title: Growth hormone-binding protein in normal and pathologic gestation: correlations with maternal diabetes and fetal growth.
abstract: To date, measurements of GH-binding protein (GHBP) during human pregnancy have been carried out using assays susceptible to interference by the elevated levels of human placental GH typical of late gestation. We recruited a large cohort of pregnant women (n = 140) for serial measurements of GHBP and used the ligand immunofunctional assay for GHBP. For normal gravidas, GHBP levels fell throughout gestation. Mean levels were 1.07 nmol/L (SE = 0.18) in the first trimester, 0.90 nmol/L (SE = 0.08) at 18-20 weeks, 0.73 nmol/L (SE = 0.05) at 28-30 weeks, and 0.62 nmol/L (SE = 0.06) at 36-38 weeks. GHBP levels in the first trimester correlated significantly with maternal body mass index (r = 0.58; P < 0.01). GHBP levels in pregnancies complicated by noninsulin-dependent diabetes mellitus (NIDDM) were substantially elevated at all gestational ages. The mean value in the first quarter (2.29 nmol/L) was more than double the normal mean (P < 0.01). In contrast, patients with insulin-dependent diabetes mellitus (IDDM) showed reduced GHBP concentrations at 36-38 weeks. The correlation between body mass index and GHBP is consistent with a metabolic role for GHBP during pregnancy, as is the dramatic elevation in GHBP observed in cases of NIDDM. At 36 weeks gestation, GHBP was significantly elevated (P < 0.01) in those women whose neonates had low birth weight (< 10th percentile). In early gestation (< 14 weeks), GHBP tended to be higher in women whose fetuses were designated to be at risk of intrauterine growth retardation (1.39 nmol/L; n = 4; compared with 1.07 nmol/L in normals), but this did not reach statistical significance. Although both NIDDM and IDDM pregnancies are at risk of fetal macrosomia, their GHBP concentrations are markedly divergent. This paradox and the roles of glucose and insulin in the regulation of GHBP during gestation warrant further investigation.
authors.affiliation: Co-operative Research Center for Diagnostic Technologies, Queensland University of Technology, Brisbane, Australia.
authors.forename: R
authors.initials: R
authors.lastname: Barnard
authors.forename: F Y
authors.initials: FY
authors.lastname: Chan
authors.forename: H D
authors.initials: HD
authors.lastname: McIntyre
mesh_terms: D002352:Carrier Proteins / Q000097:blood*; D015331:Cohort Studies; D003922:Diabetes Mellitus, Type 1; D003924:Diabetes Mellitus, Type 2; D005314:Embryonic and Fetal Development; D005260:Female; D005317:Fetal Growth Retardation; D005865:Gestational Age; D006801:Humans; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D009994:Osmolar Concentration; D011247:Pregnancy / Q000097:blood*; D011254:Pregnancy in Diabetics / Q000097:blood*; D012016:Reference Values; D012307:Risk Factors
chemical_list: D002352:Carrier Proteins; C051815:somatotropin-binding protein