Impaired Follistatin Secretion in Cirrhosis

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Impaired Follistatin Secretion in Cirrhosis. / Rinnov, Anders Rasmussen; Plomgaard, Peter; Pedersen, Bente Klarlund; Gluud, Lise Lotte.

In: The Journal of clinical endocrinology and metabolism, Vol. 101, No. 9, 09.2016, p. 3395-3400.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Rinnov, AR, Plomgaard, P, Pedersen, BK & Gluud, LL 2016, 'Impaired Follistatin Secretion in Cirrhosis', The Journal of clinical endocrinology and metabolism, vol. 101, no. 9, pp. 3395-3400. https://doi.org/10.1210/jc.2016-1923

APA

Rinnov, A. R., Plomgaard, P., Pedersen, B. K., & Gluud, L. L. (2016). Impaired Follistatin Secretion in Cirrhosis. The Journal of clinical endocrinology and metabolism, 101(9), 3395-3400. https://doi.org/10.1210/jc.2016-1923

Vancouver

Rinnov AR, Plomgaard P, Pedersen BK, Gluud LL. Impaired Follistatin Secretion in Cirrhosis. The Journal of clinical endocrinology and metabolism. 2016 Sep;101(9):3395-3400. https://doi.org/10.1210/jc.2016-1923

Author

Rinnov, Anders Rasmussen ; Plomgaard, Peter ; Pedersen, Bente Klarlund ; Gluud, Lise Lotte. / Impaired Follistatin Secretion in Cirrhosis. In: The Journal of clinical endocrinology and metabolism. 2016 ; Vol. 101, No. 9. pp. 3395-3400.

Bibtex

@article{dbfac7051fb747c585ea0544bf8575f7,
title = "Impaired Follistatin Secretion in Cirrhosis",
abstract = "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.",
author = "Rinnov, {Anders Rasmussen} and Peter Plomgaard and Pedersen, {Bente Klarlund} and Gluud, {Lise Lotte}",
year = "2016",
month = sep,
doi = "10.1210/jc.2016-1923",
language = "English",
volume = "101",
pages = "3395--3400",
journal = "Journal of Clinical Endocrinology and Metabolism",
issn = "0021-972X",
publisher = "Oxford University Press",
number = "9",

}

RIS

TY - JOUR

T1 - Impaired Follistatin Secretion in Cirrhosis

AU - Rinnov, Anders Rasmussen

AU - Plomgaard, Peter

AU - Pedersen, Bente Klarlund

AU - Gluud, Lise Lotte

PY - 2016/9

Y1 - 2016/9

N2 - 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.

AB - 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.

U2 - 10.1210/jc.2016-1923

DO - 10.1210/jc.2016-1923

M3 - Journal article

C2 - 27399349

VL - 101

SP - 3395

EP - 3400

JO - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

SN - 0021-972X

IS - 9

ER -

ID: 177292247