Changes In Growth Hormone Secretion Research Articles

Suppression of hyperinsulinemia restores growth hormone secretion and metabolism in obese mice.

The well-balanced secretion between insulin and growth hormone (GH) is essential in regulating substrate metabolism, energy metabolism, and body composition. High insulin and low GH levels are often observed in obesity, contributing to reduced energy expenditure and further fat accumulation. Although suppression of hyperinsulinemia is proposed as a treatment for obesity, changes in GH secretion and energy metabolism following this treatment are not thoroughly studied. This leaves unexplained observations, such as unchanged lean mass following insulin reduction. In this study, high-fat diet-induced obese (DIO) and normal chow-fed lean mice on a C57BL/6J background were treated for 7 weeks with diazoxide (1250 mg/kg in food), a KATP channel opener that suppressed insulin secretion. Diazoxide treatment for 10 days was sufficient to increase pulsatile GH secretion in DIO mice before any significant body weight change. The restored insulin-GH balance in DIO mice was followed by improvement in substrate and energy metabolism in a prolonged treatment period (4-6 weeks), including reduced fat mass, increased lipid oxidation and energy expenditure, as well as improved insulin sensitivity and metabolic flexibility. These metabolic benefits occurred along with the changes in the expression level of genes regulated by the insulin-GH balance. When applying diazoxide to normal chow-fed normoinsulinemic lean mice, none of the above metabolic effects was observed, suggesting that the metabolic changes following diazoxide treatment were mediated through the suppression of hyperinsulinemia. These results suggest that suppression of hyperinsulinemia by diazoxide restores GH secretion and improves substrate and energy metabolism in DIO mice.

Malnutrition, Frailty, and Sarcopenia in Patients With Cirrhosis: 2021 Practice Guidance by the American Association for the Study of Liver Diseases.

Malnutrition, Frailty, and Sarcopenia in Patients With Cirrhosis: 2021 Practice Guidance by the American Association for the Study of Liver Diseases.

Cadmium chronotoxicity at pituitary level: effects on plasma ACTH, GH, and TSH daily pattern

Cadmium is an endocrine disruptor that has been shown to induce chronotoxic effects. The present study was designed to evaluate the possible cadmium effects on the daily secretory pattern of adrenocorticotropin hormone (ACTH), growth hormone (GH), and thyroid-stimulating hormone (TSH) in adult male Sprague-Dawley rats. For this purpose, animals were treated with cadmium at two different doses [25 and 50 mg/l cadmium chloride (CdCl(2))] in the drinking water for 30 days. Control age-matched rats received cadmium-free water. After the treatment, rats were killed at six different time intervals throughout a 24-h cycle. Cadmium exposure modified the 24-h pattern of plasma ACTH and GH levels, as the peak of ACTH content between 12:00 and 16:00 h in controls appeared at 12:00 h in the group treated with the lowest dose used, while it appeared between 16:00 and 20:00 h in rats exposed to 50 mg/l CdCl(2). In addition, the peak of GH content found at 04:00 h in controls moved to 16:00 h in rats exposed to 25 mg/l CdCl(2), and the highest dose used abolished 24-h changes of GH secretion. The metal treatment did not modify ACTH secretory pattern. Exposure to cadmium also increased ACTH and TSH medium levels around the clock with both doses used. These results suggest that cadmium modifies ACTH and TSH medium levels around the clock, as well as disrupted ACTH and GH secretory pattern, thus confirming the metal chronotoxicity at pituitary level.

Growth hormone and insulin-like growth factor of naked carp ( Gymnocypris przewalskii) in Lake Qinghai: Expression in different water environments

Here, we report the cloning and characterization of growth hormone (GH), insulin-like growth factor-I (IGF-I) and IGF-II from naked carp ( Gymnocypris przewalskii), a native teleost fish of Lake Qinghai in the Qinghai-Tibet Plateau of China. The GH of naked carp encodes for a predicted amino acid sequence showing identities of 63%, 63%, 91% and 94% with cherry salmon, rainbow trout, zebrafish and grass carp, respectively. Compared to common carp and goldfish, evolutionary analysis showed that genome duplication has had less influence on the relaxation of purifying selection in the evolution of naked carp GH. Sequence analysis of naked carp IGF-I (ncIGF-I) and ncIGF-II showed a high degree of homology with known fish IGF-I and IGF-II. To investigate effects of salinity and ionic composition of the aquatic environment on the GH–IGF axis in naked carp, male fish held in river water were assigned randomly to 4 groups: RW (river-water), RW + Na (NaCl in RW), RW + Mg (MgCl 2 in RW) and LW (lake-water) groups. The concentrations of Na + in RW + Na and Mg 2+ in RW + Mg were equal to the concentrations of these ions in lake-water. After 2 days of exposure, the plasma IGF-I levels in the RW + Na and LW groups were significantly higher than the control group (RW), and the plasma GH levels of the LW group were also significantly higher than the RW group. The somatostatin (SS) levels in the hypothalamus significantly increased in the RW + Na group. After 5 days of exposure, these hormone levels did not differ significantly among groups. These results indicate that while the plasma GH and IGF-I levels are osmosensitive, the absence of a change in GH secretion in RW + Na might be partly due to a transiently increased release of hypothalamic SS induced by the stress of neutral-saline water. This is the first report of a salinity-induced increase of GH–IGF-I circulating levels in Cypriniformes.

Growth hormone (GH) deficiency in acromegaly: significance of GH stimulatory tests in relation to the twenty-four hour GH secretion

Aims: Radiation therapy for pituitary adenomas frequently leads to growth hormone (GH) deficiency. Whether radiation in acromegaly, due to a GH-secreting pituitary adenoma, induces a comparable change in GH secretion is not known.

Plasma levels of total and active ghrelin in acromegaly and growth hormone deficiency

Ghrelin is an endogenous growth hormone (GH) secretagogue recently isolated from the stomach. Although it possesses a strong GH releasing activity in vitro and in vivo, its physiological significance in endogenous GH secretion remains unclear. The aim of this study was to characterize plasma ghrelin levels in acromegaly and growth hormone deficiency (GHD). We investigated plasma total and active ghrelin in 21 patients with acromegaly, 9 patients with GHD and 24 age-, sex- and BMI-matched controls. In all subjects, we further assessed the concentrations of leptin, soluble leptin receptor, insulin, IGF-I, free IGF-I and IGFBP-1, 2, 3 and 6. Patients with acromegaly and GHD as well as control subjects showed similar levels of total ghrelin (controls 2.004+/-0.18 ng/ml, acromegalics 1.755+/-0.16 ng/ml, p=0.31, GHD patients 1.704+/-0.17 ng/ml, p=0.35) and active ghrelin (controls 0.057+/-0.01 ng/ml, acromegalics 0.047+/-0.01 ng/ml, p=0.29, GHD patients 0.062+/-0.01 ng/ml, p=0.73). In acromegalic patients plasma total ghrelin values correlated negatively with IGF-I (p<0.05), in GHD patients active ghrelin correlated with IGF-I positively (p<0.05). In the control group, total ghrelin correlated positively with IGFBP-2 (p<0.05) and negatively with active ghrelin (p=0.05), BMI (p<0.05), WHR (p<0.05), insulin (p=0.01) and IGF-I (p=0.05). Plasma active ghrelin correlated positively with IGFBP-3 (p=0.005) but negatively with total ghrelin and free IGF-I (p=0.01). In conclusion, all groups of the tested subjects showed similar plasma levels of total and active ghrelin. In acromegaly and growth hormone deficiency plasma ghrelin does not seem to be significantly affected by changes in GH secretion.

Short-term gluten challenge in children with coeliac disease does not impair spontaneous growth hormone secretion.

Growth retardation in children with coeliac disease has been attributed to impaired growth hormone (GH) secretion observed in stimulation tests. This study aimed at investigating the possible change in spontaneous GH secretion during a standardised gluten challenge. Twelve children with previous enteropathy suggesting coeliac disease and a normal pre-challenge biopsy on a gluten-free diet were included; eight of them completed all parts of the study, including repeated 24-h GH sampling. At the start and the end of a 5-6 weeks standardised gluten challenge, blood was drawn at a constant rate for 24 h and collected for GH analysis at 20-min intervals. The graph of plotted GH values was analysed by means of a computer program (PULSAR). No significant changes were seen in the measures of maximum GH peak, baseline GH values, area under the curve over the baseline (AUCb), the number of GH peaks or mean GH concentration. GH secretion rate (GHt) increased slightly. None of the characteristics of the 24-h profile was significantly correlated to the change of IGF-I. No impaired GH secretion was found. Thus, we speculate that decreased growth rate in celiac disease may not be primarily caused by changes in GH secretion. Instead it may be caused by changed peripheral sensitivity to GH.

Age-related changes in growth hormone secretion: should the somatopause be treated?

Growth hormone (GH) secretion declines progressively with aging, and many age-related changes resemble those of the adult GH deficiency (GHD) syndrome, including a decrease in lean body mass; an increase in body fat, especially in the visceral/abdominal compartment; adverse changes in lipoproteins; and a reduction in aerobic capacity. The increase in central obesity can further inhibit GH secretion. GH replacement is effective in reversing many of these changes in adult GHD, and GH is now FDA approved for treatment of adults with documented GHD or hypopituitarism, although there is still only limited experience with its long-term benefits, side effects, and risks. This early experience with GHD has led to speculation that replacing GH or stimulating its secretion may also be beneficial in normal aging, and to widespread off-label use of GH in this context; however, there are still very few well controlled studies of the effects and side effects of GH or GH secretagogues in aging. All published studies are of 6 months or shorter treatment periods. From this limited experience there is a consensus that GH has effects on body composition, but reports disagree on effects on psychological or physical functional performance. Older adults are much more susceptible to the dose-related side effects of GH, including peripheral edema, carpal tunnel syndrome, and a variable decrease in insulin sensitivity; and it is not known whether chronic GH treatment affects the risk of malignancy or has other long-term risks. Thus while short-term results are somewhat encouraging, the evidence on risks and clinically pertinent benefits is still lacking to support the use of GH in normal aging outside of clinical studies. In evaluating patients with clinical features suggesting GHD, which can be quite nonspecific, it is important to assess the presence or absence of true GH deficiency by the context (pituitary disease or its treatment, childhood GHD) and by appropriate GH stimulation tests before considering GH replacement.

Age-Related Changes in Growth Hormone Secretion: Should the Somatopause Be Treated?

Age-Related Changes in Growth Hormone Secretion: Should the Somatopause Be Treated?

Growth hormone status in adults treated for acute lymphoblastic leukaemia in childhood.

Growth hormone status was assessed in a cohort of 32 (16 male) adults who had received cranial irradiation (XRT) in childhood as part of their treatment for acute lymphoblastic leukaemia (ALL) and compared with 35 age matched young adults (18 male). Height and weight were measured in all subjects and the heights of the patients at XRT were obtained from their case notes. Each patient and control underwent two provocative tests of growth hormone (GH) secretion using insulin (0.2 IU/kg body weight) and arginine (20 g/m2). Basal serum insulin like growth factor-1 (IGF-1) and IGFBP-3 (binding protein-3) concentrations were also measured. The patient group had a significantly lower peak GH response to both provocative tests (P < 0.01), and lower IGF-1 and IGFBP-3 levels compared with the normal controls (P < 0.01). Nine of the patient group were severely GH deficient (peak GH response < 9 mU/l to both provocative agents) and a further 12 patients were GH insufficient (peak GH response < 20 mU/l to both tests with at least one peak GH response > 9 mU/l). Overall a significant median change in height from XRT to final height of -0.5 SDS was found which was even greater in the severely GH deficient group (median change in height of -2.1 SDS). These data suggest that a significant proportion of adults treated with cranial XRT in childhood with irradiation doses between 18-25 Gy, as part of their treatment for ALL, are severely GH deficient now and should be considered for GH replacement. Changes in GH secretion evolve with time following irradiation-induced damage to the hypothalamic-pituitary axis; therefore long-term surveillance will be required in those remaining patients, in whom GH status is considered currently to be insufficient or even normal.

Short-Term Modulation of the Androgen Milieu Alters Pulsatile, But Not Exercise- or Growth Hormone (GH)-Releasing Hormone-Stimulated GH Secretion in Healthy Men: Impact of Gonadal Steroid and GH Secretory Changes on Metabolic Outcomes1

Gonadal steroids are known to alter GH secretion as well as tissue metabolism. The present study was designed to examine the effects of short term (2- to 3-week) alterations in gonadal steroids on basal pulsatile (nonstimulated) and exercise- and GH-releasing hormone-stimulated GH secretion, urinary nitrogen excretion, and basal and exercise-stimulated oxygen consumption. Two protocols were conducted, which reflect a total of 18 separate studies. In the first paradigm, 5 healthy young men were each studied in a double blind, randomized manner during 3 different gonadal hormone manipulations, in which serum testosterone was varied from hypogonadal (induced by leuprolide) to eugonadal (saline injections) to high levels (testosterone enanthate, 3 mg/kg.week, i.m.). There was a washout period of 8 weeks between treatments. In the second protocol, 3 of the original subjects were studied after 2 weeks of treatment with stanozolol (0.1 mg/kg.day). Two to 3 weeks after the desired changes in serum testosterone, each subject was admitted to the General Clinical Research Center for study. The hypogonadal state (serum testosterone, 33 ng/dL) increased urinary nitrogen loss (by 34%; P < 0.005) and decreased basal metabolic rate (by 12%; P < 0.02) compared with the eugonadal state (testosterone, 796 ng/dL). High dose testosterone (1609 ng/dL) further decreased urinary nitrogen loss over the eugonadal state (by 16%; P < 0.05). Stanozolol yielded the lowest urinary nitrogen excretion of all (P < 0.03). Like urinary nitrogen, the basal metabolic rate showed the greatest change between the hypogonadal and eugonadal states (12%; P < 0.02), with a lesser change during high dose testosterone treatment (4%). Analogously, end-exercise oxygen consumption rose by 11% between the hypogonadal and eugonadal states (P < 0.05). Between the hypogonadal and eugonadal states, no significant changes in pulsatile (nonstimulated), exercise-stimulated, or GRF-stimulated GH secretion or serum insulin-like growth factor I concentrations were observed. Raising testosterone to supraphysiological levels increased pulsatile GH secretion by 62% over that with leuprolide and by 22% over that with saline (P < 0.05). High dose testosterone treatment also increased serum insulin-like growth factor I concentrations by 21% and 34% over those during the eugonadal and hypogonadal states, respectively (P < 0.01). Testosterone did not affect either exercise- or GRF-stimulated GH secretion. In protocol 2, stanozolol did not affect any parameter of GH secretion. To examine the interaction between GH secretion and testosterone on urinary nitrogen excretion and basal metabolic rate, a one-way analysis of covariance was undertaken. Statistical examination of GH production as the covariate and testosterone (by tertile) as the interactive factor demonstrated significant relationships between serum testosterone levels and either urinary nitrogen (P < 0.02) or basal metabolic rate (P < 0.01), but not GH secretion (P = NS). In summary, these results demonstrate that short term modulation of the androgen milieu affects metabolic outcome without necessitating changes in GH secretion. These results have significance for both normal physiology and for the treatment of hypogonadal GH-deficient patients.

The effect of immunization against somatostatin and β-agonist administration alone and in combination on growth and carcass composition in young steers

AbstractThe effect of active immunization against somatostatin and β-agonist administration alone and in combination on growth, carcass composition and endocrine responses was investigated in young steers given a pelleted diet of dried grass and barley (0·7: 0·3) ad libitum for 16 weeks. Immunization alone increased growth rate by proportionately 0·10 but had no effect on plasma growth hormone (GH) or insulin-like growth factor-1 (IGF-1) concentrations (P &gt; 0·10). Carcass protein content was unchanged but fat content tended to be increased. This was possibly associated with increased (P &lt; 0·10) plasma insulin concentrations observed in these animals. Cimaterol administration significantly increased growth rate (P &lt; 0·05) and carcass weight (P &lt; 0·01). Carcass protein content was significantly (P &lt; 0·01) increased and carcass fat was significantly (P &lt; 0·001) reduced. Administration of cimaterol to immunized animals resulted in an enhancement of the repartitioning effect of the pagonist although growth rates were intermediate between the separate treatments. The mechanism by which this was achieved is unclear. Plasma IGF-1 concentrations tended (P &lt; 0·10) to be lower in these animals compared with controls. Plasma insulin concentrations were also reduced (P &lt; 0·05) in these animals. Both immunized animals and those given cimaterol alone showed an increased GH response to a single intravenous injection of growth hormone releasing factor (GRF) (P &lt; 0·05). Animals given the combined treatment however showed a reduced response suggesting that the effects were not mediated through direct changes in GH secretion. The improved lean:fat ratio in the carcass was observed to be mediated through an enhancement of the lipolytic response to the /J-agonist with only small effects on protein accretion. It is suggested that immunoneutralization of somatostatin may increase the sensitivity of adipose tissue to lipolytic stimuli. This could occur through changes in the secretion of gastrointestinal or pancreatic hormones as a result of neutralization of the inhibitory influences of somatostatin. Further work is required to clarify these effects.

Age-related changes of growth hormone secretion and somatotroph function in Japanese Black Steers

Growth hormone (GH) is a vital component for the regulation of animal growth. The circulating levels of GH decrease with age in bull calves (McAndrews et al., 1993) and in steers (Verde and Trenkle, 1987), and are higher in large Simmental steers than in small Angus steers (Grigsby and Trenkle, 1986). Japanese Black cattle, known as Wagyu, is early-matured and small frame size, and has an ability to deposit the high amount of intramuscular fat. The present study was conducted to clarify the age-related changes of GH secretion and somatotroph function in Japanese Black steers, since the information about endocrine profiles of Japanese Black cattle has been scantly.

Effect of fetal alcohol exposure on postnatal pituitary adenosine 3', 5'-cyclic phosphate content and growth hormone release.

This study examines the influence of fetal ethanol (ETOH) exposure and pair-feeding dams on postnatal, releasing factor-induced pituitary growth hormone (GH) release and adenosine 3',5'-cyclic phosphate (cAMP) accumulation. Fetuses were exposed to ETOH in utero by feeding dams a 36% (calories derived from ETOH: 6.6% v/v) ETOH liquid diet. Postnatal body weights were measured at sacrifice to evaluate the influence of ETOH on growth. Pituitary weight and protein content were measured to determine if changes in GH secretion or cAMP are proportional to the overall effect of ETOH on the pituitary. Pituitaries from 1-, 10-, and 60-day-old pups were explanted and incubated without hormones or with either somatostatin [somatotropin-release inhibiting factor (SRIF); 10(-9) M], or GH-releasing factor (GRF; 5 x 10(-9) M). Radioimmunoassays were used to determine tissue cAMP content, after extraction, and media GH concentration. Results indicate that fetal ETOH exposure specifically reduces the weight of both male and female pups. However, by 60 days of age, this reduction is not different from that found in pups of pair-fed controls, and both groups weighed less than pups of ad libitum controls. Furthermore, both pituitary weight and protein content were proportionately reduced in ETOH-exposed pups. In regard to releasing factor sensitivity, compared with pituitaries from ad libitum controls, the capacity of GRF to simulate GH release was diminished in 10-day-old males (p < 0.006) exposed to ETOH. On the other hand, the capacity of GRF to stimulate cAMP accumulation was generally enhanced by prenatal ETOH exposure. The capacity of SRIF to depress GH release was diminished in ETOH pups, compared with both pair-fed and ad libitum-fed controls (p < 0.0001). This difference in GH release was more apparent in pituitaries from females than males (p < 0.001). However, the depressed SRIF response was not associated with altered cAMP accumulation. These data suggest that fetal ETOH exposure has a sexually dimorphic effect on pituitary sensitivity to GH-releasing factors that may be related to altered regulation of GH release and susceptibility to growth retardation.

Angiogenic activity of anterior pituitary tissue and growth hormone on the chick embryo chorio-allantoic membrane : A novel action of GH

A useful system to evaluate the angiogenic activity of hormones and growth factors is the chorioallantoic membrane (CAM) of chick embryos. The present studies examined the angiogenic activity of chicken anterior pituitary glands and both fibroblast growth factor (FGF) and growth hormone (GH). Grafts of anterior pituitary gland evoked an angiogenic response on the CAM which was lost if the adenohypophyseal tissue was first boiled. The magnitude of the angiogenic response to anterior pituitary glands increased with the age of the donor (from a minimum 15 days of embryonic development to a maximum between 2 and 6 weeks old). In view of the similarity of the profile of the angiogenic response and the reported changes in GH secretion, the angiogenic activity of GH was then examined. Considerable angiogenic responses were observed with GH; there being increases (P < 0.05) in number of new blood vessels on the CAM of chick embryos on which native chicken GH or native bovine GH or recombinant bovine GH were added. These data support GH having an angiogenic action.

A new somatostatin analog with optimized ring size inhibits neointima formation induced by balloon injury in rats without altering growth hormone release

Summary We report on the synthesis and pharmacological properties of a new series of somatostatin analogs. Two lower homologs of lysine, 2,3-diaminopropanoic acid and 2,4-diaminobutyric acid, were prepared and used for cyclization via amide formation with the side chain of aspartic or glutamic acid in place of natural cystine present in many somatostatin analogs. One resulting compound, although having low binding affinities for somatostatin receptors, displayed a strong potency in inhibiting neointima formation induced by balloon injury in rats at the dose of 100 ug·kg−1·d−1 . This dissociation of the antiproliferative effect from the endocrine effect seems to indicate that myointimal growth is not related to a change in growth hormone secretion.

Metabolic acidosis inhibits growth hormone secretion in rats: mechanism of growth retardation

To test the hypothesis that growth retardation in nonanion gap acidosis may be associated with impairment of growth hormone (GH) secretory patterns, we examined GH secretion in rats made acidotic with ammonium chloride ingestion. Considerable growth retardation was demonstrated in pair-fed and acidotic rats after 1 wk of ammonium chloride ingestion compared with control. With stable metabolic acidosis sustained on the 8th day of experiment, pulsatile secretion of GH was evaluated by blood samples drawn every 10 min for 6 h. Using deconvolution analysis to quantitate in vivo GH secretory rates, we found significant inhibition of pulsatile GH secretion in acidotic rats. Changes in amplitude of GH pulses and mean mass of GH pulses correlated with changes in body weight. These studies showed that chronic metabolic acidosis causes growth impairment, reduced food efficiency, and amplitude-specific inhibition of pulsatile secretion of GH. We propose that this GH axis suppression, whether mediated by decreased nutrients or not, contributes significantly to growth failure in children with renal tubular acidosis. Because a similar degree of inhibition of GH secretion was seen in pair-fed rats, we infer that insufficient calorie intake in metabolic acidosis may contribute to disruption of normal GH secretion patterns. These changes in GH secretion were specific, because acidotic rats were different from pair-fed controls in that they showed no change in either half-life of GH in circulation or in pulse frequency. Such observations offer a rationale for more detailed clinical investigations into the impact of metabolic acidosis on physiological regulation of pulsatile GH secretion in humans.

Interaction between the α2-adrenergic system and nursing in the regulation of growth hormone secretion in the neonatal rat

Separation of neonatal rats from their mothers decreases, while a subsequent period of suckling (nursing) increases, serum growth hormone (GH) levels in neonatal rats. Milk-borne (humoral) factors and neural factors inherent in mother-offspring interaction have been implicated in these phenomena. Conflicting reports have demonstrated the alpha 2-adrenergic agonist clonidine to increase and to decrease serum GH levels in 10-day-old rats. The present experiments were aimed at testing whether an interaction between the alpha 2-adrenergic system and the nursing-induced changes in GH secretion could account for the discrepancy. Rat pups were treated with clonidine (150 micrograms/kg) or the alpha 2-adrenergic antagonist yohimbine (10 mg/kg), and the drug treatment was combined with separation of the mothers and nursing. Yohimbine did not affect serum GH levels in separated two-day-old pups (i.e. basal levels of the hormone), but prevented the nursing-induced increase in serum GH concentration. In two-day-old pups, clonidine had no effect on basal GH levels but, like yohimbine, prevented the increase in serum GH normally associated with nursing. Both yohimbine and clonidine prevented active sucking behavior, i.e. the pups did not search for and/or attach to the nipples of their mothers. Moreover, the pups treated with yohimbine and clonidine were cooler to the touch than the littermate controls. In eight-day-old pups, yohimbine prevented the nursing-induced increase in serum GH and decreased GH levels below the saline-injected, separated control.(ABSTRACT TRUNCATED AT 250 WORDS)

The Somatotropic Axis in Puberty

Sex steroids markedly affect GH pulsatility by altering GH pulse amplitude without affecting GH pulse frequency. The type of sex steroid (testosterone or estrogen) appears to determine the timing of the pubertal growth spurt although both steroids appear to influence the amount of GH released from the pituitary. GH levels also affect gonadal secretion of sex steroids. The effects of the two are synergistic, but there is a real therapeutic dilemma of what to increase and when in children who are deficient in either GH or gonadotrophin secretion. Augmented GH pulsatility, particularly during the day, may alter markedly the interpretation of standard endocrine tests. Finally, the insulin resistance arising from an increased circulating concentration of GH may have important implications for the management of insulin-dependent diabetes during puberty.

Effect of ether stress on growth hormone during development in the neonatal rat.

Stress in adult rats causes an inhibition of growth hormone (GH) secretion which might be mediated by corticotropin-releasing factor (CRF). The response of neonates to stress differs from that observed in adults, including changes in GH secretion that are independent of CRF. The present study examines the effects of ether exposure, a stress known to elicit CRF release, on serum GH in the neonatal period. Preliminary experiments indicated that ether elicits increases in serum adrenocorticotropic hormone and corticosterone, and that the latter response is blocked by pretreatment with dexamethasone. Corticosterone was measured as an indicator of hypothalamo-pituitary-adrenal (HPA) axis stimulation for subsequent studies. Rat pups of 5, 8, 10, 15, 18 or 30 days were divided into three groups. Baseline animals were taken for decapitation directly from the mother. Ether animals were exposed to ether fumes for 1 min, returned to the mother after a brief recovery period, and killed 30 min later. Handled control animals were removed from the mother briefly, returned, and similarly killed at 30 min. Blood was assayed for GH and corticosterone. Handling itself stimulated both GH and corticosterone on postnatal days 10 and 15 and suppressed GH and corticosterone on days 5 and 30. Ether significantly lowered GH and increased corticosterone when compared to this handling control from day 8 to 18, but values in ether-treated animals were different from baseline animals only at 5 and 30 days of age. These results indicate that ether stress produces a mild decrease in GH by day 5 postnatally and throughout the neonatal period which is only apparent in relation to 'handled' controls.(ABSTRACT TRUNCATED AT 250 WORDS)