|
|
||||||||
Departamento de Fisiología, Facultad de Medicina, Universidad Complutense, Madrid 28040, Spain
(Requests for offprints should be addressed to A López-Calderón; Email: ALC{at}med.ucm.es)
Gram-negative bacterial infection or treatment of animals with bacterial lipopolysaccharide (LPS) induces a catabolic state with proteolysis, liver injury and an inhibition of the insulin-like growth factor-I (IGF-I) system. The purpose of this work was to elucidate the role of Kupffer cells in LPS-induced inhibition of the IGF-I/IGF-binding protein-3 (IGFBP-3) system. Adult male Wistar rats were either pretreated with the Kupffer cell inhibitor gadolinium chloride (10 mg/kg, i.v., 24 h prior to LPS exposure) or saline vehicle. Rats received two i.p. injections of 1 mg/kg LPS (at 17:30 and 08:30 h the following day) and were killed 4 h after the second injection. LPS administration induced a significant decrease in body weight and in serum concentrations of IGF-I and IGFBP-3 (P < 0.01), as well as in their gene expression in the liver. LPS-injected rats had increased serum concentrations of ACTH, corticosterone (P < 0.05), tumour necrosis factor-
(TNF-
) and nitrites (P < 0.01). Pretreatment of the animals with gadolinium chloride blocked the inhibitory effect of LPS on body weight, and on serum concentrations of IGF-I, IGFBP-3 and nitrites, as well as growth hormone receptor (GHR), IGF-I and IGFBP-3 gene expression in the liver. In contrast, gadolinium chloride administration did not modify the stimulatory effect of LPS on serum concentrations of ACTH, corticosterone and TNF-
. These results suggest that Kupffer cells are important mediators in the inhibitory effect of LPS on GHR, IGF-I and IGFBP-3 gene expression in the liver, leading to a decrease in serum concentrations of IGF-I and IGFBP-3.
This article has been cited by other articles:
![]() |
Xiaoyang Wang, G. Hellgren, C. Lofqvist, Wenli Li, A. Hellstrom, H. Hagberg, and C. Mallard White Matter Damage After Chronic Subclinical Inflammation in Newborn Mice J Child Neurol, September 1, 2009; 24(9): 1171 - 1178. [Abstract] [PDF] |
||||
![]() |
A I Martin, M Lopez-Menduina, E Castillero, M Granado, M A Villanua, and A Lopez-Calderon Ptgs2 activation by endotoxin mediates the decrease in Igf1, but not in Igfbp3, gene expression in the liver J. Endocrinol., August 1, 2008; 198(2): 385 - 394. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Granado, A. I. Martin, M. Lopez-Menduina, A. Lopez-Calderon, and M. A. Villanua GH-releasing peptide-2 administration prevents liver inflammatory response in endotoxemia Am J Physiol Endocrinol Metab, January 1, 2008; 294(1): E131 - E141. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Priego, M. Granado, E. Castillero, A. I. Martin, M A. Villanua, and A. Lopez-Calderon Nitric oxide production by hepatocytes contributes to the inhibitory effect of endotoxin on insulin-like growth factor I gene expression. J. Endocrinol., September 1, 2006; 190(3): 847 - 856. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | CONTACT US | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |