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PubMed1988

Stimulation of pituitary luteinizing hormone secretion by gonadotropin-releasing hormone is not coupled to beta-luteinizing hormone gene transcription.

The physiological stimulation and inhibition of release of several peptide and protein hormones appears to be associated with transcription of the respective peptide- and protein hormone-encoding genes. In the current studies we investigated whether this was also true for the rat pituitary LH system. Using an anterior pituitary primary tissue culture system, we have analyzed the effects of 10(-9) M GnRH on beta LH gene transcription using a transcription run-on assay, and on nuclear beta LH RNA levels using a highly sensitive solution hybridization-S1-nuclease protection assay. GnRH-stimulated release of LH does not appear to be coupled to a significant change in the rate of beta LH gene transcription, but is associated with both a 2- to 3-fold increase in levels of the beta LH primary transcript and processing intermediates and a rapid decrease in the levels of fully processed beta LH mRNA in the nucleus. No significant change in beta LH cytoplasmic mRNA levels, however, was associated with GnRH-stimulated release of LH, in vitro. Our findings suggest that unlike several other peptide and protein hormone systems, stimulated release of beta LH by GnRH in vitro is not associated with an increase in beta LH gene transcription or cytoplasmic mRNA levels.

Animals↗
PubMed1993

Localization of promoter sequences required for thyrotropin-releasing hormone and thyroid hormone responsiveness of the glycoprotein hormone alpha-gene in primary cultures of rat pituitary cells.

The glycoprotein hormone alpha-gene is regulated by multiple hormones in different pituitary and placental cell types. In thyrotropes, the alpha-gene is stimulated by TRH and repressed by thyroid hormone (T3). We used transient expression assays in primary cultures of rat pituitary cells to examine regulation of the alpha-promoter (alpha Luc) by TRH and T3. The -846 alpha Luc activity was stimulated 3.4-fold by TRH and repressed 44% by T3. GnRH and cAMP stimulated -846 alpha Luc by 8.3- and 8.6-fold, respectively. T3 blocked TRH stimulation, but it had no effect on stimulation by GnRH or cAMP, suggesting that the T3-mediated effects are thyrotrope specific. TRH and T3 responsiveness was preserved with deletions to -346 basepairs (bp). TRH responsiveness was lost after deletion to -280 bp, whereas T3-mediated repression was eliminated by further deletion to -180 bp. A series of DNA fragments between -420 and -180 was linked to -132 alpha Luc to study TRH and T3 responses in greater detail. Sequences between -346 to -180 bp conferred TRH responsiveness and T3 inhibition. TRH responsiveness was not seen after 3'-deletions of this fragment to -244 or -280 bp. These results together with the 5'-deletions provide evidence for two interdependent TRH regulatory regions: one between -346 to -280 bp and another between -244 to -180 bp. T3-dependent repression only requires sequences between -244 and -180 bp. Site-directed cluster mutations were created in each of these two regulatory domains. A mutation in region 1 (-346 to -328 bp) eliminated TRH stimulation, but retained basal suppression by T3.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Differential secretion of chicken growth hormone variants after growth hormone-releasing hormone stimulation in vitro.

Variants of growth hormone (GH) are present in most vertebrates. Chicken GH (cGH) undergoes posttranslational modifications that contribute to its structural diversity. Although the 22-kDa form of GH is the most abundant, some other variants have discrete bioactivities that may not be shared by others. The proportion of cGH variants changes during ontogeny, suggesting that they are regulated differentially. The effect of growth hormone-releasing hormone (GHRH) on the release of cGH variants was studied in both pituitary gland and primary cell cultures, employing sodium dodecyl sulfate polyacrylamide gel electrophoresis, Western blotting, and densitometry. GHRH (2 nM, 2 h) stimulated the secretion of most of the size variants of cGH although the amplitude of increase was not equal for each one. A differential effect on the secretion of GH size variants, particularly on the 22- (monomer) and 26-kDa (putatively glycosylated) cGH isoforms was found in both systems. In the whole pituitary culture, the proportion of the 26-kDa immunoreactive cGH increased 35% while the 22 kDa decreased 31% after GHRH treatment in comparison with the controls. In the primary cell culture system, the proportion of the glycosylated variant increased 43% whereas the monomer and the dimer decreased 22.26 and 29%, respectively, after GHRH stimulation. Activators of intracellular signals such as 1 mM 8-bromo-cAMP and 1 microM phorbol myristate acetate had a similar effect to that obtained with GHRH. The data support the hypothesis that GH variants may be under differential control and that GHRH promotes the release of a glycosylated cGH variant that has an extended half-life in circulation.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2002

Growth hormone-releasing hormone and gonadotropin-releasing hormone stimulate nitric oxide production in 17beta-estradiol-primed rat anterior pituitary cells.

It was reported that neuronal nitric oxide synthase (nNOS) was expressed only in gonadotrophs and folliculo-stellate cells in the anterior lobe of the pituitary gland. However, recent studies have demonstrated the occurrence of nNOS in the somatotrophs and lactotrophs. In the present study, we investigated effects of growth hormone-releasing hormone (GHRH), gonadotropin-releasing hormone (GnRH), and 17beta-estradiol on nitric oxide (NO) release in cultured rat anterior pituitary cells in vitro. The NO2- level in the incubation medium of the rat anterior pituitary cells was dependent on the cell density. Pretreatment with 10 microM 17beta-estradiol resulted in an increase in medium NO2- level. GHRH and GnRH failed to change medium NO2- levels, but they elicited increases in medium NO2- levels in estrogen-treated cells. The GHRH-induced increase in NO2- level was inhibited by Nomega-nitro-L-arginine methyl ester, a NOS inhibitor. These findings suggest that GnRH and GHRH could activate nNOS in the gonadotrophs and the somatotrophs, respectively.

Animals↗
PubMed2003

Growth hormone-releasing hormone and growth hormone secretagogues in normal aging.

Growth hormone (GH) secretion declines with aging, and parallels between normal aging and the signs and symptoms of adult GH deficiency have led to interest in the potential utility of replacing or stimulating GH to promote physical and psychological function and to prolong the capacity for independent living in older adults. The aging pituitary remains responsive to GH-releasing hormone (GHRH) and to ghrelin-mimetic GH secretagogues (GHS), and these agents have both theoretical and practical potential advantages as alternatives to the use of GH itself in this setting. Studies of the long duration and large scale needed to test the efficacy of GHRH or GHS on clinically important endpoints cannot be designed or conducted without first obtaining promising results in studies of smaller size focused on manageable intermediate endpoints, and all studies published to date have been of this latter type. GHRH and GHS both stimulate GH secretion, and, when given repeatedly, elevate IGF-I levels to within younger adult normal ranges. When GHRH treatment is continued for several months, these hormonal changes yield an increase in lean body (muscle) mass. GHRH, like GH, reduces body fat, but similar effects have not yet been shown with GHS. GHRH treatment has not yielded consistent improvements in physical function, although it may have a stabilizing effect. Chronic treatment with a short-acting GHRH did not improve sleep, possibly due to lack of sustained activity throughout the night. Compared to placebo, GHRH treatment improved certain tests of cognitive performance. These results, while encouraging, do not yet support the routine use of GHRH or GHS in normal aging.

Aging↗
PubMed1976

[A study on serum luteinizing hormone response to luteinizing hormone-releasing hormone iny hyper- and hypothyroidism (author's transl)].

In order to study the mechanism of gonadal dysfunction in patients with abnormal thyroid function, the pituitary luteinizing hormone (LH) response to 200 mug of luteinizing hormone-releasing hormone (LH-RH) was investigated in 20 untreated and 18 treated hyperthyroid patients and in 21 untreated and 8 treated hypothyroid patients in addition to 29 matched control subjects. Serum LH levels were measured by double-antibody radioimmunoassay technique with HLH kit Daiichi. In untreated hyperthyroid men, the slightly elevated mean basal level and the exaggerated mean response to LH-RH of LH were observed, and in treated hyperthyroid men, both values were found to be similar to those of matched control men. Furthermore, in these patients, the maximal increments and the net increments of responses to LH-RH of LH were correlated with serum thyroxine levels and Thyopac-3 values. In most untreated and treated hyperthyroid premenopausal women with and without menstrual disturbances, the basal levels and the responses to LH-RH of LH were similar to those of matched control premenopausal women. In untreated hyperthyroid postmenopausal women, the mean basal level of LH was elevated, although the mean LH response to LH-RH was similar to that of matched control postmenopausal women, and in treated hyperthyroid postmenopausal women, the mean basal level and the mean response to LH-RH of LH were similar to those of matched control postmenopausal women. Furthermore, in these patients, the basal levels were correlated with serum thyroxine levels. In untreated and treated hypothyroid men, the mean basal level and the mean response to LH-RH of LH were similar to those of untreated and treated hyperthyroid postmenopausal women. In most untreated and treated hypothyroid premenopausal women with and without menstrual disturbances, the basal levels were observed to be inconsistent, and the LH responses to LH-RH were similar to those of matched control premenopausal women. In untreated and treated hypothyroid postmenopausal women, the mean basal level and the mean response to LH-RH of LH were similar to those of matched control postmenopausal women. These data indicate that the ability of the pituitary to secrete LH in patients with abnormal thyroid function was augmented in hyper- and hypothyroid men, and augmented in hyper-, but normal in hypothyroid postmenopausal women. Therefore, it is concluded that the cause of gonadal dysfunction at least in the premenopausal women with abnormal thyroid function lies not inside but outside the pituitary gland.

Adolescent↗
PubMed2005

Growth hormone releasing hormone receptor (GHRH-r) gene mutation in Indian children with familial isolated growth hormone deficiency: a study from western India.

BACKGROUND: Various mutations of the growth hormone releasing hormone receptor (GHRH-R) gene have been recently described to cause familial isolated growth hormone (GH) deficiency (FIGHD), with the GHRH-R nonsense mutation E72X reported in patients with FIGHD from South Asia. The molecular genetic basis of FIGHD in Indian children is not known. OBJECTIVE: To look for the GHRH-R E72X non-sense mutation in our patients with FIGHD and describe its clinical phenotype. PATIENTS AND METHOD: A total of 31 patients from 22 families diagnosed 4-20 years previously, 20 patients with familial IGHD-IB from 11 families and 11 patients with non-familial isolated GH deficiency (NFIGHD) (phenotypes IGHD-IB in eight patients and -IA in three) were included. Twenty-eight of 31 patients with IGHD-IB came from two states of Western India, 27 of them Hindus from 18 families (three consanguineous) and one from an inbred Moslem kindred. RESULTS: Twenty-two of the patients (71%) (18 FIGHD and four NFIGHD) had a homozygous G-->T transversion in exon 3, with this GHRH-R gene mutation E72X in 90% (18/20) of patients with FIGHD, 36% (4/11) of NFIGHD, altogether 78% (22/28) with phenotype IB. One parent pair with IGHD had homozygous E72X mutation, the rest were heterozygous carriers. Two siblings with IGHD due to homozygous E72X mutation were also heterozygous carriers for GH-1 gene 6.7 kb deletion, inherited from their mother, heterozygous for both GH-1 and GHRH-R mutations. Initial chronological age was 10.89 +/- 3.69 years, bone age 6.4 +/- 3.4 years, and mean height SDS was -5.83 +/- 1.41. The clinical phenotype, with sharp features, lean habitus, lack of frontal bossing or hypoglycemia, was characteristic. The mean peak GH was 1.25 +/- 0.75 ng/ml, IGF-I and IGFBP-3 below -2 SDS with no response to GHRH in those tested. MRI (n = 10) showed pituitary hypoplasia, mean vertical height 2.61 +/- 0.76 mm. Among the other 7/11 NFIGHD patients, four with phenotype IB were negative for genotypes tested in this study; of three patients with phenotype IA, two had the GH-1 gene 6.7 kb deletion, and one was a compound heterozygote with 6.7 and 7.6 kb deletions. CONCLUSIONS: The majority of patients with FIGHD from different communities belonged to non-consanguineous Hindu families from Western India. The GHRH-R gene E72X mutation was found in 71% of this series, in 90% of FIGHD, 36% of NFIGHD, and in 78% with phenotype IB. The characteristic phenotype helped in suspecting this mutation. GHRH-R gene mutations may be the most reasonable candidate for IGHD-IB with the E72X mutation predominating in the Indian subcontinent. More extensive studies need to be undertaken.

Adolescent↗
PubMed1985

Evidence of a circulating growth hormone stimulating factor other than growth hormone releasing hormone in a patient with pituitary tumour and acromegaly.

This study is a report on the growth hormone (GH) stimulatory effect of serum and plasma from a patient with notably active acromegaly due to a GH producing pituitary adenoma. Pituitary adenomatous tissue from 7 patients with GH producing adenomas, one with a prolactin (Prl) producing adenoma, one with a TSH producing adenoma, and one with a non-secreting adenoma, were cultured in vitro for 8-10 days. Media were changed every 48-72 h and contained Neumann Tytell buffer with the addition of 1) foetal calf serum, 2) patients' own serum or plasma, 3) serum or plasma from the patient with notably active acromegaly. GH release expressed as microgram GH/1/48-72 h between day 6 and 8 in culture did not differ when adenomatous tissue was cultured in buffer, foetal calf serum or the patients' own serum or plasma. In contrast, GH release was increased in 9/10 patients, when media contained serum or plasma from the patient with notably active acromegaly. This GH stimulatory effect was demonstrated in vitro in human pituitary adenomatous tissue from patients with pathological as well as normal GH secretion in vivo. Furthermore, this GH releasing plasma in a concentration of 10% increased GH release in cultures of dispersed rat anterior pituitary cells. In the same system, synthetic growth hormone-releasing hormone (GRF)-44 stimulated the release of GH in a dose-dependent manner. However, at all dose levels including maximally stimulating doses of GRF, an additive effect on GH release was seen with 10% of the GH releasing plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1995

Growth hormone (GH)-releasing heptapeptide, but not GH-releasing hormone, inhibits thyrotropin-stimulated thyroid hormone secretion and cAMP formation in cultured human thyroid follicles.

Synthetic heptapeptide growth hormone-releasing peptide-1 (GHRP-1) potently stimulates GH release in many species, including humans. We investigated the direct in vitro effect of this peptide, compared to growth hormone-releasing hormone (GHRH), on cultured human thyroid follicles. The results indicate that whereas GHRP-1 (6-600 micrograms/l) or GHRH (6-600 micrograms/l) alone had no effect on basal triiodothyronine (T3) secretion or cAMP formation, the heptapeptide (6-600 micrograms/l), but not GHRH (6-1200 micrograms/l), dose-dependently inhibited thyrotropin (TSH)-stimulated T3 secretion and cAMP formation. Moreover, GHRP-1 also dose-dependently inhibited forskolin-stimulated T3 secretion. It would seem, therefore, that the GHRP-1-induced inhibitory effect on thyroid function is located downstream of cAMP formation, without necessarily excluding an additional inhibitory action at a pre-cAMP site. These results additionally demonstrate differences in the mode of action of GHRP-1 and GHRH.

Cells, Cultured↗
PubMed1996

Acute administration of recombinant human growth hormone inhibits the somatotrope responsiveness to growth hormone-releasing hormone in childhood.

In adulthood the growth hormone (GH) response to growth hormone-releasing hormone (GHRH) is inhibited by previous acute administration of either GH or GHRH and it is restored by substances that inhibit hypothalamic somatostatin release. Because in children the GH response to GHRH is not affected by previous neurohormone administration, it has been suggested that in childhood a GH increase is not able to trigger the somatostatin-mediated negative GH autofeedback mechanism. To verify this hypothesis, in 25 children (8 girls and 17 boys; 15 prepubertal and 10 in pubertal stages II-IV) with familial short stature (normal height velocity and insulin-like growth factor I levels) we studied the effect of acute i.v. administration of different recombinant human GH doses (group 1, N = 5, 0.06 U/kg; group 2, N = 6, 0.01 U/kg; group 3, N = 7, 0.005 U/kg at - 150 min) or saline on the GH response to GHRH (1 microgram/kg i.v. at 0 min). In another group (N = 7), we studied the effect of 0.005 U/kg iv recombinant human GH or saline on the GH response to GHRH combined with arginine (0.5 g/kg i.v. over 30 min), which likely inhibits hypothalamic somatostatin release. Serum GH increases after recombinant human GH were dose-dependent (GH peak, mean +/- SEM, 171.7 +/- 24.4, 33.3 +/- 3.9 and 21.8 +/- 5.1 micrograms/l, respectively). The administration of recombinant human GH strongly inhibited the GHRH-induced GH rise in all groups (group 1, 7.1 +/- 1.7 vs 23.1 +/- 7.6 micrograms/l, p < 0.05; group 2, 9.5 +/- 2.8 vs 26.9 +/- 8.5 micrograms/l, p < 0.05; group 3, 9.1 +/- 2.7 vs 34.8 +/- 7.2 micrograms/l, p < 0.02). The GH response to arginine + GHRH (56.9 +/- 13.3 micrograms/l) was higher than that to GHRH alone recorded in group 1 (p < 0.005), group 2 (p < 0.01) and group 3 (p < 0.01), while exogenous recombinant human GH failed to inhibit it (45.0 +/- 9.4 micrograms/l). Our results demonstrate that in childhood, as well as in adulthood, recombinant human GH administration inhibits the somatotrope responsiveness to GHRH. This inhibitory effect is likely to be mediated by hypothalamic somatostatin release.

Arginine↗
PubMed1977

Luteinizing hormone release after two injections of synthetic luteinizing hormone releasing hormone in the ewe.

Anoestrous ewes were given two injections of 30 mug synthetic luteinizing hormone releasing hormone (LH-RH) separated by one of the following intervals: 1-5, 3, 6, 12 or 24 h. The first injection caused an increase in the plasma LH concentration in each animal. The response to the second injection was dependent on the interval between the injections. When the second injection was administered 1-5 h after the first it caused a further increase in the LH concentration to maximal levels which were significantly greater than those induced in the other anoestrous groups. When the second injection was administered 3 h after the first, there was no significant difference between the responses to the two injections although the time to reach the maximal LH concentration was shorter and the height of the LH peak was greater in each animal following the second injection. When the second injection was administered 6, 12 or 24 h after the first, the LH response was significantly less, in terms of height and area of the induced peak, than following the first injection. The LH response to the second injection was particularly low in the 12 and 24 h groups. Two injections of 30 mug synthetic LH-RH were also administered at 1-5 h intervals to ewes on either day 10 of the oestrous cycle or at onset of oestrus. The pattern of LH responses in all these animals was similar to that observed in anoestrous ewes injected at 1-5 h intervals. The total LH release, as assessed in terms of the induced peaks, was significantly greater in the onset of oestrus group than in the day 10 group or any of the anoestrous groups. Presumably the sensitization-desensitization sequence of the pituitary gland to LH-RH which has been demonstrated, together with the effects of sex steroid hormones, must play an important part in the development and decay of the natural preovulatory LH peak.

Anestrus↗
PubMed1988

Galanin abolishes the inhibitory effect of cholinergic blockade on growth hormone-releasing hormone-induced secretion of growth hormone in man.

In five healthy normal male volunteers, pretreatment with the cholinergic muscarinic antagonist pirenzepine (30 mg i.v.) almost abolished the growth hormone (GH) response to a maximal dose (120 micrograms i.v.) of growth hormone-releasing hormone (GHRH) (GH response at 40 min 5.6 + 1.3 mU/l with GHRH and pirenzepine vs 40.8 +/- 5.3 mU/l with GHRH alone, P less than 0.02). Concomitant i.v. infusion of galanin (40 pmol/kg/min) with pirenzepine not only restored but significantly potentiated the GH response to GHRH (GH at 40 min 72.2 +/- 10.5 mU/l, P less than 0.001 vs GHRH and pirenzepine, P less than 0.02 vs GHRH alone). Previous studies have proposed that cholinergic pathways control GH release via somatostatin and this study suggests that galanin may act by modulating hypothalamic somatostatinergic tone either directly or, possibly, by facilitating cholinergic neurotransmission.

Adult↗
PubMed1989

Effects of hypothyroidism, tri-iodothyronine and glucocorticoids on growth hormone responses to growth hormone-releasing hormone and His-D-Trp-Ala-Trp-D-Phe-Lys-NH2.

The aim of this study was to investigate the role of thyroid hormones and glucocorticoids on GH secretion. Secretion of GH in response to GH-releasing hormone (GHRH) (5 micrograms/kg) was markedly (P less than 0.001) decreased in hypothyroid rats in vivo (peak GH responses to GHRH, 635 +/- 88 micrograms/l in euthyroid rats vs 46 +/- 15 micrograms/l in hypothyroid rats). Following treatment with tri-iodothyronine (T3; 20 micrograms/day s.c. daily for 2 weeks) or cortisol (100 micrograms/day s.c. for 2 weeks) or T3 plus cortisol, a marked (P less than 0.01) increase in GH responses to GHRH was observed in hypothyroid rats (peak GH responses, 326 +/- 29 micrograms/l after T3 vs 133 +/- 19 micrograms/l after cortisol vs 283 +/- 35 micrograms/l after cortisol plus T3). In contrast, none of these treatments modified GH responses to GHRH in euthyroid animals. Hypothyroidism was also associated with impaired GH responses to the GH secretagogue, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 (GHRP-6). Secretion of GH in response to GHRP-6 in vivo was reduced (P less than 0.01) in hypothyroid rats (peak GH responses, 508 +/- 177 micrograms/l in euthyroid rats vs 203 +/- 15 micrograms/l in hypothyroid rats). In-vitro studies carried out using monolayer cultures of rat anterior pituitary cells derived from euthyroid and hypothyroid rats showed a marked impairment of somatotroph responsiveness to both GHRP-6 and somatostatin in cultures derived from hypothyroid rats. In summary, our data suggest that thyroid hormones and glucocorticoids influence GH secretion by modulating somatotroph responsiveness to different GH secretagogues.

Animals↗
PubMed1994

Cortisol inhibition of growth hormone-releasing hormone-stimulated growth hormone release from cultured sheep pituitary cells.

Cortisol inhibits growth hormone (GH) release in short-term culture and is stimulatory in long-term cultures of rat and human pituitary cells. This study sought to determine the in vitro effects of cortisol on GH release and the signal transduction pathways mediating the effects of cortisol on GH release from cultured ovine somatotrophs. Pituitary cells were dispersed with collagenase and placed in culture medium for 4 days. The data indicate that cortisol inhibited growth hormone-releasing hormone (GHRH)-stimulated GH release by at least 2 h. In short-term culture GHRH-, forskolin- and dibutyryl cyclic AMP-stimulated GH release were inhibited by cortisol, suggesting an effect distal to the membrane and involving a protein kinase A (PKA)-dependent pathway. GH release initiated by KCl was inhibited by cortisol, but GH release caused by the calcium ionophore A23187 was unaffected. This suggests a possible action of cortisol on the calcium channels. The inhibition by cortisol of the calcium-dependent secretion of GH release appeared to play a smaller role in mediating cortisol inhibition of GH release than that seen with PKA. Attempts to overcome cortisol inhibition of GH release using puromycin, arachidonic acid or pertussis toxin were unsuccessful. Since cortisol inhibition of GH release does not occur via the mechanisms found in other cell types, cortisol inhibition of pituitary cell secretions appears to be cell-specific rather than utilizing a single inhibitory mechanism. The majority of cortisol actions on the somatotroph appear to act at a site distal to the production of cyclic AMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

The hormonal regulation of the oestrogen receptor in rat liver: an interplay involving growth hormone, thyroid hormones and glucocorticoids.

The regulation of the formation of the hepatic oestrogen receptor (ER) in adult female rats was studied by assaying steady state levels of ER and ER messenger RNA under different endocrine conditions. Hypophysectomy (HX) drastically reduced ER levels from 67.5 +/- 7.9 to 8.4 +/- 0.5 (means +/- S.E.M.) fmol/mg cytosolic protein. Continuous infusion of growth hormone (GH) to HX animals tripled ER and doubled ER mRNA levels. Treatment with triiodothyronine (T3) in a high dose (10 micrograms/day) doubled ER mRNA levels. The effects of T3 were dose-dependent, since a lower dose (1 microgram/day) increased neither ER nor ER mRNA levels. ER mRNA concentrations were increased by GH to 481 +/- 44% and by T3 to 372 +/- 35% of HX control levels 4 h after single injections of the hormones in HX animals. The glucocorticoid dexamethasone (DEX) alone increased neither ER nor ER mRNA levels in HX animals. DEX and GH in combination increased ER 5-fold and ER mRNA 2-fold compared with control levels in HX animals, whereas DEX and T3 in combination increased neither ER nor ER mRNA levels. Treatment with prolactin affected neither ER nor ER mRNA levels in HX rats. Insulin-like growth factor I (IGF-I) mRNA and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA levels were measured. GAPDH mRNA levels were increased 2.5-fold in HX rats by DEX and T3 in combination and almost 2-fold by DEX and GH in combination. IGF-I mRNA levels in HX rats were increased 4.5-fold by continuous infusion of GH alone, 6-fold by GH and T3 in combination, and 2.5-fold by GH and DEX in combination. These data indicate that both GH and T3 act directly on the liver to increase ER mRNA levels. GH, the most important of these hormones, also acts at the translational and/or post-translational level to increase ER protein levels. DEX treatment suppresses the stimulatory effects of T3, but not of GH.

Animals↗
PubMed2002

Relation of growth hormone response to growth hormone-releasing hormone to estimation of milk production via deuterium oxide dilution in beef cattle.

Current methods of estimating milk production in beef cows can be time-consuming, labor-intensive, and subject to high variability. The weigh-suckle-weigh (WSW) method requires repeated separation of offspring from their dams. Machine milking requires that animals be acclimated to the equipment prior to the estimation. The objective of Exp. 1 was to validate a deuterium oxide (D2O) dilution method of estimating milk production in cattle. In Exp. 1, Holstein calves (n = 5) averaging 29+/-2 d of age and 52.6+/-2.5 kg (+/- SE) were used as the model. Blood was collected for baseline D2O measurements followed by an injection of 300 mg D2O/kg BW. Syringes were weighed before and after the injection to gravimetrically determine the dose. Another blood sample was collected after D2O was allowed to equilibrate with body water for 2 h, and on each of the next five consecutive days, prior to feeding. Actual milk intake was measured by disappearance (i.e., amount of milk replacer offered to the calf minus the amount refused). Deuterium oxide in plasma was measured by mass spectrometry and milk intake was computed from the disappearance curve of D2O in blood plasma for each calf. Accumulated milk intake estimated by D2O dilution was highly correlated (y = 0.9x + 0.6; R2 = 0.99; P < 0.001) with actual milk intake. The objectives of Exp. 2 were to determine whether 1) D2O dilution was comparable to a standard measure of milk production in beef heifers and 2) growth hormone (GH) response to GH-releasing hormone (GHRH) in heifers at weaning is predictive of subsequent milk production. Deuterium oxide dilution and WSW were compared using 14 first-calf Angus heifers and their calves. Deuterium oxide dilution was used to estimate milk production of 40 first-calf Angus heifers that had been challenged with GHRH at weaning. Results indicate that the D2O dilution method is correlated (R2 = 0.89; P = 0.04) to the WSW estimation of milk production. Growth hormone response to GHRH in weanling heifers is positively related (R2 = 0.22; P = 0.03) to their subsequent milk production. Deuterium oxide dilution in calves offers an additional approach to the estimation of milk production of the dam in typical beef cattle production settings.

Animals↗
PubMed1986

Pulsatile or continuous infusion of luteinizing hormone-releasing hormone and hormonal concentrations in prepubertal beef heifers.

An experiment was conducted to determine if exogenous luteinizing hormone-releasing hormone (LHRH) administered iv intermittently as pulses (P) or by continuous sc infusion (I) using osmotic minipumps could sustain pulsatile LH release and induce estrous cyclicity in prepubertal heifers. Prepubertal heifers were assigned randomly to: 1) receive pulses of LHRH (n = 6; 2.5 micrograms LHRH/2 h for 72 h), 2) be infused with LHRH (n = 11; 1.25 micrograms LHRH/h for 72 h), or 3) serve as controls (n = 16). Blood was collected at 20-min intervals for 8 h (0900 to 1700 h) from six heifers in each group on d 1, 2, 3 (during treatment), and on d 4 (during 8 h after terminating LHRH treatments). Heifers given LHRH had higher (P less than .01) LH concentrations than controls. Preovulatory-like LH surges occurred in three I, two P and no control heifers during treatment. Pulse frequencies of LH (no. LH pulses/8 h) were greater (P less than .001) for P heifers than for I and control heifers due to pulsatile LHRH treatment. Serum estradiol was higher (P less than .01) during treatment for LHRH-treated heifers than for controls. Serum follicle-stimulating hormone, cortisol, and progesterone were unchanged during treatment. High levels of cortisol on d 1 declined (P less than .001) to baseline by d 2. Characteristic progesterone rises or short luteal phases occurred within 10 d of treatment initiation in more (P less than .05) LHRH-treated heifers (I = 45%, P = 33%) than controls (6%), although days to first observed estrus and first ovulation were unaffected by treatments. Although both continuous and pulsatile administration of LHRH successfully induced LH and estradiol release as well as preovulatory-like LH surges in some heifers, earlier initiation of estrous cycles was not achieved. Estrous cycles appeared to be delayed by exposure to continuous LHRH infusions during the peripubertal period.

Animals↗
PubMed1998

Effect of growth hormone releasing hormone on luteinizing hormone stimulated progestin biosynthesis in cultured rat ovarian granulosa cells.

In the present study, we examined the effects of growth hormone releasing hormone (GHRH) on luteinizing hormone (LH)-stimulated progestin biosynthesis. Granulosa cells from pregnant mare serum gonadotropin (PMSG)-treated immature rats were cultured in vitro in the absence or presence of ovine. National Institute of Health LH (100 ng/ml) with various doses of GHRH (10(-9), 10(-8) and 10(-7) mol/l) for 24 h. At the end of the incubation period, the incubation media were collected and levels of progesterone, 20 alpha-hydroxypregn-4-en-3-one and cyclic adenosine 3',5'-monophosphate (cAMP) were measured. GHRH significantly stimulated progesterone production and cAMP accumulation in media in a dose-dependent manner in the basal state (p < 0.01 and p < 0.001, respectively). In the presence of LH, GHRH significantly inhibited LH-stimulated progesterone production in a dose-dependent manner (p < 0.01), whereas increasing concentrations of GHRH produced progressive increases in cAMP accumulation (p < 0.05). Since increasing concentrations of GHRH produced progressive decreases in the ratio of progesterone to 20 alpha-hydroxypregn-4-en-3-one production in the LH-stimulated state (p < 0.01), GHRH may be involved in modulation of key steroidogenic steps concerned with progesterone degradation rather than formation in LH-stimulated rat granulosa cells. These results suggest that GHRH may regulate the effects of LH in granulosa cells and play an important role in the reproductive process.

Analysis of Variance↗