Antiproteolytic action of insulin in burn-injured rats.
BACKGROUND
Negative nitrogen balance is a typical metabolic response to burn injury resulting in decreased muscle mass and activity. Since insulin is an anabolic hormone, using insulin as a prophylactic agent in burned patients has received some attention. The present study was carried out to investigate the systemic effect of insulin on burn injury-induced muscle wasting.


METHODS
A 15-20% total body surface area (TBSA) scald burn injury was inflicted on the shaved dorsum of rats. Rats were treated with a daily subcutaneous insulin injection for 3 days (0.25-1.0 U/day). After the treatment, a variety of insulin-dependent physiological parameters were monitored. Overall body protein degradation rates were determined by measuring the urinary tyrosine. Also, protein degradations were measured in diaphragm muscles, splenocytes, and peripheral blood mononuclear cells to directly confirm the antiproteolytic activity of insulin.


RESULTS
Administration of insulin to burn-injured rats restored body weight primarily by reducing accelerated protein degradation and regaining the intracellular protein content in individual skeletal muscle. The measured physiological parameters showed no possible side effects. Protein degradation in immune cells was also suppressed after the therapy.


CONCLUSIONS
Results indicate that lower dose insulin particularly suppresses protein degradation without causing secondary effects. It may be a useful approach to preventing burn injury-induced muscle wasting and also has a potential to improve immune response.
Solomon
Vered
V
Shriners Burns Hospital, Surgical Services and Center for Engineering in Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, 02114, USA.
Madihally
Sundararajan
S
Mitchell
Richard N
RN
Yarmush
Martin
M
Toner
Mehmet
M
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D002056:Burns / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D003345:Corticosterone / Q000097:blood; D006321:Heart / Q000187:drug effects; D007328:Insulin / Q000097:blood / Q000627:therapeutic use*; D007668:Kidney / Q000187:drug effects; D007700:Kinetics; D008099:Liver / Q000187:drug effects; D008297:Male; D009124:Muscle Proteins / Q000378:metabolism; D018482:Muscle, Skeletal / Q000187:drug effects; D011506:Proteins / Q000187:drug effects* / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
D001786:Blood Glucose; D007328:Insulin; D009124:Muscle Proteins; D011506:Proteins; D003345:Corticosterone