, Greece. 4. Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Abstract
OBJECTIVE: There are limited data on the role of activin A and its binding protein, follistatin, in nonalcoholic fatty liver disease (NAFLD). The main aim was the evaluation of serum activin A and follistatin levels in patients with biopsy-proven NAFLD vs. METHODS: This was a case-control study. Fifteen patients with nonalcoholic simple steatosis (SS), 16 with steatohepatitis (NASH), and 52 (24 lean and 28 obese) controls were recruited. Activin A and follistatin were measured using ELISA. RESULTS: Activin A levels showed a trend towards progressive increase (p=0.010) from the controls (lean: 356±25, 95% CI 305-408; obese 360±20, 95% CI 320-401pg/ml) to SS (407±28, 95% CI 347-466pg/ml) and NASH patients (514±70 95% CI 364-664pg/ml); this association became non-significant after adjusting for adiposity. Follistatin was not different between groups (lean controls: 1.11±0.08, 95% CI 0.95-1.28; obese controls: 1.00±0.07, 95% CI 0.86-1.14; SS: 0.86±0.07, 95% CI 0.70-1.02; NASH: 1.14±0.09, 95% CI 0.90-1.37ng/ml; p=0.13). Within the NAFLD group of patients, follistatin was associated with NASH independently from activin A, gender and age, a relationship however likely reflecting the effect of adiposity. CONCLUSIONS: Activin A is higher in patients with NASH than both lean and obese controls. Future clinical studies are needed to confirm and expand these findings, whereas mechanistic studies exploring underlying mechanisms are also warranted.
OBJECTIVE: There are limited data on the role of activin A and its binding protein, follistatin, in nonalcoholic fatty liver disease (NAFLD). The main aim was the evaluation of serum activin A and follistatin levels in patients with biopsy-proven NAFLD vs. METHODS: This was a case-control study. Fifteen patients with nonalcoholic simple steatosis (SS), 16 with steatohepatitis (NASH), and 52 (24 lean and 28 obese) controls were recruited. Activin A and follistatin were measured using ELISA. RESULTS:Activin A levels showed a trend towards progressive increase (p=0.010) from the controls (lean: 356±25, 95% CI 305-408; obese 360±20, 95% CI 320-401pg/ml) to SS (407±28, 95% CI 347-466pg/ml) and NASHpatients (514±70 95% CI 364-664pg/ml); this association became non-significant after adjusting for adiposity. Follistatin was not different between groups (lean controls: 1.11±0.08, 95% CI 0.95-1.28; obese controls: 1.00±0.07, 95% CI 0.86-1.14; SS: 0.86±0.07, 95% CI 0.70-1.02; NASH: 1.14±0.09, 95% CI 0.90-1.37ng/ml; p=0.13). Within the NAFLD group of patients, follistatin was associated with NASH independently from activin A, gender and age, a relationship however likely reflecting the effect of adiposity. CONCLUSIONS:Activin A is higher in patients with NASH than both lean and obese controls. Future clinical studies are needed to confirm and expand these findings, whereas mechanistic studies exploring underlying mechanisms are also warranted.
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