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Articles in PresS, published online ahead of print May 21, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00122.2002
Submitted on March 20, 2002
Accepted on May 17, 2002
1 Pituitary Research Unit, Garvan Institute, Sydney, NSW, Australia
2 Australian Sports Drug Testing Laboratory, Australian Government Analytical Laboratories, Sydney, NSW, Australia
3 Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, VA, USA
* To whom correspondence should be addressed. E-mail: k.ho{at}garvan.org.au.
20-kDa (20K) GH is generated from alternative splicing of the primary transcript of full-length 22K GH. We have studied the regulation of 20K GH over a range of pathophysiological conditions and in response to pharmacological stimulation using isoform specific ELISAs. Mean 24-h levels of 20K and 22K GH were higher in acromegaly and lower in GH deficiency than in normal subjects, with the 20K/22K ratio not different between the three groups. In normal subjects, 20K GH was secreted in a pulsatile manner throughout the day, with peaks coinciding with those of 22K GH. However, the half-life of 20K GH (18.7±0.8min) was significantly longer than that of 22K GH (14.7±0.8 min; P<0.02). Insulin-induced hypoglycemia, androgen and oral estrogen caused a parallel and proportionate increase in both isoforms. Octreotide suppressed 20K less rapidly than 22K GH in blood. Administration of recombinant 22K GH in normal subjects rapidly reduced the 20K GH levels. In conclusion, 20K GH is co-secreted with and circulates at a constant proportion of 22K GH. 20K GH level is reduced by administration of exogenous 22K GH, suggesting rapid negative feedback regulation on pituitary release.
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