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Study breakdown

Blocking Somatostatin Receptor-2 Improves Steroid-Induced Muscle and Bone Wasting in Rats

Animal StudyPreliminary evidence
The takeaway

A somatostatin-2 receptor antagonist (BIM-23627) improved the catabolic effects of chronic glucocorticoid treatment in rats, partially restoring GH signaling and reducing muscle/bone wasting.

Key finding

Somatostatin subtype-2 receptor antagonist BIM-23627 partially reversed glucocorticoid-induced catabolism in rats by reducing somatostatin's GH-inhibi

What the researchers found

Somatostatin subtype-2 receptor antagonist BIM-23627 partially reversed glucocorticoid-induced catabolism in rats by reducing somatostatin's GH-inhibitory tone, improving GH/IGF-1 axis activity and reducing muscle and bone loss from chronic steroids.

Why it matters

Relevant for neuropeptides, hormone-optimization.

How the study worked

animal-study study on neuropeptides, hormone-optimization.

What this study cannot tell us

See abstract.

How to read the evidence

preliminary evidence.

When this study was published

Published in 2005.

The bigger picture

Advances peptide/biomarker research.

Questions still open

  • Further research needed.
  • Clinical translation to evaluate.

Common questions

What was studied?
Blocking Somatostatin Receptor-2 Improves Steroid-Induced Muscle and Bone Wasting in Rats
What was found?
A somatostatin-2 receptor antagonist (BIM-23627) improved the catabolic effects of chronic glucocorticoid treatment in rats, partially restoring GH signaling and reducing muscle/bone wasting.

Read the original research

The somatostatin subtype-2 receptor antagonist, BIM-23627, improves the catabolic effects induced by long-term glucocorticoid treatment in the rat.

Regulatory peptides, 125(1-3), 85-92

Citation

Tulipano, Giovanni; Rossi, Elena; Culler, Michael D; Taylor, John E; Bonadonna, Stefania; Locatelli, Vittorio; Cocchi, Daniela; Giustina, Andrea. (2005). The somatostatin subtype-2 receptor antagonist, BIM-23627, improves the catabolic effects induced by long-term glucocorticoid treatment in the rat.. Regulatory peptides, 125(1-3), 85-92.