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Contrasting Effects of Growth Hormone and Insulin-Like Growth Factor I on the Biological Activities of Endotoxin in the Rat¹

Metabolism Unit, Center for Metabolism and Endocrinology, Department of Medicine, and Molecular Nutrition Unit, Center for Nutrition and Toxicology, NOVUM, Karolinska Institute at Huddinge University Hospital, S-141 57 Huddinge, Sweden

Address all correspondence and requests for reprints to: Wei Liao, M.D., Ph.D., Center for Nutrition and Toxicology, NOVUM, Karolinska Institute, S-141 57 Huddinge, Sweden. E-mail: wei.liao{at}cnt.ki.se

We previously demonstrated that GH potentiates the biological activities of endotoxin in the rat. In the present study, we wanted to determine if the potentiating effects of GH on the biological activities of endotoxin could be reproduced by insulin-like growth factor I (IGF-I). Endotoxin (5 mg/kg BW) was injected in rats primed with or without GH or IGF-I for 3 days. As expected, endotoxin administration markedly increased circulating tumor necrosis factor (TNF) and interferon- (IFN) and induced organ injury, hypoglycemia, and hyperlipidemia. In GH-primed rats, endotoxin induced a further increase of serum IFN (but not TNF); and five out of six of those rats died within 15 h after giving endotoxin. However, little difference between endotoxin-treated rats with and without IGF-I priming could be seen. Furthermore, IGF-I infusion altered blood glucose, urea, and circulating IGF-I levels more than GH infusion. Therefore, IGF-I does not enhance the biological activities of endotoxin in the rat, suggesting that the enhancement of endotoxin effects by GH is via an IGF-I-independent pathway. Priming rats by GH (but not by IGF-I) induced a further increased response of serum IFN but not TNF to subsequent endotoxin challenge, suggesting that IFN rather than TNF is likely to be involved in this process.

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