MODULATION OF IGF MESSENGER-RNA ABUNDANCE DURING STRETCH-INDUCED SKELETAL-MUSCLE HYPERTROPHY AND REGRESSION

Citation
Sm. Czerwinski et al., MODULATION OF IGF MESSENGER-RNA ABUNDANCE DURING STRETCH-INDUCED SKELETAL-MUSCLE HYPERTROPHY AND REGRESSION, Journal of applied physiology, 76(5), 1994, pp. 2026-2030
Citations number
29
Categorie Soggetti
Physiology
ISSN journal
87507587
Volume
76
Issue
5
Year of publication
1994
Pages
2026 - 2030
Database
ISI
SICI code
8750-7587(1994)76:5<2026:MOIMAD>2.0.ZU;2-8
Abstract
Increased load on a muscle (synergistic overload or stretch) results i n muscle hypertrophy. The expression of insulin-like growth factor I ( IGF-I) mRNA in rat skeletal muscle is increased during synergistic ove rload-induced hypertrophy. Although it has also been established that fasting animals lose muscle protein, it has been shown that compensato ry muscle hypertrophy occurs in adult fasting rats that are undergoing a net loss of body weight. The purpose of this investigation was to d etermine whether a relationship exists between IGF-I mRNA levels and m uscle growth and regression. This was accomplished by examining whethe r IGF-I mRNA levels were altered during muscle hypertrophy after stret ch and regression and the effect of fasting on IGF-I mRNA levels durin g stretch-induced hypertrophy. Patagialis (PAT) muscle weights increas ed 13 and 44% at 2 and 11 days of stretch, respectively. However, afte r removal of the stretch stimulus on day 11, PAT weights began to decr ease, reaching control weights by 18 days. During the first time point (2 days), PAT muscle IGF-I mRNA remained constant. IGF-I mRNA abundan ce was threefold greater than contralateral control levels by 11 days of stretch. IGF-I mRNA levels decreased but remained significantly abo ve control levels throughout the regression of hypertrophy (13, 18, an d 25 days). Pasting did not alter PAT muscle response to stretch. Afte r 11 days of stretch, PAT muscle weight increased 60% compared with co ntralateral control muscles and IGF-I mRNA levels increased threefold. This study supports a role for IGF-I in muscle hypertrophy but not mu scle atrophy.