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PubMed1993

Intranasal administration of growth hormone-releasing hormone(1-29)-NH2 in children with growth hormone deficiency: effects on growth hormone secretion and growth.

The growth-promoting potential of growth hormone-releasing hormone(1-29)-NH2 (GHRH(1-29)-NH2) in a new formulation for intranasal use was examined in a 6-month pilot study of eight short prepubertal children. The maximal plasma concentration of growth hormone (GH) was below 12 micrograms/l in two stimulation tests (arginine, insulin), but above 12 (24-90) micrograms/l after intravenous GHRH, 1 microgram/kg. GHRH, 50 micrograms/kg, was insufflated intranasally three times per day over 6 months. On day 1, GHRH insufflations were followed by distinct GHRH and GH plasma peaks, ranging from 1.2 to 5.4 micrograms/l and from 10 to 85 mIU/l, respectively. Peak amplitudes were variably reduced after 6 weeks in most patients, and further reduced at 6 months. GHRH antibodies (initially negative) were positive in three patients after 6 weeks. The mean knemometric growth rate rose from 0.24 to 0.48 mm/week after 6 weeks of treatment (p = 0.03) and then rapidly declined; the mean 6-month stadiometric height velocity did not increase. Local tolerance was good in one patient; most others reported sneezing immediately after insufflation, rhinorrhoea and mild mucosal burning. Treatment was discontinued in two patients after 6 and 12 weeks. It is concluded that intranasal GHRH, though non-invasive, is not suitable in its present form for use in children, because of decreasing absorption and effectiveness with concomitant development of antibodies and local reactions.

Administration, Intranasal↗
PubMed1997

Developmental pattern of fetal growth hormone, insulin-like growth factor I, growth hormone binding protein and insulin-like growth factor binding protein-3.

AIMS: To evaluate the developmental pattern of fetal growth hormone (GH), insulin-like growth factor I (IGF-I), GH binding protein (GHBP) and IGF binding protein-3 (IGF-3); to determine the implications for fetal growth. METHODS: Serum GH, IGF-I, GHBP and IGFBP-3 were measured in 53 fetuses, 41 aged 20-26 weeks (group A) and 12 aged 31-38 weeks (group B). Fetal blood samples were obtained by direct puncture of the umbilical vein in utero. Fetal blood samples were taken to rule out beta thalassaemia, chromosome alterations, mother to fetus transmissible infections, and for maternal rhesus factor. GHBP was determined by gel filtration chromatography of serum incubated overnight with 125I-GH. GH, IGF-I and IGFBP-3 were determined by radioimmunoassay. RESULTS: Fetal serum GH concentrations in group A (median 29 micrograms/l, range 11-92) were significantly higher (P < 0.01) than those of group B (median 16.7 micrograms/l, range 4.5-29). IGF-I in group A (median 20 micrograms/l, range 4.1-53.3) was significantly lower (P < 0.01) than in group B (median 75.2 micrograms/l, range 27.8-122.3). Similarly, IGFBP-3 concentrations in group A (median 950 micrograms/l, range 580-1260) were significantly lower than those of group B (median 1920 micrograms/l, range 1070-1770). There was no significant difference between GHBP values in group A (median 8.6%, range 6.6-12.6) and group B (median 8.3%, range 6-14.3). Gestational age correlated positively with IGF-I concentrations (P < 0.0001) and IGFBP-3 (P < 0.0001) and negatively with GH (P < 0.0001). GHBP values did not correlate with gestational age. Multiple regression analysis showed a negative correlation between GH:IGF-I ratio and fetal growth indices CONCLUSIONS: The simultaneous evaluation of fetal GH, IGF-I, IGFBP-3 and GHBP suggests that the GH-IGF-I axis might already be functional in utero. The progressive improvement in the efficiency of this axis in the last part of gestation does not seem to be due to an increase in GH receptors.

Biomarkers↗
PubMed1997

Growth response to growth hormone (GH) treatment relates to serum insulin-like growth factor I (IGF-I) and IGF-binding protein-3 in short children with various GH secretion capacities. Swedish Study Group for Growth Hormone Treatment.

The purpose of the study was to evaluate the relationship between the 1-yr (n = 193) and 2-yr (n = 128) growth response and the individual serum concentrations of insulin-like growth factor I (IGF-I) and IGF-binding protein 3 (IGFBP-3) before and during GH treatment. Our study group of prepubertal short children had from very low to high GH secretory capacity, estimated during an arginine-insulin tolerance test, and the ages ranged from 3-15 yr at the start of treatment. Their serum levels of IGF-I and IGFBP-3 were low before treatment compared to those in an age-related reference group of prepubertal children and increased significantly from the start to 1 month of GH treatment. The mean increase in height SD score was 0.80 SD score after 1 yr of GH treatment and 1.26 SD score after 2 yr, with a wide range. In univariate analyses the highest correlation coefficients to the 2-yr growth response were found to be vs. the following variables from the start of treatment: IGF-I SD score (r = -0.49), log maximum GH concentration (log GHmax) during the arginine-insulin tolerance test (r = -0.47), difference between the height SD score of the individual child and the midparental height SD score (diffSD score; r = -0.45), IGFBP-3 SD score (r = -0.39), age (r = -0.30), short term change in IGFBP-3 SD score (r = 0.37), and IGF-I SD score (r = 0.34). In multivariate stepwise regression analysis, 41% of the variation in the 2-yr growth response could be explained by IGF-I SD score or log GHmax together with age at the start of treatment, weight SD score at 1 yr of age, and diffSD score. When both IGF-I SD score and GHmax were included and when the short term changes in IGF-I SD score were added, 46% and 58% of the variation, respectively, could be explained. The regression algorithms using different combinations of variables and their corresponding prediction intervals are also presented.

Adolescent↗
PubMed1992

Growth hormone and insulin-like growth factor regulate insulin-like growth factor-binding protein-1 in Laron type dwarfism, growth hormone deficiency and constitutional short stature.

Insulin-like growth factors (IGFs) mediate the effects of growth hormone (GH), and the insulin-like growth factor-binding proteins (IGFBPs) modulate the actions of IGFs in tissues. We studied the circulating levels of IGFBP-1 in 6 children and 9 adults with Laron type dwarfism (LTD), in 11 children and 21 adults with growth hormone deficiency (GHD), and in 8 children with constitutional short stature. Compared with the situation in healthy children, the basal serum IGFBP-1 concentration was 5.4-fold higher in LTD children, 4.1-fold higher in GHD children, and 3.8-fold higher in children with short stature (p < 0.02 vs controls in all groups). In adult patients with multiple pituitary hormone deficiency (MPHD), the IGFBP-1 concentration was 2-fold elevated, but it was normal in adult LTD patients. Intravenous (N = 10) or subcutaneous (N = 9) administration of IGF-I (75 micrograms.kg-1 and 150 micrograms.kg-1, respectively) in LTD children resulted in a rapid 50-60% fall in serum insulin (p < 0.02), a decline in blood glucose and a concomitant 40-60% rise of IGFBP-1 levels (p < 0.05). Treatment for seven days with IGF-I (150 micrograms.kg-1 x d-1) resulted in a decrease by 34% and 44% of serum IGFBP-1 level in two out of three children with LTD. After prolonged GH therapy, the IGFBP-1 level fell in GHD children by 29% (p < 0.05), in GHD adults by 52% (p < 0.02) and in children with constitutional short stature by 17% (p < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Linear regression analysis of ultrasound follicular growth series: statistical relationship of growth rate and calculated date of growth onset to total growth period.

Linear regression analysis was used to assess the serial growth of carefully measured individual mean follicular diameters as a function of menstrual age in a group of normal volunteers in natural, unstimulated cycles (n = 18). Follicle diameter (FD) growth, as measured with serial pelvic ultrasonography, can be shown to be essentially linear (mean R2, 0.92) with respect to time up to the point of ovulation. Growth rate (k) and the calculated date of growth onset (Do) are obtainable from the individual regression equations. Because an approximation of the date of ovulation (Dov, measured by menstrual age at the date of peak mean follicular size) is an available parameter, total growth period (TGP) is calculated with the equation (TGP = Dov - Do). Do, k, and TGP are highly correlated with one another. The mean parameters (+/- standard deviation) are Do = 4.29 +/- 2.77 day, k = 0.24 +/- 0.07 cm/day, TGP = 10.32 +/- 2.35 day, peak FD = 2.34 +/- 0.28 cm, and Dov = 14.61 +/- 2.00 day. The internal correlation of these parameters predicts that information from the first several scans in an individual series may be used to forecast date of ovulation. This may represent an improvement over the use of follicle size or menstrual age alone in planning for human chorionic gonadotropin administration, insemination timing, follicular aspiration and other interventions.

Adult↗
PubMed1991

Growth regulation in the gobiid teleost, Gillichthys mirabilis: roles of growth hormone, hepatic growth hormone receptors and insulin-like growth factor-I.

Studies of the teleost Gillichthys mirabilis were undertaken to assess the role of GH in regulating hepatic GH receptors, insulin-like growth factor-I (IGF-I) activity and cartilage growth. Hypophysectomized G. mirabilis were injected with saline vehicle or with 10, 100 or 1000 ng tilapia GH (tGH)/g every other day for 2-3 weeks. Growth, judged by increased body weight and length, was inhibited by hypophysectomy and stimulated by increasing tGH doses. Hepatic GH receptors, measured by 125I-labelled tGH binding, were decreased 50% by hypophysectomy. An additional dose-dependent reduction in binding was observed 24 h after tGH injection, but MgCl2 stripping of membranes suggested receptor occupation by exogenous tGH. IGF-I activity, measured by 35SO4 incorporation into oral cartilage explants in vitro, was decreased 50% by hypophysectomy and increased to 200% of intact control levels after injection of 1000 ng tGH/g. In a second experiment, 35SO4 incorporation by oral cartilage from hypophysectomized fish injected with 10, 100 or 1000 ng tGH/g was stimulated to intact control levels. Effects of feeding and tGH injection on in-vitro responsiveness of oral cartilage to recombinant bovine IGF-I (rbIGF-I; 10-1000 ng/ml) were also assessed. Oral cartilage from fed fish showed a parabolic dose-response curve, whereas oral cartilage from starved fish had a lower basal rate of 35SO4 incorporation and a linear dose-response relationship. Oral cartilage from hypophysectomized G. mirabilis showed a significantly attenuated response to rbIGF-I which was restored by tGH injection, suggesting that the GH status of the animal is important for sensitivity of target tissue to IGF-I. Because of its similarity to other vertebrate systems, G. mirabilis presents a good teleost model of growth regulation and of the functions and interactions of GH and IGF-I.

Animals↗
PubMed1991

Serum insulin-like growth factors and insulin-like growth factor binding proteins in the human fetus. Relationships with growth in normal subjects and in subjects with intrauterine growth retardation.

IGF-I, IGF-II, and their binding proteins (BP) were studied in sera obtained by direct puncture of umbilical cords in utero between 20 and 37 wk of gestation in 103 normal fetuses and in 16 fetuses with intrauterine growth retardation, as well as in the cord blood of 37 normal newborns of 38- to 42-wk pregnancies. In normal fetuses, IGF-I levels were approximately 50 ng/mL and IGF-II levels approximately 350 ng/mL up to the 33rd wk of pregnancy. Thereafter, both increased to reach values two to three times higher at term. Correlations were found between fetal placental lactogen levels and those of IGF-I and IGF-II, which is consistent with the hypothesis that placental lactogen is involved in the regulation of IGF synthesis in the fetus. With weight (either measured at birth or deduced from echographical data) as index of fetal size, IGF-I levels were significantly (p less than 0.001) higher in fetuses with weights above the mean for gestational age than in fetuses with weights below the mean, whereas IGF-II levels were similar in the two groups. Similarly, IGF-I (but not IGF-II) levels in fetuses with intrauterine growth retardation were significantly lower than those in normal fetuses of the same age (p less than 0.01). These findings suggest that, during the latter months of intrauterine life, IGF-I (but not IGF-II) is involved in the control of fetal size. Total fetal BP concentrations were approximately 1/3 those of adults. The fetal electrophoretic profile obtained by Western-ligand blotting bore a strong resemblance to that of subjects with growth hormone deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Constitution↗
PubMed1995

Effects of maternal protein malnutrition on fetal growth, plasma insulin-like growth factors, insulin-like growth factor binding proteins, and liver insulin-like growth factor gene expression in the rat.

We examined the effects of maternal dietary protein restriction on fetal growth and expression of IGF-I and -II, and IGF-binding proteins (IGFBP). We sought to dissociate the respective effects of maternal protein versus calorie restriction on growth indices and IGF synthesis by the neonates of protein-restricted dams. Pregnant Wistar rats (six to eight per group) fed a low (5%) protein diet throughout gestation had impaired body weight gain compared with controls fed a normal (20%) protein diet (by 45%, p < 0.001). Their serum and liver IGF-I concentrations and liver IGF-I mRNA concentrations were also reduced by 60, 80, and 50%, respectively. Serum IGFBP-3 was reduced by 60% in protein-restricted dams within 1 to 2 h after delivery (p < 0.001 versus controls), although IGFBP-1, -2, and -4 were not significantly affected by the dietary protein intake. In pups of protein-restricted dams, the mean body and liver weight at birth was 15-20% less than that observed in the progeny from normal protein-fed dams (p < 0.01). Their plasma and liver IGF-I concentrations were 30 and 60% lower, respectively, whereas liver IGF-I mRNA abundance was reduced by 50% (p < 0.01). In contrast, neonatal plasma IGF-II and liver IGF-II mRNA concentrations were not significantly affected by the maternal protein malnutrition. Also, the plasma levels of IGFBP were not altered in the growth-retarded pups. Maternal protein restriction did not affect fetal and placental growth, plasma and liver IGF-I levels, and liver IGF-I mRNA abundance in 20-d-old fetuses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

A four year dose-response study of recombinant human growth hormone treatment of growth hormone deficient children: effects on growth, bone growth and bone mineralization.

To evaluate the effects of two regimens of recombinant human GH (rhGH) on growth, bone growth and bone mineralization in GH deficient children, we studied two groups (A and B), each including 16 GH deficient children matched for sex, age, body mass index, height, height velocity and bone age/chronological age ratio (BA/CA). Group A was treated with a weekly rhGH dose of 1IU/kg and group B with 0.5IU/kg. After four years of therapy, we evaluated the auxological outcome, bone morphometry (metacarpal index: MI) and bone mineralization by quantitative roentgen microdensitometry at the middle region of the II metacarpal and ultra-distal radius. Height increased significantly in both groups, being significantly higher in group A after four years of therapy, while BA/CA remained similar in the two groups. Bone growth (measured by the MI), and bone mineral density at the metacarpal (mostly trabecular bone) and at the ultra-distal radial (mostly cortical bone) site did not differ in the two groups, nor did these three parameters differ from normal controls. In conclusion, after four years a greater height gain was achieved by the higher dose of rhGH compared with the conventional dose, but there were no differences in bone growth and mineralization.

Body Height↗
PubMed1993

Effect of growth hormone administration frequency on 24-hour growth hormone profiles and levels of other growth related parameters in girls with Turner's syndrome. Dutch Working Group on Growth Hormone.

OBJECTIVE: The optimal dose and frequency of GH administration in Turner's syndrome is unknown. There is some evidence that a schedule which mimics normal pulsatile GH secretion may be more effective than a single daily dose. We therefore wished to study the influence of the frequency of GH administration on 24-hour GH profiles and levels of other growth-related factors in Turner's syndrome. DESIGN: Four weeks after initiation of 0.05 microgram/kg/day ethinyl oestradiol, we compared twice daily (b.i.d.-fractionated dose) with once daily (o.d.) s.c. injections of 6 IU GH/m2/day in a 2-week cross-over design with a 2-week washout interval. Each treatment period was concluded with 24-hour GH profile tests. Pretreatment plasma/serum levels of GH, IGF-I, binding proteins for GH (GHBP) and IGF-I (IGFBP-3) were used as a basis for comparison of the levels found after each regimen. A one-compartment open model was used for estimation of pharmacokinetic parameters. SUBJECTS: Ten previously untreated girls with Turner's syndrome aged > or = 11 years. MEASUREMENTS: Plasma levels of GHBP by standardized binding assay; GH, IGF-I, and IGFBP-3 serum/plasma levels by radioimmunoassay. RESULTS: There were significantly higher maximum GH levels and a greater area under the curve with o.d. than with b.i.d. GH, while GH clearance was greater with b.i.d. The pharmacokinetic values with o.d. injections were in conformity with values for healthy and GH-deficient children. Pretreatment GHBP levels tended to be high compared with values in healthy prepubertal children. These levels decreased with GH therapy, significantly so with b.i.d. GH only. There was a significant increase in levels of IGF-I and IGFBP-3, irrespective of regimen. The IGF-I to IGFBP-3 ratio, a possible indicator of the growth response, rose significantly and comparably with both regimens. There was no consistent diurnal variation with either regimen in GHBP, IGF-I or IGFBP-3 levels. Four-hourly levels of GH, GHBP, IGF-I and IGFBP-3 were not correlated. CONCLUSIONS: Although the 24-hour profiles differed during once or twice daily administration of the same total growth hormone dose, the diurnal pattern and mean levels of factors involved in the biological effects of GH are comparable for both regimens.

Adolescent↗
PubMed1995

Long-term results of growth hormone therapy in children with short stature, subnormal growth rate and normal growth hormone response to secretagogues. Dutch Growth Hormone Working Group.

BACKGROUND AND OBJECTIVE: Growth hormone treatment in children with idiopathic short stature (ISS) leads to growth acceleration in the first years, but the effect on final height is still poorly documented. We therefore studied the long-term effect of GH therapy in children with idiopathic short stature. DESIGN: We have treated 27 prepubertal children with ISS with recombinant human GH (rhGH) in an initial dosage of 2 IU/m2 body surface/day subcutaneously, which was doubled either after the first year if the height velocity increment was less than 2 cm/year, or thereafter if height velocity fell below the P50 for bone age. Growth and bone maturation of the treatment group (ISS group, n = 21) were compared to those of an untreated control group with ISS (ISS controls, n = 27) and of a group of rhGH treated children with isolated GH deficiency (GHD group, n = 7). RESULTS: In 9 patients of the ISS group still on treatment, height standard deviation score (HSDS) for chronological age increased from -3.8 +/- 0.7 to -2.3 +/- 0.9 (mean +/- standard deviation) over 6 years, while in matched ISS controls HSDS for age did not change. HSDS for age in the GHD group increased from -3.9 +/- 0.6 to -1.8 +/- 0.7 after 4 years, significantly more than the ISS group. Bone maturation was accelerated in the ISS and GHD groups. HSDS for bone age and predicted adult height did not change in either group. Final height in 12 children of the ISS group was -2.6 +/- 1.0 SDS. In the untreated controls final height was similar. A low integrated GH concentration over 24 hours, a low GH peak to provocative stimuli, and minimal initial BA delay predicted a favourable outcome. CONCLUSION: rhGH treatment in this group of children with idiopathic short stature did not increase average final height. Part of the heterogeneity of the response can be attributed to the variation in endogenous GH secretion and initial bone age delay.

Body Height↗
PubMed1993

Auxology and response to growth hormone treatment of patients with intrauterine growth retardation or Silver-Russell syndrome: analysis of data from the Kabi Pharmacia International Growth Study. International Board of the Kabi Pharmacia International Growth Study.

Using the database from the Kabi Pharmacia International Growth Study, 105 patients with intrauterine growth retardation (IUGR) (82 males, 23 females) and 45 with Silver-Russell syndrome (SRS) (32 males, 13 females) with persistent postnatal growth failure were studied. Patients with IUGR had a birth length and birth weight more than 2 SD below the mean for gestational age. Their height deficit at the start of GH treatment was -3.0 SDS at a median chronological age of 8.7 years and a median bone age of 7.0 years. Mean paternal and maternal heights were 166 and 153 cm, respectively. The median dose of GH was 0.5 IU/kg/week, given at a median frequency of five injections/week. The median height SDS for chronological age after 1, 2 and 3 years of GH treatment were -2.5, -2.1 and -1.9, respectively. In the 45 patients with SRS, median chronological age and median bone age at the start of treatment were 6.7 and 3.2 years, respectively, and mean paternal and maternal heights were 167.5 and 160 cm, respectively. The median dose of GH was 0.7 IU/kg/week, given at a median frequency of six injections/week. The median height SDS for chronological age at the start of treatment and after 1, 2 and 3 years were -3.5, -2.9, -2.8 and -2.2, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Birth Weight↗
PubMed1990

Stimulation of bone matrix apposition in vitro by local growth factors: a comparison between insulin-like growth factor I, platelet-derived growth factor, and transforming growth factor beta.

Many recent in vitro studies have shown effects of insulin-like growth factor I (IGF I), platelet-derived growth factor (PDGF), and transforming growth factor-beta (TGF beta) on the proliferation and differential functions of bone-forming osteoblasts; however, the question whether these factors might ultimately lead to a net increase or decrease in bone formation has been difficult to assess. In this study, we have used an autoradiographic method based on the incorporation of [3H]proline into freshly synthesized bone matrix to determine the overall effects of these factors on bone matrix apposition in 21-day-old fetal rat calvariae. IGF I, PDGF, and TGF beta increased bone matrix apposition in a dose-dependent manner up to 2-fold within 48 h. In addition, they partially or completely reversed the inhibition of bone matrix apposition observed with PTH. Exogenously added TGF beta was significantly more potent than equimolar concentrations of PDGF or IGF I in stimulating bone formation. Matrix apposition was greatest when IGF I, PDGF, and TGF beta were added simultaneously to the culture medium, indicating that these factors can enhance each other in stimulating bone formation. In conclusion, our results provide direct evidence that IGF I, PDGF, and TGF beta are capable of stimulating bone formation in vitro.

Animals↗
PubMed2004

A longitudinal study of intrauterine growth and the placental growth hormone (GH)-insulin-like growth factor I axis in maternal circulation: association between placental GH and fetal growth.

The aim of the study was 1) to evaluate the association of maternal serum levels of placental GH and IGF-I with fetal growth, and 2) to establish reference data for placental GH, IGF-I, and IGF-binding protein-3 (IGFBP-3) in normal pregnancies based on longitudinal measurements. A prospective longitudinal study of 89 normal pregnant women was conducted. The women had, on the average, seven blood samples taken and three ultrasound examinations performed. All had normal umbilical artery pulsatility indexes during pregnancy and gave birth to singletons between 37 and 42 wk gestation with birth weights above -2 SD. Placental GH levels were detectable in all samples from as early as 5 wk gestation and increased significantly throughout pregnancy to approximately 37 wk when peak levels of 22 ng/ml (range, 4.64-69.22 ng/ml) were reached. Subsequently, placental GH levels decreased until birth. The change in placental GH during 24.5-37.5 wk gestation was positively associated with fetal growth rate (P = 0.027) and birth weight (P = 0.027). Gestational age at peak placental GH values (P = 0.007) was associated with pregnancy length. A positive association between the change in placental GH and the change in IGF-I levels throughout gestation was found in a multivariate analysis (r(2) = 0.42; P < 0.001). There was no association between placental GH and IGFBP-3 levels. The change in IGF-I throughout gestation (P = 0.039), but not placental GH, was significantly positively associated with placental weight at birth. We found a significant association between placental GH and fetal growth. In addition, we found a highly significant association between the increase in placental GH and the increase in IGF-I. The gestational age at peak placental GH levels was associated with pregnancy length.

Adult↗
PubMed1996

High-affinity growth hormone binding protein, insulin-like growth factor I and insulin-like growth factor binding protein 3 in adults with growth hormone deficiency.

The high-affinity growth hormone binding protein (GHBP) circulates in human blood and represents the extracellular domain of the growth hormone (GH) receptor. The effects of GH deficiency on GHBP in adults are not clear. The aim of this study was to evaluate serum GHBP levels in adults with GH deficiency and to assess whether GHBP measurement may contribute to the diagnosis of adult GH deficiency, based on a two-step model. We measured insulin-like growth factor I (IGF-I), IGF binding protein 3 (IGFBP-3) and GHBP levels in serum samples of 36 patients with adult-onset GH deficiency. The GHBP levels were measured by FPLC size-exclusion chromatography; IGF-I and IGFBP-3 levels were measured by RIA. Serum GHBP levels were elevated above the upper limit of the 95% confidence interval in 26 patients, whereas IGF-I and IGFBP-3 levels were low in 10 patients and in 16 patients, respectively. The combination of low serum IGF-I and low IGFBP-3 levels was found in 10 patients. In nine patients, serum IGF-I levels were low, with elevated GHBP levels. Low serum IGF-I, low IGFBP-3 and elevated GHBP levels were found in five patients. Only four out of 36 patients had serum IGF-I, IGFBP-3 and GHBP levels that were within the 95% confidence interval of the control values. We conclude that adults with acquired GH deficiency have elevated GHBP levels in comparison to healthy subjects. We suggest that measurement of GHBP levels might contribute to the diagnosis of adult GH deficiency, though further research is required to study the additional value of GHBP measurements.

Adult↗
PubMed2000

Epidermal growth factor and insulin-like growth factor I upregulate the expression of the epidermal growth factor system in rat liver.

BACKGROUND/AIM: Both epidermal growth factor and insulin-like growth factor I play a role in connection with the liver. In the present study, the possible interaction of these two growth factor systems was studied by investigating the effect of epidermal growth factor or insulin-like growth factor I treatment on the expression of the epidermal growth factor receptor, and its activating ligands, transforming growth factor-alpha and epidermal growth factor. METHODS: Fifty-five male rats received no treatment, human recombinant epidermal growth factor or human recombinant insulin-like growth factor I for either 3 or 7 days. The amount of epidermal growth factor receptor, transforming growth factor-alpha, and epidermal growth factor mRNA was quantitated by a calibrated user-friendly RT-PCR assay (CURT-PCR), and the expression of transforming growth factor-alpha and epidermal growth factor peptides was quantitated by ELISA. RESULTS: Control liver (n=16) contained a mean (+/-SD) value of 12.7+/-7.4x10(-18) mol epidermal growth factor receptor mRNA, 3.8+/-2.0x10(-18) mol transforming growth factor-alpha mRNA and 0.8+/-0.4x10(-18) mol epidermal growth factor mRNA per microg total RNA and 9.8+/-1.6 fmol/mg protein epidermal growth factor and 144+/-22 fmol/mg protein transforming growth factor-alpha. Both epidermal growth factor and insulin-like growth factor I treatment increased the expression of mRNA for transforming growth factor-alpha and epidermal growth factor receptor, as well as the expression of transforming growth factor-alpha peptide. The level of epidermal growth factor receptor and transforming growth factor-alpha mRNA expression was found to correlate both in control and growth factor-treated animals, whereas the expression of epidermal growth factor receptor and epidermal growth factor showed no correlation. Marked differences were seen upon activation of the two growth factor systems, as epidermal growth factor, but not insulin-like growth factor I treatment, increased the plasma concentration of urea and decreased the concentration of insulin-like growth factor I and the liver enzymes, alanine aminotransferase and alkaline phosphatase. CONCLUSION: Our results show that epidermal growth factor and insulin-like growth factor I, which belong to two different growth factor systems, both induce a correlated upregulation of transforming growth factor-alpha and epidermal growth factor receptor mRNA in rat liver. Although marked differences were observed after treatment with either epidermal growth factor or insulin-like growth factor I on the liver as reflected in the plasma concentrations of e.g. liver enzymes, a common motif in their action involves an upregulation of the expression of the epidermal growth factor system.

Animals↗
PubMed1983

The effect of growth hormone treatment alone or growth hormone with supplemental zinc on growth rate, serum, and urine zinc and copper concentrations and hair zinc concentration in patients with growth hormone deficiency.

Previous studies suggest that growth hormone (GH) may increase daily zinc requirements to meet the demand of growing bone and to replace increased urinary losses. We tested the hypothesis that zinc or copper availability might be limiting factors in the response of children receiving GH replacement. Ten patients with GH deficiency were followed for GH-induced changes in urine and serum zinc and copper during acute (0.3 IU/kg/day X 5 days) and chronic GH treatment (0.1 IU/kg/tiw). Zinc was measured in hair collected every 3 months. Zinc sulfate (220 mg/day) was given to half the patients during the second year of treatment. There was no evidence of zinc or copper deficiency, and zinc supplements did not venhance growth response to GH during the second year of treatment. We conclude that GH treatment in children does not alter serum or urine zinc or copper or hair zinc, and zinc supplementation does not improve growth in children with GH deficiency.

Adolescent↗
PubMed1988

Atenolol enhances growth hormone release to exogenous growth hormone-releasing hormone but fails to alter spontaneous nocturnal growth hormone secretion in boys with constitutional delay of growth.

We tested the hypothesis that selective beta 1-adrenergic blockade will enhance growth hormone (GH) secretion in boys with constitutional delay of growth in response to both exogenously administered growth hormone-releasing hormone as well as to endogenous GH-releasing hormone pulsations. The study group comprised eight healthy, short, prepubertal boys ranging from 7 2/12 to 15 0/12 yr old with bone ages delayed 15 to 42 months. All had demonstrated GH levels of greater than 10 ng/ml following a pharmacologic or physiologic stimulus. During two consecutive nights, blood samples were withdrawn every 20 min for GH determination between 2000 and 0800 h. Immediately after each 0800 h blood withdrawal, 1 microgram/kg of GH-releasing hormone (1-40)-OH was administered intravenously to each subject and blood was withdrawn every 15 min for an additional 2 h. During the day before the second overnight sampling period each subject received atenolol, 25 mg orally, at 1030 and 1600 h to induce beta-adrenergic blockage. The six subjects in whom beta-adrenergic blockade could be documented had enhanced GH release after GH-releasing hormone administration on the atenolol treatment day both in terms of higher peak GH levels achieved (p less than 0.05) as well as greater total GH secretion (3916 +/- 701 versus 5624 +/- 986 ng/ml.min, p less than 0.01). In contrast, there were no differences in endogenous, unstimulated nocturnal GH pulse characteristics between study and control days.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗