Chapter 16 — Quiz
IGF-1, Myostatin Inhibitors, and the Muscle-Building Peptides
22 items. Answer before opening the key.
1. Muscle hypertrophy results from:
A. an increase in the number of muscle fibers in adults B. net protein accretion — synthesis exceeding breakdown, integrated over time C. increased circulating IGF-1 acting on satellite cells D. reduced myostatin expression alone
2. The dominant signal driving muscle hypertrophy is:
A. dietary protein intake B. circulating growth hormone C. mechanical loading D. satellite cell number
3. Satellite cells contribute to muscle growth principally by:
A. secreting IGF-1 into the circulation B. proliferating and fusing into existing fibers, supplying additional nuclei C. replacing damaged fibers with new ones D. inhibiting myostatin locally
4. IGF-1 is:
A. produced mainly by the pituitary B. a 70-amino-acid polypeptide produced largely in the liver in response to GH C. a small molecule structurally related to testosterone D. identical to insulin in sequence
5. Approximately what proportion of circulating IGF-1 is bound to IGF binding proteins?
A. about 10% B. about half C. upward of 99% D. none — IGF-1 circulates free
6. Mecasermin is approved for:
A. sarcopenia in adults over 65 B. severe primary IGF-1 deficiency in children C. muscle wasting in muscular dystrophy D. performance enhancement under medical supervision
7. The most prominent labeled safety concern with mecasermin is:
A. hepatotoxicity B. hypoglycemia C. injection site necrosis D. immune suppression
8. IGF-1 LR3 differs from native IGF-1 principally in that it:
A. binds a different receptor B. has reduced binding-protein affinity and extended activity C. can be taken orally D. is a smaller molecule
9. The fact that IGF-1 LR3 is known by a code rather than a generic name tells you:
A. nothing; naming is arbitrary B. that it is a peptide rather than a protein C. something about its regulatory history — it never reached serious clinical development D. that it is a cosmetic ingredient
10. Myostatin (GDF-8) is:
A. a positive regulator of muscle growth B. a negative regulator of muscle growth — a brake C. a growth hormone secretagogue D. an IGF binding protein
11. Myostatin signals through:
A. the IGF-1 receptor B. the activin receptor type IIB and Smad2/3 C. the GH receptor and JAK/STAT D. a G-protein-coupled receptor
12. Belgian Blue and Piedmontese cattle show "double muscling" because they carry:
A. an inserted growth hormone transgene B. naturally occurring loss-of-function mutations in the myostatin gene C. elevated circulating IGF-1 D. a follistatin overexpression mutation
13. The most important limitation of the double-muscled cattle as evidence for a myostatin drug is:
A. cattle physiology is unrelated to human physiology B. the mutations have never been sequenced C. a developmental knockout is not the same experiment as adult pharmacological blockade D. the effect is too small to be relevant
14. In myostatin-null animals, force per unit of muscle cross-sectional area has been reported to be:
A. increased proportionally with mass B. unchanged C. reduced D. impossible to measure
15. Follistatin is best described as:
A. a 15-residue peptide B. an endogenous glycoprotein of roughly 35–40 kDa that inhibits myostatin and related family members C. a synthetic myostatin analog D. a receptor found on muscle fibers
16. The central finding of the myostatin-pathway programs in muscle disease was that:
A. the drugs failed to engage the target B. lean mass increased without corresponding reliable improvement in strength or function C. function improved but lean mass did not D. neither mass nor function changed
17. In this chapter's rating system, "myostatin / follistatin inhibitors for muscle disease" is rated ⚠️ because:
A. no human data exists B. human data exists and is disappointing C. the mechanism is unproven D. the compounds are unapproved
18. A surrogate endpoint is legitimate for regulatory purposes when:
A. it is cheaper and faster than the outcome B. it is biologically plausible C. it has been validated — shown that intervention-induced change in it reliably produces the corresponding change in the outcome D. the sponsor prespecifies it
19. Contemporary consensus definitions of sarcopenia lead with:
A. low muscle mass B. low muscle strength C. low body weight D. low serum IGF-1
20. Chapter 8 reported that on GLP-1 receptor agonists, lean mass falls while measured physical function improves. Together with this chapter, that pair demonstrates:
A. that lean mass measurements are unreliable B. that GLP-1 drugs build muscle indirectly C. that mass is not function — a dissociation that can run in either direction D. that myostatin inhibitors should be combined with GLP-1 drugs
21. The correct statement of the IGF-1 and cancer relationship is:
A. IGF-1 causes cancer B. IGF-1 has no relationship to cancer risk C. higher circulating IGF-1 has been associated with increased risk of several cancers in observational studies; confounding is substantial and no causal claim is established D. the association has been disproven by genetic studies
22. Why is "follistatin-344 for performance in healthy adults" rated ❌ in a stronger sense than a compound with simply no data?
A. because it is illegal B. because the disease trials that did run failed on function, which is evidence against the claim rather than merely absence of evidence for it C. because it is a protein rather than a peptide D. because it is expensive