Commentary

Abstract

HIGHLIGHTED TOPICScommentaryPublished Online:01 Mar 2001https://doi.org/10.1152/jappl.2001.90.3.1165MoreSectionsPDF (47 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat The first Highlighted Topics article in this issue of the Journal of Applied Physiology, “IGF-I antibody prevents increases in protein synthesis in epitrochlearis muscles from refed, diabetic rats,” by Fedele et al. (p. 1166–1173), shows a potential compensatory role of insulin-like growth factor I (IGF-I) for stimulating skeletal muscle protein synthesis in diabetic rats. This study tested the effect of immune neutralization of locally produced IGF-I on rates of protein turnover in incubated epitrochlearis muscles after fasting and subsequent refeeding. Antibodies against IGF-I reduced protein synthesis rates in muscles from both diabetic and nondiabetic animals. Muscles from diabetic rats that were incubated with anti-IGF-I did not increase protein synthesis as a result of refeeding after a 48-h fast. However, muscles from control diabetic animals as well as muscles from control and antibody-treated nondiabetic animals all exhibited higher protein synthesis rates after refeeding. The deleterious effects of immunoneutralizing IGF-I were thus most pronounced in the diabetic animals during conditions that necessitated an anabolic response. The findings from this study suggest that IGF-I may compensate for insulin during hypoinsulinemic conditions to facilitate anabolism.The second Highlighted Topics article featured in this issue, “Skeletal muscle focal adhesion kinase, paxillin, and serum response factor are loading dependent,” by Gordon et al. (p. 1174–1183), focuses on skeletal muscle adaptations in response to mechanical loading. A complete picture of the molecular events linking mechanical loading to the size and strength of skeletal muscle is still largely unknown. Although calcineurin has been implicated in the hypertrophic response of skeletal muscle to increased physiological loads, a recent study suggests that calcineurin overexpression alone does not result in skeletal muscle hypertrophy and that calcineurin requires upstream activity-dependent effectors (possibly nerve-mediated activity or mechanical loading) (Dunn et al.,J Cell Biol 151: 663–672, 2000). In their study, Gordon et al. show that the mechanochemical signaling protein focal adhesion kinase (FAK) varies its concentration and/or phosphorylation state in skeletal muscle in association with muscle loading status. In addition, the investigators found that changes in FAK were associated with changes in the concentration of the serum response factor (SRF), which is necessary for skeletal α-actin gene transcription and has been shown to lie downstream of FAK in cultured myoblasts (Wei et al.,Am J Physiol Heart Circ Physiol 278: H1736–H1743, 2000). Thus FAK may be a potential upstream mechanochemical signaling component of the SRF pathway or even other pathways (e.g., calcineurin), all of which may be involved in loading-induced regulation of skeletal muscle mass.This article has no references to display. Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 90Issue 3March 2001Pages 1165-1165 Copyright & PermissionsCopyright © 2001 the American Physiological Societyhttps://doi.org/10.1152/jappl.2001.90.3.1165History Published online 1 March 2001 Published in print 1 March 2001 Metrics