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Insulin growth factor‐1 decreases muscle atrophy following denervation
Author(s) -
Day Charles S.,
Buranapanitkit Boonsin,
Riano Felix A.,
Tomaino Matthew M.,
Somogyi George,
Sotereanos Dean G.,
Kuroda Ryosuke,
Huard Johnny
Publication year - 2002
Publication title -
microsurgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.031
H-Index - 63
eISSN - 1098-2752
pISSN - 0738-1085
DOI - 10.1002/micr.21742
Subject(s) - reinnervation , denervation , medicine , atrophy , muscle atrophy , myocyte , neuromuscular junction , amyotrophy , gastrocnemius muscle , regeneration (biology) , endocrinology , anatomy , skeletal muscle , biology , neuroscience , microbiology and biotechnology
Despite modern microsurgical techniques for nerve repair, functional outcome following proximal injury is often unsatisfactory because irreversible muscle atrophy may develop before reinnervation occurs. Because insulin growth factor‐1 (IGF‐1) has been shown to improve muscle regeneration after injury, and may have a role in muscle preservation following denervation, the purpose of this investigation was to evaluate the histological, immunohistochemical, and electrophysiological differences between normal, denervated, and IGF‐1‐injected denervated muscle over an 8‐week period. Denervated mice gastrocnemius muscles demonstrated a decrease in muscle weight, a decrease in myofiber diameter, an absence of muscle regeneration, an early increase in the number of neuromuscular junctions (NMJs), and a decrease in fast‐twitch and maximum tetanic strength as compared to normal muscle up to 8 weeks following denervation. IGF‐1‐injected denervated muscle, on the other hand, sustained muscle diameter and muscle weight, maintained a smaller number of NMJs, and relatively sustained fast‐twitch and maximum tetanic strength as compared to normal muscle over 8 weeks. These data suggest that IGF‐1 may help prevent muscle atrophy and secondary functional compromise after denervation. © 2002 Wiley‐Liss, Inc. MICROSURGERY 22:144–151 2002