| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Departments of Cellular and Molecular Physiology and of Surgery, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033
The purpose of the present study was to determine whether burn-induced changes in various components of the insulin-like growth factor (IGF) system are mediated by the actions of endogenous glucocorticoids or tumor necrosis factor (TNF). To address this aim, a 30% total body surface area full-thickness scald burn was produced in anesthetized rats, and the animals were studied 24 h later. Separate groups of time-matched control and burned rats were pretreated with either an antagonist to glucocorticoids (RU-486) or to TNF (TNF-binding protein; TNFBP). Thermal injury decreased the plasma concentration of IGF-I (38%) as well as the IGF-I mRNA abundance in muscle and kidney (31 and 48%, respectively). While RU-486 prevented the burn-induced decrease in plasma IGF-I, it did not ameliorate the reduction in tissue IGF-I mRNA. Burn increased the plasma concentration of IGF-binding protein (IGFBP)-1 as well as the mRNA content of IGFBP-1 in liver and kidney (15- to 20-fold). These burn-induced increases were partially or largely prevented by RU-486. In contrast, burn decreased the plasma concentration of IGFBP-3 (30%). Burn concomitantly decreased hepatic IGFBP-3 mRNA abundance (42%) but increased IGFBP-3 mRNA in kidney and muscle (50% and 10-fold, respectively). RU-486 largely prevented the burn-induced changes in IGFBP-3 mRNA in kidney and muscle but failed to attenuate the decreases in plasma and liver. Finally, burn injury decreased hepatic acid-labile subunit (ALS) mRNA by 80% and increased the mRNA content of IGFBP-related protein-1 (mac25) in liver by twofold, and these changes were not modified by pretreatment with RU-486. The above-mentioned changes in the IGF system were associated with a burn-induced decrease in muscle protein content that was prevented by RU-486. TNFBP failed to completely ameliorate any of the burn-induced changes in the IGF system. These results demonstrate that glucocorticoids, but not TNF, mediate many but not all of the burn-induced changes in the IGF system.
insulin-like growth factor-binding proteins 1 and 3; acid-labile subunit; mac25; muscle protein; RU-486; tumor necrosis factor-binding protein; rats
This article has been cited by other articles:
|
|
 |
|
  C. H. Lang, D. Huber, and R. A. Frost Burn-induced increase in atrogin-1 and MuRF-1 in skeletal muscle is glucocorticoid independent but downregulated by IGF-I Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2007; 292(1): R328 - R336. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Lopez-Bermejo, J. Khosravi, J. M. Fernandez-Real, V. Hwa, K. L. Pratt, R. Casamitjana, M. M. Garcia-Gil, R. G. Rosenfeld, and W. Ricart Insulin Resistance Is Associated With Increased Serum Concentration of IGF-Binding Protein-Related Protein 1 (IGFBP-rP1/MAC25). Diabetes, August 1, 2006; 55(8): 2333 - 2339. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. H. Lang, B. J. Krawiec, D. Huber, J. M. McCoy, and R. A. Frost Sepsis and inflammatory insults downregulate IGFBP-5, but not IGFBP-4, in skeletal muscle via a TNF-dependent mechanism Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2006; 290(4): R963 - R972. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. J. Krawiec, R. A. Frost, T. C. Vary, L. S. Jefferson, and C. H. Lang Hindlimb casting decreases muscle mass in part by proteasome-dependent proteolysis but independent of protein synthesis Am J Physiol Endocrinol Metab, December 1, 2005; 289(6): E969 - E980. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. R. Almon, W. Lai, D. C. DuBois, and W. J. Jusko Corticosteroid-regulated genes in rat kidney: mining time series array data Am J Physiol Endocrinol Metab, November 1, 2005; 289(5): E870 - E882. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
X. Li, S. N. Rana, E. J. Kovacs, R. L. Gamelli, I. H. Chaudry, and M. A. Choudhry Corticosterone suppresses mesenteric lymph node T cells by inhibiting p38/ERK pathway and promotes bacterial translocation after alcohol and burn injury Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2005; 289(1): R37 - R44. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. A. Frost, G. J. Nystrom, and C. H. Lang Epinephrine stimulates IL-6 expression in skeletal muscle and C2C12 myoblasts: role of c-Jun NH2-terminal kinase and histone deacetylase activity Am J Physiol Endocrinol Metab, May 1, 2004; 286(5): E809 - E817. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. H. Lang, R. A. Frost, N. Deshpande, V. Kumar, T. C. Vary, L. S. Jefferson, and S. R. Kimball Alcohol impairs leucine-mediated phosphorylation of 4E-BP1, S6K1, eIF4G, and mTOR in skeletal muscle Am J Physiol Endocrinol Metab, December 1, 2003; 285(6): E1205 - E1215. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Q. Hong-Brown, C. R. Brown, R. N. Cooney, R. A. Frost, and C. H. Lang Sepsis-induced muscle growth hormone resistance occurs independently of STAT5 phosphorylation Am J Physiol Endocrinol Metab, July 1, 2003; 285(1): E63 - E72. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Kumar, R. A. Frost, and C. H. Lang Alcohol impairs insulin and IGF-I stimulation of S6K1 but not 4E-BP1 in skeletal muscle Am J Physiol Endocrinol Metab, November 1, 2002; 283(5): E917 - E928. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Spies, M. R. K. Dasu, N. Svrakic, O. Nesic, R. E. Barrow, J. R. Perez-Polo, and D. N. Herndon Gene expression analysis in burn wounds of rats Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2002; 283(4): R918 - R930. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
