PLASMA LEVELS OF GROWTH HORMONE IN FEMALE RATS OF DIFFERENT AGES

1978 ◽  
Vol 88 (4) ◽  
pp. 676-690 ◽  
Author(s):  
Staffan Edén ◽  
Kerstin Albertsson-Wikland ◽  
Olle Isaksson

ABSTRACT Radioimmunoassayable growth hormone (GH) was determined in fed and fasted female rats of different ages. In 6–40 day-old rats blood was collected at hourly intervals in groups of rats at different time intervals during the day. Within each age group the variation in plasma GH was considerable. In 6–14 day-old rats plasma GH was generally elevated. By day 18 levels declined, lowest on day 22 and by day 26 again increasing. In 14 day-old rats the median plasma level of GH was 22 ng/ml, in 22 day-old rats < 5 ng/ml and in 40 day-old rats 43 ng/ml. In 14 day-old rats levels ranged from < 5 ng/ml – 148 ng/ml, in 22 day-old rats from < 5 ng/ml – 34 ng/ml and in 40 day-old rats from < 5 ng/ml – > 200 ng/ml. A 20 h fasting period was associated with a significant decrease in plasma GH. In 45 day-old rats, the variations in plasma GH of individual animals were studied by obtaining sequential blood samples from unrestrained, undisturbed animals with implanted intra-aortic cannulae. In these rats GH secretion was characterized by an episodic release, occurring every 2–4 h. After a 20 h fasting period major peaks were depressed and occurred less frequently. It is concluded that there is an age-related as well as a circadian rhythm in growth hormone secretion in the rat and that sequential sampling of blood is essential for the evaluation of the secretory pattern.

1994 ◽  
pp. 167-192 ◽  
Author(s):  
Richard F. Walker ◽  
Sei-Won Yang ◽  
Ryuji Masuda ◽  
Cheng-Shih Hu ◽  
Barry B. Bercu

1987 ◽  
Vol 253 (4) ◽  
pp. E354-E359
Author(s):  
K. Ishikawa ◽  
H. Katakami ◽  
L. A. Frohman

The inhibitory effect of centrally administered thyrotropin-releasing hormone (TRH) on the plasma growth hormone (GH) response to GH-releasing hormone (GHRH) in the rat was studied in relation to the anatomic loci involved. Experiments were performed in animals with bilateral electrolytic lesions in the medial preoptic (MPO) area or with anterolateral hypothalamic deafferentation and in sham-operated controls. Blood samples were obtained every 10 to 20 min from and drugs were injected into freely moving animals with indwelling cannulas in the right atrium and lateral cerebral ventricle. In control animals, the plasma GH response to GHRH, 1 microgram iv, was almost completely inhibited by TRH, 1 microgram icv, injected 5 min previously. In animals with either MPO lesions or anterolateral hypothalamic deafferentation in which median eminence somatostatin immunochemical staining was almost completely eliminated, the GH response to GHRH was enhanced and TRH did not exhibit any inhibitory effect. These results, together with the previous observation that the inhibitory effect of TRH is blocked by prior treatment with anti-somatostatin serum, suggest that the effect of TRH is mediated by stimulation of somatostatin-containing neurons in the periventricular nucleus of the MPO area.


1995 ◽  
Vol 144 (1) ◽  
pp. 83-90 ◽  
Author(s):  
E Magnan ◽  
L Mazzocchi ◽  
M Cataldi ◽  
V Guillaume ◽  
A Dutour ◽  
...  

Abstract The physiological role of endogenous circulating GHreleasing hormone (GHRH) and somatostatin (SRIH) on spontaneous pulsatile and neostigmine-induced secretion of GH was investigated in adult rams actively immunized against each neuropeptide. All animals developed antibodies at concentrations sufficient for immunoneutralization of GHRH and SRIH levels in hypophysial portal blood. In the anti GHRH group, plasma GH levels were very low; the amplitude of GH pulses was strikingly reduced, although their number was unchanged. No stimulation of GH release was observed after neostigmine administration. The reduction of GH secretion was associated with a decreased body weight and a significant reduction in plasma IGF-I concentration. In the antiSRIH group, no changes in basal and pulsatile GH secretion or the GH response to neostigmine were observed as compared to controls. Body weight was not significantly altered and plasma IGF-I levels were reduced in these animals. These results suggest that in sheep, circulating SRIH (in the systemic and hypophysial portal vasculature) does not play a significant role in pulsatile and neostigmine-induced secretion of GH. The mechanisms of its influence on body weight and production of IGF-I remain to be determined. Journal of Endocrinology (1995) 144, 83–90


1989 ◽  
Vol 121 (2) ◽  
pp. 177-184 ◽  
Author(s):  
Silvano G. Cella ◽  
Valerio Moiraghi ◽  
Francesco Minuto ◽  
Antonina Barreca ◽  
Daniela Cocchi ◽  
...  

Abstract. Age-related changes in GH secretion were studied in the dog. In preliminary experiments, administration of GH-relasing hormone (GHRH-40, 2 μg/kg, iv) or the α2-adrenoceptor agonist clonidine (4 μg/kg, iv) elicited significantly higher plasma GH rises in 3 to 4 years old than in 10 to 14 years old beagle dogs. The pulsatile patterns of GH secretion in both young and old dogs under baseline conditions and after prolonged fasting or clonidine administration were studied. Samples were taken every 10 min from 09.00 to 15.00 h from five young and five old dogs of both sexes. Under baseline conditions, GH peak frequency, total peak area, and integrated GH secretion were significantly lower in old than in young dogs. In old dogs, 5-day complete fasting or 14-day clonidine administration (75 μg/dog, po, twice daily) increased the frequency and amplitude of spontaneous GH bursts, the total peak area, and the integrated GH secretion. After either stimulus, the GH secretory pattern was quantitatively and qualitatively indistinguishable from that of young dogs under baseline conditions. Similarly, the foregoing indices were significantly increased in young dogs by either stimulus, except for the inability of clonidine to affect peak frequency. These data demonstrate that the defective GH secretion in old dogs is not irreversible, since it is normalized when old dogs are exposed to central nervous system-directed stimuli.


2004 ◽  
Vol 82 (6) ◽  
pp. 950-965 ◽  
Author(s):  
M L Perreault ◽  
C D Rollo

Photoperiod affects most of the features altered in transgenic growth hormone (TG) mice, and laboratory rats and mice retain some sensitivity to photoperiod. We examined growth, feeding, longevity, and reproduction of TG mice and normal control mice (Mus musculus L., 1758) in 12 h light : 12 h dark (LD) and 24 h light (LL) photoperiods. Sexual dichotomy in growth and hepatic gene expression are considered to require gender-specific patterns of growth hormone secretion that are absent in TG mice. Regardless, in the LD photoperiod mature TG females were 82.8% (46.8 g) of the mass of TG males (56.5 g, p < 0.05), whereas control mice showed no size dichotomy (≈33 g). Mature masses of TG males and of control mice of either gender were unaffected by the LL photoperiod. TG females, however, reached a mature mass 92% (50.9 g) of that of mature TG males in the LL photoperiod, attenuating the sexual size dichotomy expressed in the LD photoperiod. Growth of females was slower than that of males, even in the control group. TG females in the LL photoperiod expressed faster growth, higher reproduction, and greater mean longevity than TG females in the LD photoperiod. Differences in age-related feeding associated with gender and photoperiod reflected differential growth rates. Females grew more slowly and ate more than males of similar age because they were smaller (i.e., had lower growth efficiencies). The LL photoperiod improved the energy balance of TG females. Possible mechanisms mediating such gender-specific effects are explored.


Diabetes ◽  
1975 ◽  
Vol 24 (9) ◽  
pp. 842-850 ◽  
Author(s):  
D. Bryce ◽  
M. Yeh ◽  
C. Funderburk ◽  
H. Todd ◽  
F. Hertelendy

Metabolism ◽  
1999 ◽  
Vol 48 (5) ◽  
pp. 665-670 ◽  
Author(s):  
Taylor J. Marcell ◽  
Robert A. Wiswell ◽  
Steve A. Hawkins ◽  
Kyle M. Tarpenning

1992 ◽  
Vol 127 (5) ◽  
pp. 416-419 ◽  
Author(s):  
Koji Nakagawa ◽  
Tatsuya Ishizuka ◽  
Chikara Shimizu ◽  
Yoshito Ito ◽  
Ichiji Wakabayashi

There is increasing evidence to suggest that supraphysiological doses of glucocorticoids suppress growth hormone secretion in vivo by augmenting somatostatin release from the hypothalamus; previously, we reported an increase in hypothalamic somatostatin content in dexamethasone-treated rats. To further examine whether the production of somatostatin really is augmented, hypothalamic somatostatin mRNA levels were determined by the Northern blot technique in female rats receiving 330 μg of dexamethasone daily for three days. In two series of experiments, hypothalamic somatostatin mRNA levels in dexamethasone-treated rats were significantly (p<0.05) increased to 133±19 (mean±sd)% and 153±38% of the controls. In the dexamethasone-treated rats, plasma growth hormone levels were markedly suppressed compared with those of the controls. These results further support the hypothesis that pharmacological doses of glucocorticoids increase the production and release of somatostatin from the hypothalamus and thus inhibit growth hormone secretion, overriding the direct stimulatory effect of glucocorticoids on growth hormone production at the pituitary level.


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