Timing of growth hormone injections and reproduction in gilts

1991 ◽  
Vol 71 (3) ◽  
pp. 717-723 ◽  
Author(s):  
J. Gilbertson ◽  
R. N. Kirkwood ◽  
P. A. Thacker

Sixty-eight Yorkshire × Landrace gilts were selected at 85 kg body weight (BW) and exposed to a mature boar for 20 min d−1 to detect puberty. At the onset of puberty, gilts were allocated to receive daily intramuscular injections of porcine growth hormone (pGH, 90 μg kg−1 BW) from either 14 to 17 d (GH17, n = 22) or from 14 to 22 d (GH22 n = 22) after puberty, inclusively. A third group of gilts served as controls (n = 24) and received vehicle buffer. A single blood sample was obtained from each gilt on days 14, 17 and 20. Also, four gilts from each pGH treatment and eight control gilts were sampled at 15-min intervals for 8 h on day 16. Gilts were slaughtered 30 d after puberty at which time their ovaries were recovered for the determination of ovulation rate. Injection of pGH resulted in elevated serum concentrations of triiodothyronine, insulin and glucose (P < 0.01). There was no significant (P > 0.1) treatment effect on mean serum concentrations of LH or FSH. However, pGH treatment tended (P = 0.1) to increase LH pulse frequency and to decrease (P = 0.01) LH pulse amplitude. The incidence of a second estrus was reduced (P < 0.01) in GH22 compared to control gilts, with GH17 being intermediate (72.7 vs. 90.9 vs. 100% for GH22, GH17 and control gilts, respectively). Ovulation rate was not affected by pGH treatment (15.1 vs. 14.3 vs 14 0 for GH22, GH17 and control gilts, respectively). The present data confirm an adverse effect of pGH on ovarian function and suggest that an altered LH pulsatility may be involved. Key words: Gilts, growth hormone, estrus, endocrinology

1996 ◽  
Vol 62 (2) ◽  
pp. 279-286 ◽  
Author(s):  
N. R. Adams ◽  
J. R. Briegel ◽  
R. D. G. Rigby ◽  
M. R. Sanders ◽  
R. M. Hoskinson

AbstractPlasma concentrations of growth hormone (GH) are elevated in sheep during undernutrition. The present study attempted to determine whether this increased secretion mediated nutritional effects on reproduction or wool growth, using sheep immunized against growth hormone-releasing hormone and given a low-quality, sub-maintenance diet. Immunization reduced plasma concentrations of GH at all times measured (P < 0·01), through reduced pulse frequency, reduced pulse amplitude, and reduced baseline concentrations. Plasma insulin-like growth factor-1 (1GF-1) was also reduced in the immunized sheep (P < 0·01). Despite this, rates of live-weight loss and wool growth were similar in immunized and control ewes. Plasma concentrations ofLH and FSH were also similar in immunized and control ewes, both during the late luteal phase and after ovariectomy and supplementation with oestradiol and progesterone. Numbers of ovarian follicles and corpora lutea were also unaffected by immunization. It is concluded that high endogenous concentrations of GH in sheep given food below maintenance are necessary to maintain plasma IGF-1, but do not affect the concentration of gonadotropins or ovarian follicular growth. Furthermore, rates of live-weight loss and the depression in wool growth in such animals were also independent of concentrations ofGH or IGF-1.


1989 ◽  
Vol 69 (4) ◽  
pp. 931-937 ◽  
Author(s):  
R. N. KIRKWOOD ◽  
P. A. THACKER ◽  
B. L. GUEDO ◽  
B. LAARVELD

Fifty-six gilts of Yorkshire and Landrace breeding were selected at 86.8 ± 0.8 kg body weight (BW) and given an intramuscular (im) injection of 400 IU PMSG plus 200 IU hCG to stimulate ovulation. From 14 d after gonadotropic stimulation, gilts were exposed to a boar to detect a subsequent spontaneous estrus. At the onset of this first observed estrus, gilts were allocated to receive daily injections (i.m.) of growth hormone (pGH, 90 μg kg−1) from either 14 d (GH14, n = 21) or 17 d (GH17, n = 20) until 22 d after the onset of the first observed estrus. A third group of gilts served as controls (n = 15) and received vehicle buffer. Blood samples were obtained by jugular vein puncture at 3-d intervals from 14 to 29 d, inclusively. Gilts were slaughtered 30–32 d after the first observed estrus at which time their ovaries were recovered for the determination of ovulation rates. All control gilts and all but one GH17 gilt exhibited normal estrous cycles. However, of the 21 gilts assigned to GH14, only 9 (43%) had normal estrous cycles (P < 0.001). In gilts exhibiting a second estrus, there was no effect of pGH treatment on the duration of the estrous cycle (20.4, 20.9 and 20.5 d) or on ovulation rate (14.6, 13.9 and 13.5) for GH14, GH17 and controls, respectively. Serum assays revealed that pGH injections resulted in decreased serum concentrations of thyroxine (P < 0.01) but increased concentrations of triiodothyronine, insulin and glucose (P < 0.001). The present data confirm an adverse effect of pGH on ovarian function. However, the adverse effect is only evident when the pGH injection regime encompasses days 14–16 of the estrous cycle. Key words: Gilts, growth hormone, estrus, ovulation rate


2001 ◽  
Vol 280 (3) ◽  
pp. E489-E495 ◽  
Author(s):  
Eleni V. Dimaraki ◽  
Craig A. Jaffe ◽  
Roberta Demott-Friberg ◽  
Mary Russell-Aulet ◽  
Cyril Y. Bowers ◽  
...  

To test whether endogenous hypothalamic somatostatin (SRIH) fluctuations are playing a role in the generation of growth hormone (GH) pulses, continuous subcutaneous octreotide infusion (16 μg/h) was used to create constant supraphysiological somatostatinergic tone. Six healthy postmenopausal women (age 67 ± 3 yr, body mass index 24.7 ± 1.2 kg/m2) were studied during normal saline and octreotide infusion providing stable plasma octreotide levels of 2,567 ± 37 pg/ml. Blood samples were obtained every 10 min for 24 h, and plasma GH was measured with a sensitive chemiluminometric assay. Octreotide infusion suppressed 24-h mean GH by 84 ± 3% ( P = 0.00026), GH pulse amplitude by 90 ± 3% ( P = 0.00031), and trough GH by 54 ± 5% ( P = 0.0012), whereas GH pulse frequency remained unchanged. The response of GH to GH-releasing hormone (GHRH) was not suppressed, and the GH response to GH-releasing peptide-6 (GHRP-6) was unaffected. We conclude that, in women, periodic declines in hypothalamic SRIH secretion are not the driving force of endogenous GH pulses, which are most likely due to episodic release of GHRH and/or the endogenous GHRP-like ligand.


1992 ◽  
Vol 134 (1) ◽  
pp. 115-125 ◽  
Author(s):  
R. Webb ◽  
G. Baxter ◽  
D. McBride ◽  
A. S. McNeilly

ABSTRACT Two experiments were carried out during the breeding season in ewes, first to investigate the effects of oral administration of a 3β-hydroxysteroid dehydrogenase (3β-HSD) inhibitor (epostane) on the number of corpora lutea, and secondly to investigate the mechanism through which epostane acts. In the first experiment Dorset Horn ewes were treated orally with 25, 50, 100 or 200 mg epostane twice daily between days 10 and 15 of the oestrous cycle. All doses of epostane resulted in an increase in the number of corpora lutea per ewe, although the response was curvilinear, with the 25 mg dose showing the largest response and the 200 mg group the smallest response. Although there was no difference between groups in the number of ewes showing oestrus, the higher doses of epostane had a detrimental effect on fertility. In the second experiment Welsh Mountain ewes were treated twice daily with 25 mg epostane from day 10 of the oestrous cycle and the ovaries were removed for analysis during either the luteal or the follicular phases. Treatment significantly increased the number of follicles >6 mm in diameter, but significantly reduced in-vitro follicular oestradiol and testosterone production. Despite a marked increase in peripheral inhibin concentrations there was no effect on in-vitro inhibin production. Epostane treatment also caused a significant reduction in peripheral FSH concentrations and an increase in mean LH concentration. The latter was due to an increase in LH pulse frequency during the luteal phase and LH pulse amplitude during the follicular phase. These results confirm that treatment of ewes with epostane orally has a significant effect on follicular steroidogenesis and causes a significant increase in the number of corpora lutea per ewe. This effect on ovulation rate is not via an increase in peripheral FSH concentration, but may be caused by a reduction in follicular steroid activity either directly on the ovary or via an alteration in the pattern of LH secretion. Journal of Endocrinology (1992) 134, 115–125


2002 ◽  
Vol 74 (3) ◽  
pp. 423-430 ◽  
Author(s):  
F. Elsaesser ◽  
M. W. Pfaffl ◽  
H. H. D. Meyer ◽  
B. Serpek ◽  
H. Sauerwein

AbstractThe intention of the current study was to gain more insight into the endocrine and molecular control mechanisms of growth in the pig. For this purpose various growth related parameters were determined in 4-month-old barrows of two extreme pig genotyes, the small, obese Göttingen Miniature (GM) and the large and lean German Landrace (DL). Mean growth hormone (GH) concentration, GH pulse frequency and GH pulse amplitude did not differ between breeds. Likewise, plasma IGF-1, thyroxine, tri-iodothyronine (T3) concentrations were similar in both breeds. However the plasma GH response (maximum level and area under curve) to a single i.v. injection of GHRH in DL was higher than in GM (P < 0·05). Furthermore, basal plasma insulin and in particular plasma cortisol concentrations were higher in GM compared with DL pigs (P 0·05 and 0·01 respectively). Analysis of cortisol during 4-h frequent blood sampling indicated higher cortisol amplitudes in GM compared with DL (P ≤ 0·01). Specific bGH-binding to hepatic membrane preparations was not different between breeds and IGF-1 m RNA concentrations determined by reverse transcription-polymerase chain reaction in liver, m. semimenbranosus and m. longissimus dorsi were similar in both breeds. I.m. treatment with recombinant porcine somatotropin (rpST; 70 µg/kg live weight) over an 8-day period in contemporary barrows increased without any breed difference, plasma IGF-1, T3 and insulin concentrations and hepatic specific bGH-binding, but did not affect thyroxine or cortisol concentrations in plasma. IGF-1 gene expression was also elevated in liver and muscle tissues in rpST-treated animals without obvious breed effects. The observations underline the complexity of the hormonal and molecular control of growth and support the notion that differences in growth potential are the consequence of differences at various levels of the somatotropic axis and apparently relate to differences in other control systems of energy metabolism such as the pituitary adrenal axis or the endocrine pancreas as well.


2003 ◽  
Vol 285 (1) ◽  
pp. E163-E170 ◽  
Author(s):  
Eleni V. Dimaraki ◽  
Craig A. Jaffe ◽  
Cyril Y. Bowers ◽  
Peter Marbach ◽  
Ariel L. Barkan

Using a continuous subcutaneous octreotide infusion to create constant supraphysiological somatostatinergic tone, we have previously shown that growth hormone (GH) pulse generation in women is independent of endogenous somatostatin (SRIH) declines. Generalization of these results to men is problematic, because GH regulation is sexually dimorphic. We have therefore studied nine healthy young men (age 26 ± 6 yr, body mass index 23.3 ± 1.2 kg/m2) during normal saline and octreotide infusion (8.4 μg/h) that provided stable plasma octreotide levels (764.5 ± 11.6 pg/ml). GH was measured in blood samples obtained every 10 min for 24 h. Octreotide suppressed 24-h mean GH by 52 ± 13% ( P = 0.016), GH pulse amplitude by 47 ± 12% ( P = 0.012), and trough GH by 39 ± 12% ( P = 0.030), whereas GH pulse frequency and the diurnal rhythm of GH secretion remained essentially unchanged. The response of GH to GH-releasing hormone (GHRH) was suppressed by 38 ± 15% ( P = 0.012), but the GH response to GH-releasing peptide-2 was unaffected. We conclude that, in men as in women, declines in hypothalamic SRIH secretion are not required for pulse generation and are not the cause of the nocturnal augmentation of GH secretion. We propose that GH pulses are driven primarily by GHRH, whereas ghrelin might be responsible for the diurnal rhythm of GH.


1998 ◽  
Vol 275 (4) ◽  
pp. R1218-R1226 ◽  
Author(s):  
Anne B. Loucks ◽  
Mark Verdun ◽  

In other energy-restricted mammals, a single large meal restores luteinizing hormone (LH) pulsatility within a few hours. To determine whether this is so in women, we measured LH pulsatility during the 5th day of low energy availability [dietary energy intake − exercise energy expenditure = 10 kcal ⋅ kg lean body mass (LBM)−1 ⋅ day−1] and during a 6th day of aggressive refeeding (90 kcal ⋅ kg LBM−1 ⋅ day−1) in 15 meals providing 4,100 kcal for an energy availability of 75 kcal ⋅ kg LBM−1 ⋅ day−1. Low energy availability raised β-hydroxybutyrate 1,000% ( P < 0.001) and reduced plasma glucose 15% ( P < 0.01), insulin 63% ( P < 0.001), and triiodothyronine 22% ( P < 0.005). In five of eight subjects, low energy availability also unambiguously suppressed LH pulse frequency 57% to 8.2 ± 1.5 pulses/24 h ( P < 10−4) and raised LH pulse amplitude 94% to 3.1 ± 0.3 IU/l ( P < 10−4), levels below the 5th and above the 95th percentile, respectively, in energy-balanced women. Aggressive refeeding restored β-hydroxybutyrate, glucose, and insulin, but not triiodothyronine. In the five women with unambiguously disrupted LH pulsatility, aggressive refeeding had no effect on LH pulse amplitude ( P > 0.9) and raised LH pulse frequency only slightly (2.4 ± 0.6 pulses/24 h, P = 0.04) and not above the fifth percentile. This striking contrast between women and other mammals may be another clue to the unidentified mechanism mediating the effect of energy availability on LH pulsatility.


1998 ◽  
Vol 84 (1) ◽  
pp. 37-46 ◽  
Author(s):  
A. B. Loucks ◽  
M. Verdun ◽  
E. M. Heath ◽  

Loucks, A. B., M. Verdun, and E. M. Heath. Low energy availability, not stress of exercise, alters LH pulsatility in exercising women. J. Appl. Physiol.84(1): 37–46, 1998.—We tested two hypotheses about the disruption of luteinizing hormone (LH) pulsatility in exercising women by assaying LH in blood samples drawn at 10-min intervals over 24 h from nine young, habitually sedentary, regularly menstruating women on days 8, 9, or 10 of two menstrual cycles after 4 days of intense exercise [E = 30 kcal ⋅ kg lean body mass (LBM)−1 ⋅ day−1at 70% of aerobic capacity]. To test the hypothesis that LH pulsatility is disrupted by low energy availability, we controlled the subjects’ dietary energy intakes (I) to set their energy availabilities (A = I − E) at 45 and 10 kcal ⋅ kg LBM−1 ⋅ day−1during the two trials. To test the hypothesis that LH pulsatility is disrupted by the stress of exercise, we compared the resulting LH pulsatilities to those previously reported in women with similar controlled energy availability who had not exercised. In the exercising women, low energy availability reduced LH pulse frequency by 10% ( P < 0.01) during the waking hours and increased LH pulse amplitude by 36% ( P = 0.05) during waking and sleeping hours, but this reduction in LH pulse frequency was blunted by 60% ( P = 0.03) compared with that in the previously studied nonexercising women whose low energy availability was caused by dietary restriction. The stress of exercise neither reduced LH pulse frequency nor increased LH pulse amplitude (all P > 0.4). During exercise, the proportion of energy derived from carbohydrate oxidation was reduced from 73% while A = 45 kcal ⋅ kg LBM−1 ⋅ day−1to 49% while A = 10 kcal ⋅ kg LBM−1 ⋅day−1( P < 0.0001). These results contradict the hypothesis that LH pulsatility is disrupted by exercise stress and suggest that LH pulsatility in women depends on energy availability.


1976 ◽  
Vol 82 (2) ◽  
pp. 467-474 ◽  
Author(s):  
T. Yamamoto ◽  
T. Ogihara ◽  
K. Miyai ◽  
Y. Kumahara ◽  
Y. Hirata

ABSTRACT A 52 year old man is described in whom the simultaneous occurrence of isolated adrenocorticotrophin (ACTH) deficiency and primary hypothyroidism was documented by the determination of six anterior pituitary hormones by specific radioimmunoassays after suitable stimulations. The urinary 17-hydroxycorticosteroids excretion was persistently reduced and was increased by repeated ACTH injections. The low basal metabolic rate, reduced serum thyroid hormones and elevated serum thyrotrophic hormone were consistent with primary hypothyroidism. After resumption of euthyroidism, secretory reserves of growth hormone and ACTH were assessed. The growth hormone response to insulin-induced hypoglycaemia was normal. No rise in plasma cortisol and ACTH was observed following insulin-induced hypoglycaemia. Plasma ACTH was not augmented by iv infusion of metyrapone. The pathogenesis of two co-existent endocrine deficiencies was discussed.


1991 ◽  
Vol 125 (6) ◽  
pp. 614-620 ◽  
Author(s):  
Jacques Allouche ◽  
Antoine Bennet ◽  
Pierre Barbe ◽  
Monique Plantavid ◽  
Philippe Caron ◽  
...  

Abstract. LH nocturnal pulsatility and bioactivity to immunoreactivity (B/I) ratio were determined in 16 patients with anorexia nervosa-related hypothalamic amenorrhea and low sex steroid levels, and in 12 normal women in the midfollicular phase. The patients were subdivided into 2 groups: IA (N=7) without, and IB (N=9) with documented recent weight gain. Blood samples were taken from each subject at 10-min intervals from 00.00 to 06.00 h. Immunoreactive LH data were analysed with cluster analysis algorithm. A pool of aliquots from all the samples was used to evaluate bioactive LH, immunoreactive LH and LH B/I ratio in each subject. LH pulse frequency was lower in Group IA than in controls, whereas it did not differ significantly between Group IB and controls. LH pulse amplitude was lower in Group IA, and higher in Group IB than in controls. LH B/I ratio was below the control range in 3/16 patients. In conclusion, persistent hypothalamic amenorrhea does not require a permanent inhibition of the GnRH pulse generator; transient inhibition of pulsatility and qualitative abnormalities of gonadotropins could be involved in the mechanism, at least in some patients.


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