Abstract
ObjectiveTo determine if a commercial myostatin reducer (Fortetropin®) would inhibit disuse muscle atrophy in dogs after a tibial plateau leveling osteotomy.DesignA prospective randomized, double-blinded, placebo-controlled clinical trial.AnimalsOne hundred client-owned dogs presenting for surgical correction of cranial cruciate ligament rupture by tibial plateau leveling osteotomy.ProceduresPatients were randomly assigned into the Fortetropin® or placebo group and clients were instructed to add the assigned supplement to the dog’s normal diet once daily for twelve weeks. Enrolled patients had ultrasound measurements of muscle thickness, tape measure measurements of thigh circumference, serum myostatin level assays, and static stance analysis evaluated at weeks 0, 8, and 12.ResultsFrom week 0 to week 8, there was no change for thigh circumference in the Fortetropin® group for the affected limb (-0.54cm, P = 0.31), but a significant decrease in thigh circumference for the placebo group (-1.21cm, P = 0.03). There was no significant change in serum myostatin levels of dogs in the Fortetropin® group at any time point (P>0.05), while there was a significant rise of serum myostatin levels of dogs in placebo group during the period of forced exercise restriction (week 0 to week 8; +2,892 pg/ml, P = 0.02). The percent of body weight supported by the affected limb increased in dogs treated with Fortetropin® (+7.0%, P<0.01) and the placebo group (+4.9%, P<0.01) at the end of the period of forced exercise restriction. The difference in weight bearing between the Fortetropin® and placebo groups was not statistically significant (P = 0.10).ConclusionDogs receiving Fortetropin® had a similar increase in stance force on the affected limb, no significant increase in serum myostatin levels, and no significant reduction in thigh circumference at the end of the period of forced exercise restriction compared to the placebo. These findings support the feeding of Fortetropin® to prevent disuse muscle atrophy in canine patients undergoing a tibial plateau leveling osteotomy.
Highlights
Loss of lean body mass can result from cachexia, sarcopenia, and disuse atrophy
There was no significant change in serum myostatin levels of dogs in the Fortetropin® group at any time point (P>0.05), while there was a significant rise of serum myostatin levels of dogs in placebo group during the period of forced exercise restriction
Dogs receiving Fortetropin® had a similar increase in stance force on the affected limb, no significant increase in serum myostatin levels, and no significant reduction in thigh circumference at the end of the period of forced exercise restriction compared to the placebo
Summary
Loss of lean body mass can result from cachexia, sarcopenia, and disuse atrophy. Cachexia is the loss of lean body mass as a result of catabolism secondary to a disease state [1]. The loss of lean body mass due to disuse muscle atrophy can result from immobilization or inactivity associated with recovery from surgery or reduction in the use of a limb secondary to pain [3]. The resultant increase in serum myostatin levels associated with the endocrine pathway can be measured and reduction of these levels is a potential target for prevention of disuse atrophy. The use of a canine-specific activin receptor type IIB decoy receptor in dogs did not reverse cardiac cachexia, but reduction of serum myostatin by an insertion of a canine myostatin propeptide gene utilizing an adeno-associated virus serotype 8 vector increased muscle mass in both healthy dogs and golden retrievers with muscular dystrophy [5,6,7]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
