Influence Of Growth Hormone Research Articles

Metabolomic profiles and development of metabolic risk during the pubertal transition: a prospective study in the ELEMENT Project.

Objectives:(1) Examine associations of a branched chain amino acid (BCAA) metabolite pattern with metabolic risk across adolescence; (2) Use Least Absolute Shrinkage and Selection Operator (LASSO) to identify novel metabolites of metabolic risk.Methods:We used linear regression to examine associations of a BCAA score with change (Δ) in metabolic biomarkers over 5-years follow-up in 179 adolescents 8–14 years at baseline. Next, we applied LASSO, a regularized regression technique well-suited for reduction of high-dimensional data, to identify metabolite predictors of Δbiomarkers.Results:In boys, the BCAA score corresponded with decreasing C-peptide, C-peptide insulin resistance (CP-IR), total (TC) and low-density-lipoprotein cholesterol (LDL). In pubertal girls, the BCAA pattern corresponded with increasing C-peptide and leptin. LASSO identified asparagine as a predictor of decreasing C-peptide (β=−0.33) and CP-IR (β=−0.012); and acetylcarnitine (β=2.098), 4-hydroxyproline (β=−0.050), ornithine (β=−0.353), and α-aminoisobutyric acid (β=−0.793) as determinants of TC in boys. In girls, histidine was a negative determinant of TC (β=−0.033).Conclusions:The BCAA pattern was associated with Δglycemia and Δlipids in a sex-specific manner. LASSO identified asparagine, which influences growth hormone secretion, as a determinant of decreasing C-peptide and CP-IR in boys, and metabolites on lipid metabolism pathways as determinants of decreasing cholesterol in both sexes.

PERTUMBUHAN DAN KELANGSUNGAN HIDUP LARVA IKAN BETOK (Anabas testudineus) YANG DIBERI PENCAHAYAAN DENGAN LAMA WAKTU BERBEDA

ABSTRACT Climbing perch (Anabas testudineus) is a kind of swamp fish which is potentially to be cultivated. Photoperiod is one of factor that influence growth from culture fish larvae. Light also influence growth hormone and make larvae easier to eat their feed because larvae usually visual feeder. The aim of this research is to determine the best photoperiod in larvae of age 3 – 27 days so as to generate growth and survival rate climbing perch of larvae highest in aquarium with defferent of photoperiod. The usage of the research are expected that different photoperiod can influence the growth and survival of climbing perch larvaes. The research was conducted on April - May 2016 in Laboratory of Budidaya Perairan, Faculty of Agriculture, Sriwijaya University. This research methods used completely randomized design (CDR) with use six treatments and three replications of photoperiod those are P1(24L:0D), P2(18L:6D), P3(12L:12D), P4(6L:18D), P5(0L:24D). The parameters of this research are growth, survival rate of climbing perch larvae and maintenance of water quality. The result showed that photoperiod has significant effect of survival rate, weight growth and length growth from climbing perch photoperiod for 24 hours each day (treatments P1) has the highest result for survival rate and growth 81.11%±2.01%, 30.68mm±0.14mm, 0.46g±0.04g. The value of water quality during larvae rearing were temperature 27 – 31 oC, pH 5.70 – 7.10, dissolved oxygen 4.56 – 7.58 mg.L-1 and ammonia 0.02 – 0.11 mg.L-1. Keywords: Climbing perch, Growth, Photoperiod, Survival rate

Influence of The -202 A/C insulin-like growth factor-binding protein-3 promoter polymorphism on individual variation in height in Korean girls.

PurposeThe most common single nucleotide polymorphism in the IGFBP3 promoter region occurs at position -202. This polymorphic variation occurs frequently and may influence growth hormone responsiveness and somatic growth. However, the effects of IGFBP3 promoter polymorphism on growth in children are unknown.MethodsRestriction fragment length polymorphism-based genotyping of the -202 single nucleotide polymorphism was performed in 146 Korean girls aged between 15 and 16 years, who were selected randomly from the Seoul School Health Promotion Center. The participants were divided into 3 groups (tall, medium, and short) according to the height percentile established from normal reference values for Korean children. The serum levels of insulin-like growth factor I (IGF-I) and IGF-binding protein-3 (IGFBP-3) were then compared according to genotype.ResultsThe genotype distribution in the participants was 79 AA (54.1%), 60 AC (41.1%), and 7 CC (4.8%). The C allele frequency at the -202 IGFBP3 position was 25.4% in this group. The mean serum IGFBP-3 concentration in girls with the AA genotype was higher than that in girls with the AC genotype in the medium (P=0.047) and short (P=0.035) groups, respectively. There was no difference in the IGF-I to IGFBP-3 molar ratio between the AA and AC genotype groups (P=0.161).ConclusionIn conclusion, the -202 polymorphism in the IGFBP3 promoter region is assumed to affect the serum concentration of IGFBP-3 in children as well as in adults. However, it is unclear whether this affects physical development according to the concentration of IGFBP-3.

Corticotropin-releasing hormone (CRH)-immunoreactive (IR) axon varicosities target a subset of growth hormone-releasing hormone (GHRH)-IR neurons in the human hypothalamus

It is a general consensus that stress is one of the major factors that suppresses growth. Previous studies revealed that the catecholaminergic and neuropeptide Y (NPY) systems, involved in the activation of stress-related neuronal circuits, influence growth hormone (GH)-release via modulating growth hormone-releasing hormone (GHRH) secretion. Indeed, catecholaminergic and NPY-immunoreactive (IR) axon varicosities abut on the surface of the GHRH neurons forming contacts. These juxtapositions appear to be real synapses and may represent the morphological substrate of the impact of stress on growth. In addition to catecholamines and NPY, there is a vast amount of evidence that corticotropin-releasing hormone (CRH), a major stress hormone, also influences GH secretion. Whether this modulatory effect is direct, or indirect, via the hypothalamic GHRH system, has not been elucidated yet.In the present study, we examined the possibility that CRH influences GH secretion via modulating the GHRH release by direct synaptic mechanisms. Since the verification of these synapses by electron microscopy is problematic in human due to the long post mortem time, in order to reveal the putative CRH-GHRH juxtapositions, light microscopic double label immunohistochemistry was utilized. In the infundibular nucleus, a subset (6%) of the GHRH perikarya received abutting CRH fiber varicosities forming multiple contacts while passing by. No gaps appeared between the contacting elements. The morphology of these CRH-GHRH juxtapositions suggests that, among other neurotransmitters/neuromodulators, CRH influences growth by modulating the hypothalamic GHRH secretion via direct synaptic mechanisms.

Growth hormone receptor polymorphisms and growth hormone response to stimulation test: a pilot study.

No gold standard pharmacological stimulation test exists for the diagnosis of growth hormone deficiency (GHD). In addition, the genetic factors that influence growth hormone (GH) responses remain unclear. This study aimed to determine whether polymorphisms in exon 6 of the GH receptor gene influence responses to the L-arginine GH stimulation test. This study included 27 prepubertal patients with confirmed GHD. GHD was defined as a peak GH level <8 ng/mL in response to pharmacological stimulation. The mean GH peak after L-arginine stimulation was 2.9±2.9 ng/mL. The included patients had the following genotypes at the third position of codon 168: AA (N.=1), AG (N.=15) and GG (N.=11). Patients carrying the AA and AG genotypes exhibited stronger responses to arginine than patients with the GG genotype (3.1±2.7 vs. 1.5±1.3 ng/mL, P=0.01). The approach employed in this study could elucidate GH profiles under physiological and pathological conditions, facilitating improved interpretation of pharmacological stimulation tests.

Does Ramadan fasting affect acylated ghrelin and growth hormone concentrations during short-term maximal exercise in the afternoon?

Ghrelin is an important stomach hormone that influences several metabolic activities and influences growth hormone (GH) release in response to change in energy homeostasis. The aim of this study was to investigate the effect of Ramadan fasting on acylated ghrelin and GH concentrations during a short-term maximal exercise. Eleven male soccer players (age, 22.11 ± 1.3 years; height, 1.76 ± 0.2 m; body mass, 75.3 ± 2.2; mean ± SD) were asked to perform a 30-s Wingate test, during which we recorded the peak (PP) and mean (MP) powers and fatigue index. Measurements were performed in the afternoon at 18:00 h, after three different occasions: (i) one week before Ramadan (BR), (ii) the first week of Ramadan (FWR), and (iii) the fourth week of Ramadan (ER). Blood samples were taken before, immediately and 60 min after the exercise. Our results show that PP and MP were affected by Ramadan fasting with a significant decrease during Ramadan (i.e. FWR and ER) in comparison with ER (p < 0.05). However, no significant difference was observed between BR and FWR (p > 0.05). Also, a significant decrease in body weight and body fat percentage was observed during Ramadan in comparison with ER. From diet record analysis, protein, fat, and carbohydrate decreased significantly during FWR (p < 0.01), often with further decreases by ER. A significant increase in plasma concentrations of ghrelin was observed during the ER (p < 0.001) compared with BR and FWR, and GH levels were significantly higher during ER (p < 0.01) in comparison with BR and FWR. However, the 30-s Wingate tests had no significant effect on plasma concentrations of ghrelin before or during Ramadan. Our study shows that the concentrations of ghrelin and GH change in the last week of Ramadan fasting, though it is unclear if these changes are related to the changes in body composition during Ramadan, or if they are responsible for the change in performance at the short-duration anaerobic test.

The influence of growth hormone on bone and adipose programming.

In utero growth hormone exposure is associated with distinct immediate growth responses and long term impacts on adult physiological parameters that include obesity, insulin resistance, and bone function. Growth hormone accelerates cellular proliferation in many tissues but is exemplified by increases in the number of cells within the cartilaginous growth plate of bone. In some cases growth hormone also potentiates differentiation as seen in the differentiation of adipocytes that rapidly fill upon withdrawal of growth hormone. Growth hormone provokes these changes either by direct action or through intermediaries such as insulin-like growth factor-I and other downstream effector molecules. The specific mechanism used by growth hormone in programming tissues is not yet fully characterized and likely represents a multipronged approach involving DNA modification, altered adult hormonal milieu, and the development of an augmented stem cell pool capable of future engagement as is seen in adipose accrual. This review summarizes findings of growth hormone's influence on in utero and neonatal cellular and metabolic profiles related to bone and adipose tissue.

Performing resistance exercise before versus after aerobic exercise influences growth hormone secretion in type 1 diabetes

We compared growth hormone (GH) and plasma glucose (PG) levels in type 1 diabetic individuals performing aerobic before resistance exercise (AR) to when resistance exercise was performed first (RA). In AR, GH secretion declined in late exercise while it rose throughout exercise in RA, resulting in higher GH in RA versus AR at exercise completion. Higher GH during RA may support PG by increasing hepatic glucose production and lipid mobilization.

Radiation-induced hypopituitarism in children with acute lymphoblastic leukemia

Background:Acute Lymphoblastic Leukemia (ALL) is the most common malignancy among children for whom radiotherapy and chemotherapy are used for treatment. When hypothalamus-pituitary axis is exposed to radiotherapy, children's hormone level and quality of life are influenced. The aim of this study is to determine late effects of radiotherapy on hormonal level in these patients.Materials and Methods:In this study 27 children with ALL, who have been referred to Shahid Ramezanzadeh Radiation Oncology Center in Yazd-Iran and received 18-24 Gy whole brain radiation with Cobalt 60 or 9 MV linear accelerator, were assessed. These patient's basic weight, height and hormonal levels were measured before radiotherapy and also after different periods of time.Results:GHD (growth hormone deficiency) after clonidine stimulation test was observed in 44% (n=12) and that in 50% of them (n=6), less than 1 year, had been passed from their radiation therapy. None of these patients demonstrated hormone deficiency in other axes.Conclusions:This study showed that even application of a 18-24 Gy radiation dose might influence growth hormone levels; therefore, we recommend reduction of radiotherapy dose in such patients whenever possible.

Oral contraception enhances growth hormone responsiveness to hyper‐ and hypoglycaemia

Plasma glucose levels influence growth hormone concentrations. Oral contraceptives are known to affect circulating growth hormone levels and glucose metabolism. While growth hormone plays an important role in hypoglycaemia counter-regulation, it has been shown that oral contraceptives increase growth hormone concentrations. In this context, we tested if serum growth hormone concentrations display a differential response on glycaemic variations in healthy women using oral contraceptives and those not using contraceptives. Fifteen healthy women with oral contraceptive treatment and 10 without participated in a stepwise hyper- and hypoglycaemic glucose clamp procedure. Serum growth hormone concentrations were measured at euglycaemic baseline and subsequently at plasma glucose plateaus of 8.8, 6.8, 4.8 and 2.8 mmol/l. Growth hormone values were significantly higher in women using oral contraceptives throughout the experiments (P = 0.001). Hyperglycaemia decreased growth hormone concentrations in women using oral contraceptives (P = 0.009), but not in those who were not using oral contraceptives (P = 0.241). Hypoglycaemia significantly elevated growth hormone concentrations in women using oral contraceptives (P = 0.009), but not in those not using oral contraceptives (P = 0.094). Maximum growth hormone values were reached at the end of the hypoglycaemic plateau, with significantly higher concentrations in the group using oral contraceptives than in the group not using oral contraceptives (P = 0.016). Healthy women on oral contraceptive treatment display an increased responsiveness of growth hormone to hypoglycaemic, as well as hyperglycaemic conditions and generally higher serum growth hormone concentrations than women without oral contraceptives. Given the known boosting effects of growth hormone on hypoglycaemic hormonal counter-regulation, oral contraceptives may thus be a pharmacological candidate contributing to combat hypoglycaemia unawareness in women with diabetes in the future.

Poor Specificity of Low Growth Hormone and Cortisol Levels During Fasting Hypoglycemia for the Diagnoses of Growth Hormone Deficiency and Adrenal Insufficiency

Fasting tests are used to identify the cause of hypoglycemia in children. The purposes of this study were to (1) determine whether growth hormone and cortisol levels obtained at the time of hypoglycemia in such tests can identify children with growth hormone and/or cortisol deficiency and (2) identify potential clinical factors that influence growth hormone and cortisol responses to hypoglycemia. The design consisted of chart review of all diagnostic fasting tests conducted over a 3-year period (n = 151). A normal growth hormone level was defined as >/=7.5 ng/mL, and a normal cortisol level was defined as >/=18 mug/dL. During the fasting tests, 84 children (median age: 1.3 years [2 days to 14.3 years]), became hypoglycemic, with blood glucose </=50 mg/dL. Diagnoses included normal, ketotic hypoglycemia, hyperinsulinism, fatty acid-oxidation defects, glycogen-storage disease, and late dumping hypoglycemia. A total of 70% had growth hormone and cortisol levels less than the "normal" thresholds regardless of diagnosis. Of various factors (age, diagnosis, fast duration, duration blood glucose level of <60 mg/dL, and blood glucose nadir), only age was positively associated with cortisol, and none were consistently related to growth hormone. A singe low growth hormone or cortisol value at the time of fasting hypoglycemia has poor specificity for the respective diagnoses of growth hormone deficiency and adrenal insufficiency.

Bone ultrasonometric features and growth hormone secretion in asthmatic patients during chronic inhaled corticosteroid therapy

Background Quantitative ultrasound bone densitometry (QUBD) is a new method to assess bone mineral density and bone microarchitecture. Corticosteroid (CS) therapy may diminish bone mass, alter bone quality and may influence growth hormone (GH) secretion and bone metabolism markers. Therefore, the aim of this study was to evaluate the effects of long-term therapy with inhaled CSs (ICSs) on structural bone characteristics and their correlations with GH secretion and bone markers in asthmatic patients. Methods In a cross-sectional study, we enrolled 60 adult patients with mild to moderate persistent asthma: 22 on chronic (>1 year) ICS therapy, 10 naive to ICSs treatment and 28 healthy control subjects. The groups were matched for age and BMI. Each subject underwent to QUBD at the phalanxes to assess bone microarchitecture by ultrasound bone profile index (UBPI), bone density by amplitude-dependent speed of sound (AdSos); test with GH-releasing hormone (GHRH) injection with calculation of peak GH and the Δ GH (peak GH–basal GH); and hormonal and bone markers measurements. Results Asthmatics treated with long-term ICS therapy showed a lower UBPI ( P < 0.01) compared to controls (49.8 ± 19.3 vs. 77.0 ± 10.1, respectively) and to asthmatics never taking ICSs (73.2 ± 9.6). In ICS-treated asthmatics, ΔGH and GH-peak showed a significant correlation with UBPI. A significant difference was observed comparing asthmatics treated with ICSs to controls and asthmatics naive to ICSs in GH response to GHRH iv bolus. Serum osteocalcin was significantly reduced in asthmatic patients treated with ICSs. Conclusions In asthmatic patients, long-term ICSs treatment produces negative effects on bone quality assessed by QUBD, and such effects are associated to an impaired GH secretion.

Seeking SOCS and sex steroids

In seeking to explain why oral estrogen inhibits the GH–IGF-I axis, a recent study has unearthed a new way that steroid hormones can influence growth hormone action. This involves suppressors of cytokine signalling (SOCS), which offer a new level of understanding in signal control and crosstalk.

Endocrine rhythms in patients with restless legs syndrome.

There is increased evidence that the dopaminergic system plays a major role in the pathophysiology of the restless legs syndrome (RLS). Dopamine is the major inhibitory factor of prolactin release and also influences growth hormone (hGH) secretion. The aim of this study was to measure the endocrine activity of RLS patients, to compare it with that of normal subjects and to detect possibly altered patterns of hormonal secretion in RLS patients. Prolactin, hGH and cortisol plasma levels were measured every 20 min for 24 hours in 10 male never-medicated RLS patients (aged 56 +/- 6 years) who have had mild to moderate symptoms for 15 +/- 10 years and in 8 age-matched male controls (aged 57 +/- 5 years). The blood samples taken during the night were paralleled by polysomnographic recordings including the assessment of periodic leg movements (PLM). Plasma levels as well as frequency and amplitude of the pulses of prolactin, hGH and cortisol were not different between RLS patients and controls. Both groups showed the same rhythms during the night- and daytime for all hormones. Cross correlations resulted in high correlation coefficients for each hormone at lag 0 (0.964,0.943 and 0.971 for mean locations of cortisol, hGH and prolactin, respectively). Concerning sleep parameters, there were no significant differences between the two groups apart from a higher PLMS arousal index in RLS patients (25.9 +/- 17.1) compared with the controls (12.0 +/- 9.2; p < 0.05). It is suggested that a possible dysfunction of the dopaminergic system in RLS does not affect the release of prolactin and hGH from the pituitary gland.

Effects of direct and indirect acetylcholine receptor agonists on growth hormone secretion in humans

Cholinergic pathways in the central nervous system positively influence growth hormone (GH) secretion. In fact pyridostigmine, a cholinesterase inhibitor, enhances both basal and GH-releasing hormone (GHRH)-induced GH secretion while, conversely, pirenzepine, an antagonist of muscarinic M 1 receptors, inhibits the GH response to GHRH and to other physiological and pharmacological stimuli. The effect of the cholinergic system on GH secretion probably takes place via inhibition of the release of endogenous somatostatin. In this study in 36 normal adults (26 males and 10 females, age 22–35 years) we compared the effects of three cholinesterase inhibitors (pyridostigmine, 120 mg p.o., n = 19; neostigmine, 10 μg/kg i.v., n = 6; physostigmine, 12.5 μg/kg i.v., n = 6) and bethanechol, a direct muscarinic receptor agonist that is mainly active on muscarinic M 3 receptors (25 μg/kg i.v., n = 5), on both basal and GHRH (1 μg/kg i.v.)-stimulated GH secretion. Pyridostigmine, neostigmine and physostigmine induced a significant GH increase (peak vs. basal levels, mean ± S.E.: 10.4 ± 1.6 vs. 0.6 ± 0.2 μg/l, P = 0.0001; 13.3 ± 1.2 vs. 0.5 ± 1.1 μg/l, P = 0.004; and 14.9 ± 3.1 vs. 2.7 ± 1.1 μg/l, P = 0.025;, respectively). These drugs also induced a similar potentiation of the GH response to GHRH (peak: 48.3 ± 5.6 vs. 16.2 ± 2.2 μg/l, P = 0.0001; 49.2 ± 2.2 vs. 19.9 ± 5.1 μg/l, P = 0.006; and 76.9 ± 12.4 vs. 18.1 ± 5.3 μg/1, P = 0.001, respectively). By contrast, bethanechol neither enhanced basal GH secretion (peak vs. basal level: 3.3 ± 1.2 vs. 2.6 ± 1.2 μg/l) nor potentiated the GH response to GHRH (peak: 16.3 ± 1.3 vs. 15.4 ± 1.6 μg/l). The present findings strongly confirm the stimulatory role of aetylcholine on GH secretion in man, showing that indirect acetylcholine receptor agonists stimulate GH secretion, while the muscarinic M 3 agonist bethanechol does not. The results exclude that cholinergic stimulation of GH secretion is mediated by muscarinic M 3 receptors, in keeping with the hypothesis that muscarinic M 1 receptors play the main role in the neuroregulation of GH secretion.

Factors Affecting Circulating Growth Hormone Binding Protein in Chickens

Growth hormone binding protein (GHBP) may be an important factor in the regulation of growth and might provide an indirect, relatively noninvasive means of predicting the status of hepatic growth hormone receptor (GHR) activity. Several factors have been reported to influence growth hormone (GH), GHR, or GHBP. Therefore, these studies were conducted to test how age, sex, nutritional status, and glucocorticoids (cortisone acetate, CA) influence serum concentrations of chicken GHBP. Serum GHBP activity was highest (mean percentage specific binding (%SB) = 12.43 ± .80) at hatch and decreased linearly (P < .0001) to 5 wk of age (%SB = 1.99 ± 1.13). There were no sex-related differences in serum GHBP activity from hatch to 5 wk of age (P > .08). Short-term nutrient deprivation (24-h) of 4-wk-old broilers also had a significant effect on serum GHBP activity (P < .0001). Measurement of serum GHBP activity with refeeding (after a 24-h period without feed) restored %SB to normal values. Feeding broilers a low-protein diet (12% CP) did not significantly affect serum GHBP activity when compared with that of broilers fed a commercial broiler diet (23% CP; P > .30). Administration of cortisone (1, 5, and 10 mg/day), every 24 h for 7 days, had no effect, at any dose, on serum GHBP activity at 48 h and 1 wk after the last injection. These results indicate that serum GHBP activity is influenced by factors such as age and feed deprivation. It remains to be determined whether these changes in GHBP are associated with changes in GHR as reported for mammalian species.

Effect of bovine somatotropin (growth hormone) treatment on gonadotropin profiles and ovarian follicle populations during the postpartum period in beef cows in low body condition

Cows in low body condition exhibit a prolonged postpartum anoestrous period and a delayed return to normal follicular function (Prado et al 1990). Previous studies have shown that the effects of body condition on gonadotrophin profiles are inconsistent (Wright et al 1990; Rhind et al 1992) indicating that the effects of body condition on ovarian function cannot be explained by changes in gonadotrophin profiles alone. Since nutritional state influences growth hormone profiles which in turn can affect ovarian function (Gong et al 1991), it was postulated that the effects of body condition on the duration of postpartum anoestrus could be mediated through changes in profiles of this hormone.The aim of the present study was to determine the effect of growth hormone on ovarian follicle development and associated gonadotrophin profiles in post-partum beef cows.

Delta sleep-inducing peptide administration does not influence growth hormone and prolactin secretion in normal women

The aim of this study was to analyze the effects of delta sleep-inducing peptide (DSIP) on growth hormone (GH) and prolactin (PRL) secretion in eight healthy women with normal cycles (aged 17–36 years). GH and PRL secretion was studied in five women after DSIP (25 μg/kg bw IV over 30 min), arginine chlorhydrate (0.5 g/kg bw IV over 30 min) and simultaneous DSIP plus arginine chlorhydrate administration. In three other women the circadian rhythm of GH and PRL was studied during DSIP (25 μg/kg bw from 2130h to 2230h) and placebo IV infusion. Serum GH and PRL levels were normal under basal conditions and no effects were noted after the infusion of DSIP. The GH and PRL circadian rhythm was not modified by DSIP administration. DSIP did not influence GH and PRL responsiveness to arginine chlorhydrate. We found that at dosages which are known to modify ECG patterns, DSIP is unable to modify spontaneous or arginine chlorhydrate-induced GH and PRL secretion.

Effect of Recombinant Human Insulin-Like Growth Factor-I on Weight Gain, Fat Content, and Hormonal Parameters in Broiler Chickens

Osmotic minipumps were implanted in 4-wk-old female broiler chickens to supply a 2-wk continuous infusion of recombinant human insulin-like growth factor-I (rhIGF-I) in three doses (.03, .1, and .3 mg/kg BW per day). At the end of the experimental period no differences in BW were detected, although abdominal fat was significantly reduced in the highest dose group. Measurement of fat content in both breast and thigh muscle indicated a different effect of IGF-I treatment on these parameters, as no reduction was observed. Determination of circulating IGF-I levels revealed a twofold increase in the .3-mg group whereas the lowest dose did not increase circulating plasma levels. The changes in IGF-I levels did not influence growth hormone levels whereas thyroxine levels were significantly decreased both in the .03- and .3-mg groups after 1 wk of treatment. At the same time plasma triiodothyronine levels were increased in the .1- and .3-mg/kg groups. These results indicate that a continuous infusion of IGF-I did not increase weight gain but may play a role as a fat repartitioning agent.

The growth hormone secretory response to fentanyl in rat: an involvement of μ type receptors

Fentanyl, a selective mu opioid receptor agonist, administered intravenously, influences growth hormone secretion in conscious male rats. A dose-response study demonstrated that the maximum growth hormone release was obtained with 10 micrograms/kg while higher doses were less or not effective. MR-2266 (6 mg/kg i.v.), a mu and kappa opioid receptor antagonist, and bremazocine (0.1 mg/kg i.v.) a mu opioid receptor antagonist with kappa agonistic properties, both potently inhibited the growth hormone response to fentanyl (10 micrograms/kg i.v.). In contrast, the effect of fentanyl on growth hormone release was not blocked in rats treated with either ICI-154129 (30 mg/kg i.v. or 150 micrograms/kg intracerebroventricularly a selective delta opioid receptor antagonist, or U-50488 (10 mg/kg i.v.), a specific kappa opioid receptor agonist. These results suggest that opioid receptors of the mu type are involved in the fentanyl-induced growth hormone release.