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

1993 ◽  
Vol 128 (2) ◽  
pp. 184-191 ◽  
Author(s):  
Bálint Kacsóh ◽  
Judith S Opp (Meyers) ◽  
William R Crowley ◽  
Clark E Grosvenor
Keyword(s):  
Growth Hormone ◽  
Neonatal Rat ◽  
Female Rats ◽  
Adrenergic System ◽  
Neonatal Rats ◽  
Humoral Factors ◽  
Adrenergic Agents ◽  
Gh Secretion ◽  
Old Rats ◽  
Serum Gh

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 α2-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 α2-adrenergic system and the nursing-induced changes in GH secretion could account for the discrepancy. Rat pups were treated with clonidine (150 μg/kg) or the α2-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. As in two-day-old pups, clonidine prevented the suckling-induced release of GH and failed to induce GH-release above that of saline-injected, separated pups. By day 10 postpartum. clonidine became capable of stimulating GH release, but only in separated male pups. The effects of CLO and nursing in male pups were not additive: either treatment alone was as effective as the combined treatment. In female rats CLO prevented the increase in serum GH levels in response to nursing. It is concluded that (1) the α2-adrenergic agents yohimbine and clonidine inhibit nursing-induced GH secretion in an indirect (perhaps hypothermia-related) manner not involving the well-established α2-adrenergic-GH releasing hormone pathway; (2) the α2-adrenergic system becomes fully functional in terms of stimulation of GH secretion between days 8 and 10; (3) the GH-releasing effects of the α2-adrenergic system are sexually dimorphic in 10-day-old rats.

Effects of refeeding of undernourished and insulin treatment of diabetic neonatal rats on IGF and IGFBP

1996 ◽  
Vol 271 (2) ◽  
pp. E223-E231 ◽  
Author(s):  
L. Goya ◽  
F. Rivero ◽  
M. A. Martin ◽  
R. Arahuetes ◽  
E. R. Hernandez ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Growth Factor ◽  
Mrna Expression ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Insulin Like Growth Factor ◽  
Neonatal Rats ◽  
Igf I ◽  
Serum Gh

The effect of refeeding and insulin treatment of undernourished and diabetic neonatal rats, respectively, on the regulation of insulin-like growth factor (IGF) and insulin-like growth factor binding protein (IGFBP) was investigated. The changes in body weight, insulinemia, glycemia, serum IGF-I, and growth hormone (GH) as well as the increase of the 30-kDa IGFBP in undernourished and diabetic neonatal rats previously shown elsewhere were reversed by refeeding and insulin treatment, respectively. Also, changes in liver mRNA expression of IGF-I and-II and IGFBP-1 and -2 were restored in refed undernourished and IGF-I and IGFBP-1 levels recovered in insulin-treated diabetic rats. However, serum GH was still below normal after rehabilitation in both situations. Thus the present results support the idea of a GH-independent IGF/ IGFBP regulation mediated by a balance of insulin and nutrients as has already been suggested in previous neonatal studies.

Is there a place for urinary growth hormone measurement?

1993 ◽  
Vol 128 (3) ◽  
pp. 197-201 ◽  
Author(s):  
Maria N Moreira-Andrés ◽  
Francisco J Cañizo ◽  
Federico Hawkins
Keyword(s):  
Growth Hormone ◽  
Screening Method ◽  
Small Sample ◽  
Point Of View ◽  
Intrasubject Variability ◽  
Gh Secretion ◽  
Lack Of Information ◽  
Low Levels ◽  
Plasma Gh ◽  
Serum Gh

The evaluation of growth hormone (GH) secretion is an important problem in pediatric endocrine practice. The diagnosis of GH insufficiency is based on the finding of a "blunted" GH response to GH provocative tests or on the demonstration of a decreased endogenous secretion. From a practical point of view, these methods are uncomfortable, expensive and time consuming. Recently, very sensitive specific assays to measure human GH in urine have been developed. We present a discussion of available data on these tests in order to estimate their role in the evaluation of a short or slowly growing child. The present available assays allow measuring very low levels of GH in a small sample of untreated urine. The main limitations of urinary GH measurement are the intrasubject variability, wide normal range, overlapping results in several GH secretory states and lack of information on GH pulsatility. However, most of these limitations also apply to other tests of GH secretion. The advantage of urinary GH tests is that they provide, in an easy procedure, information on serum GH concentration. There is good correlation between urinary and serum GH concentration and several findings suggest that urinary GH excretion reflects changes in plasma GH levels during the period of urine collection. Therefore, the usefulness of urinary GH measurement is that of a simpler and cheaper screening method for assessing integrated serum GH concentration in clinical practice.

EFFECTS OF OESTRADIOL-17β, OESTRADIOL BENZOATE AND THE SYNTHETIC OESTROGEN RU 2858 ON SEXUAL DIFFERENTIATION IN THE NEONATAL FEMALE RAT

1975 ◽  
Vol 67 (3) ◽  
pp. 419-424 ◽  
Author(s):  
CYNTHIA DOUGHTY ◽  
JANET E. BOOTH ◽  
P. G. McDONALD ◽  
R. F. PARROTT
Keyword(s):  
Rat Brain ◽  
Sexual Differentiation ◽  
Neonatal Rat ◽  
Female Rats ◽  
Sexual Receptivity ◽  
Female Rat ◽  
Neonatal Rats ◽  
Oestradiol Benzoate ◽  
Ovarian Cyclicity ◽  
Neonatal Rat Brain

SUMMARY Groups of neonatal female rats were treated for the first 5 days of life with oestradiol-17β, oestradiol benzoate or a synthetic oestrogen, 11β-methoxy-17-ethynyl-1,3,5(10)-oestratriene-3,17β-diol (RU 2858), in daily doses ranging from 0·5 to 1000 ng. Oestradiol-17β had no effect on adult ovarian cyclicity or sexual receptivity after ovariectomy and oestrogen + progesterone treatment. Ovarian cyclicity was prevented by 100 ng or more oestradiol benzoate/day, and by all doses of RU 2858. Only rats receiving 50 ng oestradiol benzoate/ day or 0·5 ng RU 2858/day showed normal receptivity. The defeminizing action of RU 2858 was at least 100 times greater than that of oestradiol benzoate; it is suggested that this greater potency is due to the low affinity of RU 2858 for the oestradiol-binding protein in the plasma of neonatal rats. These results indicate that defeminization of the neonatal rat brain can be induced by physiological amounts of oestrogen, and are discussed with reference to the action of testosterone.

Inhibition of foetal growth hormone (GH) and thyrotrophin (TSH) secretion after maternal administration of somatostatin

1984 ◽  
Vol 106 (3) ◽  
pp. 393-399 ◽  
Author(s):  
Elio Roti ◽  
Giuseppe Robuschi ◽  
Alessandro Alboni ◽  
Rossella Emanuele ◽  
Lorenzo d' Amato ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Cord Blood ◽  
Pregnant Women ◽  
Marked Decrease ◽  
Maternal Blood ◽  
Gh Secretion ◽  
Foetal Growth ◽  
Tsh Secretion ◽  
Maternal Administration ◽  
Serum Gh

Abstract. Somatostatin (SRIF) was infused (500 μg over 30 min) into 68 pregnant women during labour. As a control, saline was infused into 26 pregnant women. Maternal blood was obtained prior to the infusion and at delivery and cord blood was obtained at delivery. The subjects were divided into 4 groups based upon the interval of time from the termination of SRIF infusion and delivery. There was a marked decrease in cord blood thyrotrophin (TSH) from 0 to 180 min and in cord blood growth hormone (GH) from 0 to 120 min following SRIF infusion. SRIF infusion did not affect cord blood iodothyronine and thyroglobulin concentrations. SRIF administration induced a small but significant (P < 0.05) decrease in serum GH concentration but had no other effect on maternal hormone values. These studies strongly suggest that SRIF crosses the human placenta and transiently suppresses foetal anterior pituitary TSH and GH secretion.

scholarly journals Effects of gender on exercise-induced growth hormone release

1999 ◽  
Vol 87 (3) ◽  
pp. 1154-1162 ◽  
Author(s):  
Laurie Wideman ◽  
Judy Y. Weltman ◽  
Niki Shah ◽  
Shannon Story ◽  
Johannes D. Veldhuis ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Area Under The Curve ◽  
Interactive Effects ◽  
Men And Women ◽  
Gh Secretion ◽  
Exercise Condition ◽  
Calculated Mass ◽  
Exercise Induced ◽  
Serum Gh ◽  
Secretion Rates

We examined gender differences in growth hormone (GH) secretion during rest and exercise. Eighteen subjects (9 women and 9 men) were tested on two occasions each [resting condition (R) and exercise condition (Ex)]. Blood was sampled at 10-min intervals from 0600 to 1200 and was assayed for GH by chemiluminescence. At R, women had a 3.69-fold greater mean calculated mass of GH secreted per burst compared with men (5.4 ± 1.0 vs. 1.7 ± 0.4 μg/l, respectively) and higher basal (interpulse) GH secretion rates, which resulted in greater GH production rates and serum GH area under the curve (AUC; 1,107 ± 194 vs. 595 ± 146 μg ⋅ l−1⋅ min, women vs. men; P = 0.04). Compared with R, Ex resulted in greater mean mass of GH secreted per burst, greater mean GH secretory burst amplitude, and greater GH AUC (1,196 ± 211 vs. 506 ± 90 μg ⋅ l−1⋅ min, Ex vs. R, respectivley; P < 0.001). During Ex, women attained maximal serum GH concentrations significantly earlier than men (24 vs. 32 min after initiation of Ex, respectively; P = 0.004). Despite this temporal disparity, both genders had similar maximal serum GH concentrations. The change in AUC (adjusted for unequal baselines) was similar for men and women (593 ± 201 vs. 811 ± 268 μg ⋅ l−1⋅ min), but there were significant gender-by-condition interactive effects on GH secretory burst mass, pulsatile GH production rate, and maximal serum GH concentration. We conclude that, although women exhibit greater absolute GH secretion rates than men both at rest and during exercise, exercise evokes a similar incremental GH response in men and women. Thus the magnitude of the incremental secretory GH response is not gender dependent.

EFFECTS OF NEONATALLY INJECTED NON-ESTERIFIED TESTOSTERONE ON REPRODUCTIVE FUNCTIONS IN FEMALE RATS

1971 ◽  
Vol 66 (4) ◽  
pp. 720-726 ◽  
Author(s):  
T. Alklint ◽  
A. Norgren
Keyword(s):  
Exposure Time ◽  
Testosterone Propionate ◽  
Female Rats ◽  
List Type ◽  
Double Dose ◽  
Neonatal Rats ◽  
Duration Of Action ◽  
Old Rats

ABSTRACT The effect of 1.5 mg testosterone (T) given to neonatal rats of various ages was compared with that of 1.5 mg testosterone propionate (Tp) injected into 5 day old rats. Androgenization of the rats was obtained: with Tp in 100 per cent, with T on day 2 in 79 per cent, with T on day 5 in 50 per cent, with T on day 10 in 18 per cent, with a double dose of T on day 5 in 61 per cent, with T on day 5 and 10 in 100 per cent. The results emphasize the importance of the duration of action of the preparation given. The possibility is considered that a minimal exposure time of more than a few hours is required to produce androgenization of 5 day old female rats.

Growth hormone responses to multiple injections of a fragment of human growth hormone-releasing factor in conscious male and female rats

1985 ◽  
Vol 106 (3) ◽  
pp. 281-289 ◽  
Author(s):  
R. G. Clark ◽  
I. C. A. F. Robinson
Keyword(s):  
Growth Hormone ◽  
Human Growth ◽  
Female Rats ◽  
Male Rats ◽  
Normal Male ◽  
Male And Female ◽  
Gh Secretion ◽  
Male And Female Rats ◽  
Hormone Responses ◽  
Males And Females

ABSTRACT The GH responses to single i.v. injections of GH-releasing factor (GRF) in conscious male rats are highly variable. Although normal male rats show a pulsatile secretory pattern of GH with pulses occurring at intervals of 3–3·5 h, the peaks occur at different times in individual animals. We have compared the GH responses of young conscious male and female rats to multiple i.v. injections of 1 μg human (h) GRF1-29NH2. The peak GH responses occurred 3–5 min after hGRF1-29NH2 injection and were lower in female than in male rats. Both males and females responded uniformly to hGRF1-29NH2 injections given 180 min apart and the GH responses became entrained with no endogenous GH pulsing. Female rats produced consistent GH peaks in response to hGRF1-29NH2 injections at 90-min intervals, whereas male rats responded only to alternate injections, so that GH peaks occurred only every 180 min despite giving GRF every 90 min. When the frequency of hGRF1-29NH2 administration was increased to once every 40 min female rats again responded consistently to each injection. Male rats responded intermittently, being able to respond to two injections 40 min apart, after which they became refractory to hGRF1-29NH2. This cycle of varying sensitivity to GRF in male rats probably underlies their 3-hourly endogenous GH secretory rhythm. Female rats can respond uniformly to repeated GRF injections, consistent with their more continuous pattern of endogenous GH secretion. Introducing a pulse of 10 μg rat GH into a series of hGRF1-29NH2 injections did not induce refractoriness to hGRF1-29NH2, suggesting that GH does not itself desensitize the pituitary to GRF. Whether the different patterns of GH secretion in males and females result from different patterns of GRF and/or somatostatin secretion remains to be determined. J. Endocr. (1985) 106, 281–289

Growth hormone in exercise: comparison of physiological and pharmacological stimuli

1976 ◽  
Vol 41 (4) ◽  
pp. 523-527 ◽  
Author(s):  
J. Sutton ◽  
L. Lazarus
Keyword(s):  
Growth Hormone ◽  
Cycle Ergometer ◽  
Serum Growth Hormone ◽  
Insulin Hypoglycemia ◽  
Arginine Infusion ◽  
Provocative Test ◽  
Gh Secretion ◽  
Ergometer Exercise ◽  
Normal Males ◽  
Serum Gh

This study was designed to compare the serum growth hormone (GH) response with quantified exercise to that obtained with other stimuli. In eight normal males, aged 21–24 yr, we studied the serum GH response to 20 min cycle ergometer exercise at 300, 600, and 900 kpm/min on three separate occasions and compared the results with those found during sleep, insulin hypoglycemia, arginine infusion, and L-DOPA. Exercise at 900 kpm/min and insulin hypoglycemia resulted in the greatest elevations in serum GH which weresignificantly greater than those found with sleep, arginine or L-DOPA. The 20-min exercise at 900 kpm/min represented 75–90% of the subjects' maximal oxygen uptake and is a suitable provocative test for GH secretion. As a screening test for pituitary GH reserve, exercise compares favorably with insulin hypoglycemia and is superior to sleep, arginine, and L-DOPA.

Synergy ofl-arginine and growth hormone (GH)-releasing peptide-2 on GH release: influence of gender

2000 ◽  
Vol 279 (4) ◽  
pp. R1455-R1466 ◽  
Author(s):  
Laurie Wideman ◽  
Judy Y. Weltman ◽  
James T. Patrie ◽  
C. Y. Bowers ◽  
Niki Shah ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Young Adults ◽  
Stimulus Type ◽  
Follicular Phase ◽  
Analysis Of Covariance ◽  
Gh Secretion ◽  
Basal Serum ◽  
Nested Anova ◽  
Early Follicular Phase ◽  
Serum Gh

We test the hypotheses that 1) growth hormone (GH)-releasing peptide-2 (G) synergizes with l-arginine (A), a compound putatively achieving selective somatostatin withdrawal and 2) gender modulates this synergy on GH secretion. To these ends, 18 young healthy volunteers (9 men and 9 early follicular phase women) each received separate morning intravenous infusions of saline (S) or A (30 g over 30 min) or G (1 μg/kg) or both, in randomly assigned order. Blood was sampled at 10-min intervals for later chemiluminescence assay of serum GH concentrations. Analysis of covariance revealed that the preinjection (basal) serum GH concentrations significantly determined secretagogue responsiveness and that sex ( P = 0.02) and stimulus type ( P < 0.001) determined the slope of this relationship. Nested ANOVA applied to log-transformed measures of GH release showed that gender determines 1) basal rates of GH secretion, 2) the magnitude of the GH secretory response to A, 3) the rapidity of attaining the GH maximum, and 4) the magnitude or fold (but not absolute) elevation in GH secretion above preinjection basal, as driven by the combination of A and G. In contrast, the emergence of the G and A synergy is sex independent. We conclude that gender modulates key facets of basal and A/G-stimulated GH secretion in young adults.

scholarly journals Acute hyperglycemia and activation of the beta-adrenergic system exhibit synergistic inhibitory actions on growth hormone (GH) releasing hormone-induced GH release

2003 ◽  
pp. 635-640 ◽  
Author(s):  
C Park ◽  
I Yang ◽  
J Woo ◽  
S Kim ◽  
J Kim ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Continuous Infusion ◽  
Adrenergic System ◽  
Beta Adrenergic ◽  
Acute Hyperglycemia ◽  
Gh Secretion ◽  
Regulatory Systems ◽  
Adrenergic Antagonist ◽  
Cholinergic Pathway ◽  
Design And Methods

OBJECTIVE: Acute hyperglycemia stimulates somatostatin (SRIH) release by the hypothalamus which, in turn, suppresses growth hormone (GH) secretion from the anterior pituitary gland. Although it has been suggested that the cholinergic pathway mediates glucose-induced SRIH release, other regulatory systems have not been examined. Therefore, we investigated whether blocking or activating the beta-adrenergic pathway alters glucose-mediated inhibition of GH release. DESIGN AND METHODS: One set of experiments was performed with a beta-adrenergic antagonist, propranolol, and the other set with a beta-adrenergic agonist, isoproterenol. Each set of experiments was performed in ten healthy subjects and consisted of four tests. Test 1, a 100 microg GHRH bolus i.v. at 0 min; test 2, 100 g glucose orally at -30 min, followed by a 100 microg GHRH bolus at 0 min; test 3, after a 100 microg GHRH bolus i.v. at 0 min, a continuous infusion of propranolol (0.2 mg/kg) or isoproterenol (0.012 microg/kg) was administered between 0 and 120 min; test 4, after a 100 g glucose oral load at -30 min, and a 100 microg GHRH bolus i.v. at 0 min, a continuous infusion of propranolol (0.2 mg/kg) or isoproterenol (0.012 microg/kg) was administered between 0 and 120 min. Blood was drawn every 10 min from -30 min to 120 min to measure GH and glucose concentrations. RESULTS: Pretreatment with glucose significantly suppressed GHRH-induced GH secretion. Propranolol infusion significantly increased the GHRH-induced GH secretion, but it did not block glucose-induced suppression of GH secretion. Isoproterenol infusion alone significantly suppressed GHRH-induced GH secretion and augmented the inhibitory action of glucose on GH release. CONCLUSION: This study demonstrates that glucose-induced suppression of GHRH-stimulated GH release is independent of beta-adrenergic tone. Since previous data supports a role for SRIH in both glucose and beta-adrenergic suppression of GH release, the current results suggest that subsets of SRIH neurons are differentially responsive to these external cues. Therefore, a combined glucose and isoproterenol test may provide a useful assessment of hypothalamic somatostatinergic activity.

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