{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T13:21:28Z","timestamp":1790860888435,"version":"4.1.0"},"reference-count":35,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Endocrinology and Metabolism"],"published-print":{"date-parts":[[2002,10,1]]},"abstract":"<jats:p>The 20-kDa growth hormone (GH) is generated from alternative splicing of the primary transcript of full-length 22-kDa GH. We have studied the regulation of 20-kDa GH over a range of pathophysiological conditions and in response to pharmacological stimulation using isoform-specific enzyme-linked immunosorbent assays (ELISAs). Mean 24-h levels of 20- and 22-kDa GH were higher in acromegaly and lower in GH deficiency than in normal subjects, with the 20-to-22-kDa ratio not different between the three groups. In normal subjects, 20-kDa GH was secreted in a pulsatile manner throughout the day, with peaks coinciding with those of 22-kDa GH. However, the half-life of 20-kDa GH (18.7 \u00b1 0.8 min) was significantly longer than that of 22-kDa GH (14.7 \u00b1 0.8 min; P &lt; 0.02). Insulin-induced hypoglycemia, androgen, and oral estrogen caused a parallel and proportionate increase in both isoforms. Octreotide suppressed 20-kDa less rapidly than 22-kDa GH in blood. Administration of recombinant 22-kDa GH in normal subjects rapidly reduced the 20-kDa GH levels. In conclusion, 20-kDa GH is cosecreted with and circulates at a constant proportion of 22-kDa GH. The 20-kDa GH level is reduced by administration of exogenous 22-kDa GH, suggesting rapid negative feedback regulation on pituitary release.<\/jats:p>","DOI":"10.1152\/ajpendo.00122.2002","type":"journal-article","created":{"date-parts":[[2015,2,27]],"date-time":"2015-02-27T15:11:19Z","timestamp":1425049879000},"page":"E836-E843","source":"Crossref","is-referenced-by-count":52,"title":["Physiological and pharmacological regulation of 20-kDa growth hormone"],"prefix":"10.1152","volume":"283","author":[{"given":"Kin-Chuen","family":"Leung","sequence":"first","affiliation":[{"name":"Pituitary Research Unit, Garvan Institute of Medical Research, St. Vincent's Hospital, Sydney, New South Wales 2010;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chris","family":"Howe","sequence":"additional","affiliation":[{"name":"Australian Sports Drug Testing Laboratory, Australian Government Analytical Laboratories, Sydney, New South Wales 2073, Australia; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lily Y.-Y.","family":"Gui","sequence":"additional","affiliation":[{"name":"Pituitary Research Unit, Garvan Institute of Medical Research, St. Vincent's Hospital, Sydney, New South Wales 2010;"},{"name":"Australian Sports Drug Testing Laboratory, Australian Government Analytical Laboratories, Sydney, New South Wales 2073, Australia; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Graham","family":"Trout","sequence":"additional","affiliation":[{"name":"Australian Sports Drug Testing Laboratory, Australian Government Analytical Laboratories, Sydney, New South Wales 2073, Australia; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes D.","family":"Veldhuis","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ken K. 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