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.
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http://dx.doi.org/10.1016/j.metabol.2016.07.009 | DOI Listing |
Cytokine Growth Factor Rev
November 2024
Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Japan. Electronic address:
Activins, multifunctional cytokines of the transforming growth factor-beta superfamily, play critical roles in the regulation of growth and differentiation in multiple biological systems. Activin activity is finely regulated by the endogenous antagonist follistatin. Early studies reported that activins are involved in renal organogenesis, but subsequent research demonstrated that activins also play a significant role in kidney regeneration following injury.
View Article and Find Full Text PDFACS Nano
December 2024
Department of Pharmaceutical Sciences, College of Pharmacy, Oregon State University, 2730 SW Moody Avenue, Portland, Oregon 97201, United States.
Metabolism
December 2024
Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA; Section of Endocrinology, Boston VA Healthcare System, Harvard Medical School, Boston, MA, USA. Electronic address:
Similar to bariatric surgery, incretin receptor agonists have revolutionized the treatment of obesity, achieving up to 15-25 % weight loss in many patients, i.e., at a rate approaching that achieved with bariatric surgery.
View Article and Find Full Text PDFCommun Biol
October 2024
Ecole Polytechnique Fédérale de Lausanne (EPFL) SV ISREC, Station 19, Lausanne, Switzerland.
The Activin-A precursor dimer can be cleaved by furin, but how this proteolytic maturation is regulated in vivo and how it facilitates access to signaling receptors is unclear. Here, analysis in a syngeneic melanoma grafting model shows that without furin coexpression, Activin-A failed to accelerate tumor growth, correlating with failure of one or both subunits to undergo cleavage in signal-sending cells, even though compensatory processing by host cells nonetheless sustained elevated circulating Activin-A levels. In reporter assays, furin-independent cleavage of one subunit enabled juxtacrine Activin-A signaling, whereas completion of proteolytic maturation by coexpressed furin or by recipient cells stimulated contact-independent activity, crosstalk with BMP receptors, and signal inhibition by follistatin.
View Article and Find Full Text PDFHypertens Res
December 2024
Laboratory of Veterinary Pharmacology, Faculty of Veterinary Medicine, Okayama University of Science, Imabari, Japan.
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