Abstract:
OBJECTIVE:Adjuvant-induced arthritis induces a catabolic response, and a decrease in circulating IGF-I. Hypermetabolism and GH insensitivity have been described in acute inflammation. The aim of this study was to analyze whether impaired IGF-I secretion in arthritic rats can be attributed to hepatic GH resistance. DESIGN AND METHODS:Male Wistar rats were injected with complete Freund's adjuvant, and 14 days afterwards arthritic and control rats were injected daily with recombinant human GH (rhGH) (3 IU/kg) or saline for 8 days. GH receptor (GHR) gene expression in the liver and the effect of rhGH on hepatic IGF-I synthesis in arthritic rats were examined. RESULTS:There was a significant decrease in hepatic concentrations of IGF-I (P < 0.01) as well as in the IGF-I gene expression in arthritic but not in pair-fed rats. In contrast, arthritis did not modify GHR mRNA levels in the liver. The 8 day administration of rhGH resulted in an increase in body weight gain in arthritic but not in control rats. There was an increase in hepatic IGF-I synthesis and in GHR mRNA levels after rhGH treatment, both in control and in arthritic rats. Two endotoxin lipopolysaccharide (LPS) (1 mg/kg) injections decreased hepatic concentrations of IGF-I and IGF-I mRNA (P < 0.01). Contrary to the results obtained in arthritic rats, mRNA expression of GHR in the liver was lower in LPS- than in saline-treated rats (P < 0.01). CONCLUSION:These data suggest that the decrease in IGF-I synthesis induced by chronic arthritis is not secondary to GH resistance.
journal_name
Eur J Endocrinoljournal_title
European journal of endocrinologyauthors
Lopez-Calderon A,Ibáñez de Caceres I,Soto L,Priego T,Martin AI,Villanua MAdoi
10.1530/eje.0.1440529subject
Has Abstractpub_date
2001-05-01 00:00:00pages
529-34issue
5eissn
0804-4643issn
1479-683Xpii
1440529journal_volume
144pub_type
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journal_title:European journal of endocrinology
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pub_type: 杂志文章,多中心研究
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更新日期:2001-10-01 00:00:00
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journal_title:European journal of endocrinology
pub_type: 杂志文章
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