Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HORMONES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources
PubMed1988

Active immunization of heifers against luteinizing hormone-releasing hormone, human chorionic gonadotropin and bovine luteinizing hormone.

Seventy crossbred heifers were allotted randomly to 10 treatment groups. Treatments consisted of active immunization against ovalbumin (OV) conjugates of luteinizing hormone-releasing hormone (LHRH), human chorionic gonadotropin (hCG) and bovine luteinizing hormone (bLH) with each of three adjuvants. The adjuvants were complete Freund's adjuvant (CFA), M103(6) and 6VR6. Control animals were immunized against OV alone using CFA. Bulls were placed with the heifers following immunization to allow comparison of pregnancy rates between groups. Blood samples were collected weekly for 14 wk to determine antibody concentrations. Significant levels of circulating LH or LHRH antibodies were detected in heifers immunized with each of the hormone conjugates. Complete Freund's adjuvant was the most effective for stimulating antibody response to these antigens; however, M103 was equally effective when used with bLH or hCG conjugates. None of the heifers in the bLH-OV-CFA, bLH-OV-M103 or LHRH-OV-CFA immunization groups was pregnant at slaughter, whereas 71% of the OV-CFA control heifers were pregnant. Fertility suppression may be achieved in the bovine by active immunization against any of these three hormone conjugates. However, the duration of this study (8 wk after immunization) does not allow evaluation of the duration of effectiveness of each of the treatments.

Adjuvants, Immunologic↗
PubMed1991

A potential code of luteinizing hormone-releasing hormone-induced calcium ion responses in the regulation of luteinizing hormone secretion among individual gonadotropes.

Luteinizing hormone-releasing hormone (LHRH) induces two Ca2+ responses in single gonadotropes: a Ca2+ spike/plateau or oscillation. Similar receptor-mediated Ca2+ signals have been reported in many cell types but their functional significance is obscure. Accordingly, we have determined the concentration-response properties of LHRH-induced luteinizing hormone (LH) release at the single cell level. We demonstrate a critical single cell LHRH threshold for LH release. Each gonadotrope had a particular LHRH threshold value and a range of different single cell thresholds was distributed in the gonadotrope population. The physiological significance of the threshold was demonstrated by a striking reduction (delta ED50 = 153 nM) of the LHRH threshold immediately before the preovulatory surge of LH release. The metestrous phenotype of secretion resembled a quantal process in contrast with the graded process of the proestrous phenotype. That is, the quantity of hormone secreted per metestrous gonadotrope was independent of LHRH concentration and more all-or-none than graded. The LHRH threshold and the quantal secretion process of metestrous gonadotropes was further studied by measuring cytosolic Ca2+ using fura-2 and digital imaging microscopy. We provide evidence suggesting that the Ca2+ spike/plateau and oscillation are the respective responses to subthreshold and suprathreshold concentrations of LHRH. It is proposed therefore that the Ca2+ oscillation and spike/plateau response form a binary intracellular signaling code that functions as an on-off switch. It is further proposed that this potential code unraveled here for the regulation of hormone secretion may also regulate other gonadotrope functions. Thus, while the Ca2+ spike/plateau response is strongly associated with LH release, it may be associated with reduced levels of LH-beta mRNA, and reduced numbers of LHRH receptors. Conversely, while the Ca2+ oscillation appears to be unrelated to LH release, it may be associated with increased levels of LH-beta mRNA, and increased numbers of LHRH receptors. This model may explain in molecular terms the long-standing observation that an invariant, albeit pulsatile, pattern of LHRH release is sufficient to support the preovulatory surge of LH release.

Animals↗
PubMed1989

Functional characterization of the rat growth hormone promoter elements required for induction by thyroid hormone with and without a co-transfected beta type thyroid hormone receptor.

We have extensively characterized the sequences of the rat growth hormone (rGH) promoter required for induction by T3 (thyroid hormone, 3,5,3'-L-triiodothyronine) in a transient transfection system. Oligonucleotides containing portions of the rGH promoter sequence with various deletions and point mutations were placed upstream of the first 137 base pairs of the rGH promoter or the heterologous herpes virus thymidine kinase promoter in chloramphenicol acetyltransferase expression vectors. The rGH137 and thymidine kinase promoters show no or minimal response to T3 in the basal state. The constructs were tested in GH4C1 rat pituitary cells and COS cells (functionally deficient in thyroid hormone receptor) with and without a co-transfected plasmid expressing a beta type c-erbA gene coding for a functional T3 receptor. Oligonucleotides containing the T3 receptor binding site confer hormone-dependent induction in a manner that is independent of either orientation or variation in position on the helix relative to the promoter. Point mutations in the sequence -189 to -173 result in loss of T3 induction, and bases between -173 and -167 were also required for a full T3 response. The minimal length to confer T3 induction to the rGH promoter was 23 base pairs (-190 to -167). Point mutations creating a perfect duplication of 7 base pairs within the receptor binding site conferred 12-fold T3 response to the rGH137 promoter, 3-fold greater than the wild type rGH237 construct. T3 inductibility was also transferred to the thymidine kinase promoter by an oligonucleotide containing the sequence -200 to -157, demonstrating that cell type specific elements located 3' to 157 of the rGH promoter are not required for thyroid hormone responsiveness.

Animals↗
PubMed1988

Rat growth hormone gene expression: both cell-specific and thyroid hormone response elements are required for thyroid hormone regulation.

The elements that we have identified in the 5'-flanking region of the rat growth hormone gene are shown in Figure 7, and the following conclusions are drawn: 1) Cell-specific expression of the rat growth hormone gene is mediated by two CSEs, which are located from -95 to -65 and from -137 to -107.2) These CSEs bind a common cell-specific trans-acting factor (GH-CSF), which is found in growth hormone-producing cells. 3) Enhanced levels of cell-specific expression may involve a protein-protein interaction when this factor binds on the same side of the DNA helix as the two CSEs. 4) A TRE is located between -208 and -178. 5) Activation of the gene by thyroid hormone appears to require both the TRE and one of the CSEs, and both are required to confer L-T3 stimulation to several heterologous promoters. 6) Our studies support the notion that stimulation by L-T3 involves the binding of the L-T3-receptor complex to the TRE, which enhances the function of the CSEs, resulting in stimulation of growth hormone gene expression.

Animals↗
PubMed1979

Cyclic release of luteinizing hormone and the effects of luteinizing hormone-releasing hormone injection in Asiatic elephants.

Cyclic changes in serum concentration of luteinizing hormone (LH) were observed throughout the estrous cycle of Asiatic elephants (Elephas maximus). The increase in serum LH was correlated with a slight increase in serum estradiol concentration and the onset of behavioral heat (willingness to mate). In a second series of studies, injection of luteinizing hormone-releasing hormone after 3 days of estrone administration induced an increase in serum LH. These studies indicate that the Asiatic elephant exhibits a cyclic LH release that can be experimentally induced by estrone and luteinizing hormone-releasing hormone administration.

Animals↗
PubMed1996

Effect of endothelin-1 in man--impact on basal and stimulated concentrations of luteinizing hormone, follicle-stimulating hormone, thyrotropin, growth hormone, corticotropin, and prolactin with and without pretreatment with nifedipine.

In healthy men, intravenous (IV) endothelin-1 suppresses the growth hormone (GH)-releasing hormone (GHRH)-stimulated increase in GH and prolactin (PRL) and augments corticotropin (ACTH)-releasing factor (CRF)-stimulated secretion of ACTH. Since some actions of endothelin-1 on pituitary function in vitro are antagonized by calcium channel antagonists, we have studied the effect of pretreatment with oral nifedipine (10 mg, given before infusion of endothelin-1 or vehicle) on basal and stimulated concentrations of pituitary hormones in a group of healthy men (N = 6). The augmentative effect of endothelin-1 on CRF-induced ACTH secretion (P < .05) was counteracted by pretreatment with nifedipine. Pretreatment with nifedipine further inhibited (P < .01) the GHRH-induced increase in plasma concentrations of GH (P < .05), which, in keeping with previous data, had already been reduced by IV endothelin-1 alone (P < .05). Thus, both endothelin-1 and nifedipine influence pituitary hormone secretion in healthy man. However, nifedipine does not ubiquitously counteract the effects of endothelin-1 since it enhances some of its actions on the pituitary and diminishes others. Endothelin-1 may therefore influence pituitary function by mechanisms other than activation of calcium channels alone.

Adrenocorticotropic Hormone↗
PubMed1986

Effects of corticotropin releasing factor and growth hormone releasing factor on pituitary hormone secretion in patients with congenital thyrotropin deficiency. Abnormal response of growth hormone to corticotropin releasing factor.

Blood concentrations of anterior pituitary hormones, ACTH, GH, TSH, PRL, LH, and FSH were determined in corticotropin releasing factor (CRF) test (synthetic ovine CRF 1.0 microgram per kg body weight) and growth hormone releasing factor (GRF) test (synthetic human pancreatic GRF-44 100 micrograms) in 2 female sibling patients with congenital isolated TSH deficiency, in their mother, in 2 patients with congenital primary hypothyroidism and in 8 normal controls. The patients with isolated TSH deficiency showed normally increased plasma ACTH and serum GH after CRF and GRF, respectively, and also showed an abnormal GH response to CRF. The serum GH showed a rapid increase to maximum levels (12.9 ng/ml) within 30 to 60 min followed by decrease. The possibility of secretion of abnormal GH could be excluded by the fact that on serum dilution, GH value gave a linear plot passing through zero. In addition, serum PRL, LH and FSH levels after CRF administration in case 1 and PRL after GRF in case 2 were also slightly increased but these responses were marginal. The mother of the patients, patients with congenital primary hypothyroidism, and normal healthy controls showed normal responses of pituitary hormones throughout the experiment. Data from the present study and a previous report show that abnormal GH response to the hypothalamic hormones (CRF, TRH and LHRH) may be observed in patients with congenital isolated TSH deficiency.

Adult↗
PubMed1987

Growth hormone response to growth hormone-releasing hormone in normal and uraemic children. Comparison with hypoglycaemia following insulin administration.

The uraemic syndrome is characterized by several endocrinological disturbances. This study was undertaken in order to evaluate the GH response to growth hormone-releasing hormone (GRH) in children with chronic renal failure (CRF) and to compare the results with those observed after insulin hypoglycaemia. Twenty-two children with CRF, 10 undergoing continuous ambulatory peritoneal dialysis (CAPD) and 12 on conservative treatment (CT), age ranges 2-15 years, were studied and the data were compared with those from 14 children with normal renal function and normal hormonal behaviour, affected by short stature (NC), and those form 13 healthy adult volunteers (NA). The GRH test (l micrograms/kg body weight, iv) was carried out in 8 CAPD, 8 CT, 9 NC and 10 NA subjects. The blood samples were taken every 30 min for 3 h in CAPD and CT and for 2 h in NC and NA starting at 09.00 h. The following hormones were measured: GH, LH, FSH, Prl, TSH and cortisol (F). The insulin test (0.1 U/kg body weight, iv) was carried out in 5 CAPD, 5 CT, 10 NC and 9 NA on blood samples taken every 30 min for 2 h, measuring GH and glycaemia. No adverse effects were observed after the infusion of GRH. GRH administration induced a prompt response in all subjects, but GH plasma levels were significantly higher in uraemic children than in adults (peak value of 43.5 +/- 8.2, 45.0 +/- 8.4, 27.8 +/- 6.0; 13.5 +/- 2.6 micrograms/ml in CAPD, CT, NC and NA, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Human anti-luteinizing hormone-releasing hormone antibodies in patients treated with synthetic luteinizing hormone-releasing hormone.

One hundred sixty-three patients who were given synthetic LH-RH therapeutically underwent monitoring of serum IgG anti-LH-RH antibodies. Five of the patients showed specific binding to antibodies. Development of anti-LH-RH antibodies was not limited to those patients with a congenital deficiency of LH-RH. Urticarial responses occurred in four patients, only one of whom had IgG antibodies. Patients who had IgG antibodies or an urticarial response underwent monitoring of their serum IgE anti-LH-RH antibodies, but none had a positive binding response. The refractory state which has been reported in patients in whom similar antibodies to LH-RH develop was not invariably observed among these patients.

Adult↗