Impaired Follistatin Secretion in Cirrhosis

Anders Rasmussen Rinnov, Peter Plomgaard, Bente Klarlund Pedersen, Lise Lotte Gluud
2016 Journal of Clinical Endocrinology and Metabolism  
Context: Follistatin is a liver-derived inhibitor of the muscle-growth inhibitor myostatin. Reduction in acute follistatin release may help explain muscle loss in liver cirrhosis. Objective: The study aimed to investigate the capacity of acute follistatin release in patients with liver cirrhosis compared to healthy control participants. Design, Setting, and Participants: To experimentally increase the glucagon-insulin ratio (mimicking the hormonal effect of exercise), we infused
more » ... tatin (to inhibit insulin secretion) and compared the acute follistatin increase in eight male cirrhosis patients with eight healthy control participants. Patients and controls received 1-hour glucagon/somatostatin and saline infusions on 2 separate days. Main Outcome Measure: Follistatin was measured during and 5 hours after termination of infusions. Results: The peak follistatin change was significantly decreased in patients with liver cirrhosis compared to healthy control participants (1.9 (interquartile range, 1.4 -2.5) versus 3.6 (interquartile range, 3.0 -4.0), respectively; P ϭ .003). Patients with liver cirrhosis demonstrated significantly decreased amounts of appendicular lean mass compared to healthy controls (27.6 Ϯ 3.8 vs 34.5 Ϯ 2.9%, respectively; P ϭ .001). Conclusions : Patients with cirrhosis show impaired capacity to acutely secrete follistatin. The decrease in acute follistatin release may contribute to the loss of muscle mass in liver cirrhosis. (J Clin Endocrinol Metab 101: 3395-3400, 2016) Figure 3. Correlation between peak follistatin change and appendicular lean mass (%). F, Patients with liver cirrhosis; Ⅺ, healthy control participants. Significant correlation between peak follistatin change and appendicular lean mass (%), P ϭ .044; r ϭ 0.51. Figure 2. Peak follistatin changes at 120 minutes after termination of glucagon/somatostatin and saline infusions. Data are presented as median mean with interquartile range. F, Saline infusion; Ⅺ, glucagon/somatostatin infusion. Peak follistatin change is significantly higher in healthy control participants than patients with liver cirrhosis after glucagon/somatostatin infusion. P ϭ 0.003.
doi:10.1210/jc.2016-1923 pmid:27399349 fatcat:jow7vqmobjgiji3oygryw55s6e