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Impaired Follistatin Secretion in Cirrhosis
Anders Rasmussen Rinnov1, Peter Plomgaard1, Bente Klarlund Pedersen1
1The Centre of Inflammation and Metabolism and the Centre for Physical Activity Research (A.R.R., P.P., B.K.P.), Rigshospitalet, University of Copenhagen, 2100 Copenhagen, Denmark; Department of Clinical Biochemistry (P.P.), Rigshospitalet, 2100 Copenhagen, Denmark; and Gastrounit, Hvidovre Hospital (L.L.G.), University of Copenhagen, 2650 Hvidovre, Denmark.
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 glucagon/somatostatin (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 = .003). Patients with liver cirrhosis demonstrated significantly decreased amounts of appendicular lean mass compared to healthy controls (27.6 ± 3.8 vs 34.5 ± 2.9%, respectively; P = .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.
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