Conflict of interest: All authors declare no conflict of interests.
Comparative Aspects of the Endotoxin- and Cytokine-Induced Endocrine Cascade Influencing Neuroendocrine Control of Growth and Reproduction in Farm Animals
Article first published online: 9 JUL 2008
© 2008 The Authors. Journal compilation © 2008 Blackwell Verlag
Reproduction in Domestic Animals
Special Issue: 16th International Congress on Animal Reproduction
Volume 43, Issue Supplement s2, pages 317–323, July 2008
How to Cite
Whitlock, B., Daniel, J., Wilborn, R., Elsasser, T., Carroll, J. and Sartin, J. (2008), Comparative Aspects of the Endotoxin- and Cytokine-Induced Endocrine Cascade Influencing Neuroendocrine Control of Growth and Reproduction in Farm Animals. Reproduction in Domestic Animals, 43: 317–323. doi: 10.1111/j.1439-0531.2008.01180.x
- Issue published online: 9 JUL 2008
- Article first published online: 9 JUL 2008
Disease in animals is a well-known inhibitor of growth and reproduction. Earlier studies were initiated to determine the effects of endotoxin on pituitary hormone secretion. These studies found that in sheep, growth hormone (GH) concentration was elevated, whereas insulin-like growth factor-I (IGF-I) was inhibited, as was luteinizing hormone (LH). Examination of the site of action of endotoxin in sheep determined that somatotropes expressed the endotoxin receptor (CD14) and that both endotoxin and interleukin-Iβ activated GH secretion directly from the pituitary. In the face of elevated GH, there is a reduction of IGF-I in all species examined. As GH cannot activate IGF-I release during disease, there appears to be a downregulation of GH signalling at the liver, perhaps related to altered nitration of Janus kinase (JAK). In contrast to GH downregulation, LH release is inhibited at the level of the hypothalamus. New insights have been gained in determining the mechanisms by which disease perturbs growth and reproduction, particularly with regard to nitration of critical control pathways, with this perhaps serving as a novel mechanism central to lipopolysaccharide suppression of all signalling pathways. This pathway-based analysis is critical to the developing novel strategies to reverse the detrimental effect of disease on animal production.