Investigation of 17kDa human growth hormone fragment in serum as a marker for human growth hormone doping

The 5th IOC World Congress Awards ~arke-Davis Awards: Medica| Science (d[la[ winners) Investigation of 17kDa Human Growth Hormone Fragment in serum as a Marker for Human Growth Hormone Doping C Howe 1, K Leung 2, K Emslie1, G Trout 1 & K Ho2 1Australian Sports Drug Testing Laboratory, Australian Government Analytical Laoratories, Pymble, Australia. 2pituitary Research Unit, Garvan Institute of Medical Research, Sydney, Australia. H u m a n growth hormone (GH) is secreted from the pituitary primarily as a peptide of molecular size 22 kDa {22K). The pituitary also contains other forms of GH, including a 17 kDa form (17K) which lacks 43 amino acid residues from the N-terminus of the 22K isoform. Little is known of the physiology of 17K GH. The aim of this study was to determine whether 17K is a reliable marker of pituitary GH secretion. As pituitary GH secretion is subject to feedback regulation, we postulated that suppression of 17K, or changes in tile ratio of 17K to 22K GH occurs with exogenous use of recombinant 22K GH. After developing a radioimmlmoassay (RIA) specific for t7K, we measured integrated 24tl 17K and 22K levels in normal, GH deficient (GHD) and acromegalic subjects, GH responses to a stimulation test, GH changes following octreotide {a somatostatin analogue) admim'stratio11 in acromegalie patients and the respective levels in GH deficient subjects after administration of recombinant 22K GH. The RIA showed <2% crossreactivity with 22K and other isoforms. The limit of detection was 0.75 ng/ml, and intra- and interassay CVs were 3.4% and 11.9% respectively. Mean 24tl 17K concentrations were higher in acromegalic (6.85(0.37 ng/ml, n=12; P<0.05) than in normal subjects (5.30_+0.47 ng/ml, i1=16). The 17K level was significantly lower in GH deficiency (3.79_+0.18 ng/ml, n=16; P<0.01) but was clearly measurable, in contrast to 22K, which was below the limit of detectability (<0.4 ng/ml). Insulin-induced hypoglyeaemia in normal subjects induced a significant increase in 17K (1.32_+0.51 to 2.39_+0.45 ng/ml) which occurred in parallel with a rise in 22K (0.53±0.24 to 7.75_+2.17 11g/ml). Octreotide treatment significantly reduced 17K, as it did 22FL Administration of recombinant hGH to GIlD subjects increased serum 22K levels in a dose-dependent fashion, while having no effect on 17K.

Heterogeneity in the Osteotrophic Response to Exercise During Different Stages of Puberty L Saxon*, S Bass & R Daly School of Health Sciences, Deakin University, Burwood, Australia Very little is known about the surface specific effects of exercise on cortical bone in humans. It has been hypothesised that exercise increases bone accrual on the periosteal surface duling premenarcheal years and on the endocortical surface after menarche 1. The aim of this study was to determine the effect of exercise on bone mass (BMC), bone geometry, and volumetric bone density (vBMD) during different stages of growth. These traits were compared in the playing and non-playing humerli of 6 pre-menareheal, and 13 post-menarcheal (1.8_+0.2 yrs) female tennis players. Bone geometry and BMC of humeral mid-third was determined using magnetic resonance imaging (MR[) and DEXA respectively. The pre- and post- menarcheal players were aged 12.1±0.7 and 14.2±0.5 yrs, had been training for 5.6_+0.7 and 6.9_+0.3 yrs, and were

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