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PubMed1992

Electron microscopic identification of luteinizing hormone-releasing hormone-immunoreactive neurons in the medial olfactory placode and basal forebrain of embryonic mice.

Luteinizing hormone-releasing hormone is a decapeptide found in the brain and nose of all vertebrates that have been examined by immunocytochemical procedures with antiserum to luteinizing hormone-releasing hormone. It regulates the release of both luteinizing hormone and follicle-stimulating hormone from the gonadotropes of the anterior pituitary gland and promotes mating behavior. After about 11 days of embryogenesis in mice, luteinizing hormone-releasing hormone-immunoreactive cells are detected by immunocytochemical procedures in the medial olfactory placode, in the primordium of the vomeronasal organ. As they leave the olfactory placode, they run under the epithelial layer of the nasal septum associated with vomeronasal and terminalis nerves. Clustered, they stream toward the primordium of the olfactory bulb, passing along its ventromedial surface. Eventually, the largest numbers reach the septal and preoptic areas of the brain. Electron microscopic immunocytochemistry showed that luteinizing hormone-releasing hormone-immunoreactive product is accumulated just outside the nuclear envelope and in the lumen of rough endoplasmic reticulum adjacent to the cell nucleus of cells in and adjacent to the olfactory placode. As luteinizing hormone-releasing hormone-immunoreactive neurons migrate, they assume a fusiform shape and the immunoreaction product extends from the area around the nucleus throughout the cytoplasm, notably in processes which extend toward the direction of migration. Before and during migration, luteinizing hormone-releasing hormone was not detected in the Golgi apparatus or neurosecretory granules. It is inferred that as far as ultrastructural evidence is concerned, these neurons do not have a secretory function before they attain their target organs.

Animals↗
PubMed1992

Urinary excretion of human growth hormone in children with short stature: correlation with pituitary secretion of human growth hormone.

Thirty-five children with short-stature underwent insulin-loading and sleep tests for assessment of secretion of human growth hormone. Correlations between the levels of human growth hormone in the serum and urine during the tests were examined to elucidate the clinical significance of urinary human growth hormone levels in short children. The concentration and total amount of human growth hormone in the urine correlated significantly with the peak concentration of serum human growth hormone (r = 0.81, p less than 0.001 and r = 0.80, p less than 0.001, respectively) and the integrated concentration of human growth hormone (r = 0.85, p less than 0.001 and r = 0.85, p less than 0.001, respectively) in the insulin-loading test. The concentration and total amount of human growth hormone in the morning urine also correlated significantly with the peak concentration of serum human growth hormone (r = 0.80, p less than 0.001 and r = 0.70, p less than 0.001, respectively) and the integrated concentration of serum human growth hormone (r = 0.80, p less than 0.001 and r = 0.72, p less than 0.001, respectively) in the sleep test. The concentration or total amount of human growth hormone in the urine differed significantly among children with human growth hormone deficiency, those with nonendocrine short stature, and those with normal stature (p less than 0.05). These data suggest that measurement of human growth hormone in the urine may be used to assess secretion of human growth hormone, serving as a screening test for human growth hormone deficiency in children.

Adolescent↗
PubMed1984

A comparison of a powerful luteinizing hormone releasing hormone analogue agonist and estrogen in the treatment of advanced prostatic cancer.

Luteinizing hormone releasing hormone agonists presently are being evaluated in the treatment of patients with metastatic prostatic cancer. To determine the comparative benefits of a specific luteinizing hormone releasing hormone agonist [6-leu (1-9) luteinizing hormone releasing hormone nonapeptide ethylamide] relative to conventional estrogen therapy 23 patients with stage D2 prostatic cancer were randomized to receive either 1 mg. luteinizing hormone releasing hormone agonist daily (12) or 3 mg. diethylstilbestrol per day (11). Both agents were effective in inducing a remission in all patients, although diethylstilbestrol was slightly faster. The early phase of treatment with the luteinizing hormone releasing hormone agonist was dominated by a transient reversible deterioration (the flare) of the patient, which was believed to be related to the agonist-induced increase in serum androgens. At 1 year of followup adverse effects in both groups have been minor but the proportion of patients with progression in the luteinizing hormone releasing hormone agonist group (6 of 12) was significantly higher than that in the diethylstilbestrol group (0 of 11). Further investigation is required to determine the role of luteinizing hormone releasing hormone agonist in the treatment of patients with advanced prostatic cancer.

Aged↗
PubMed1994

Pharmacological characterization of a biosynthetic trisulfide-containing hydrophobic derivative of human growth hormone: comparison with standard 22 K growth hormone.

Growth hormone is the classical anabolic hormone which promotes organ growth after binding to somatogenic target cell receptors, present in various target tissues. The present study elucidated the pharmacological characteristics in vitro and in vivo of human growth hormone and a recently identified by-product of a recombinant human growth hormone preparation; i.e. a trisulfide-containing (cys 182-cys 189) hydrophobic, folding derivative of growth hormone, hydrophobic derivative-growth hormone. Standard growth hormone and hydrophobic derivative-growth hormone possessed similar characteristics in vitro, both as regards binding to the somatogenic receptor on the human IM-9 cell line, and the prolactin receptor-mediated proliferation of rat Nb2 cells. This indicates that no change occurs in the binding characteristics in spite of a change in conformation of the molecule. Using an ELISA assay that detected standard and hydrophobic derivative-growth hormone equally well, the plasma pharmacokinetical profiles of the preparations following a single intravenous or subcutaneous dose were indistinguishable. Thus, following initial disposition of hydrophobic derivative-growth hormone and standard growth hormone into a volume, V1, of one to two times the plasma volume, almost 90% of either compound disappeared from plasma during the alpha-phase of the plasma decay curve. Similar half-lives of 4-5 min. were found for hydrophobic derivative-growth hormone and standard growth hormone during this phase, indicating rapid removal of drug from the circulation. Also, the AUC and Cmax values for standard and hydrophobic derivative-growth hormone did not differ following intravenous or subcutaneous administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Urinary growth hormone estimation in diagnosing severe growth hormone deficiency.

Urinary growth hormone was measured in 54 children with short stature who had growth hormone deficiency that was initially diagnosed pharmacologically (arginine and L-dopa) and physiologically (mean growth hormone concentration during sleep evaluated twice). Based on the growth hormone response to pharmacological tests the subjects were subdivided into three groups: group A, 20 subjects with normal response (peak concentration > 8 micrograms/l); group B, 20 subjects with response between 4 and 8 micrograms/l; and group C, 14 subjects with response < 4 micrograms/l. In group A four subjects had an abnormally low nocturnal mean growth hormone concentration (< or = 3.3 micrograms/l). In group C seven subjects had multiple pituitary hormone deficiency and abnormal magnetic resonance imaging. All subjects had urine collected from 8.00 pm to 8.00 am for 4-5 consecutive nights. A positive correlation was found between serum nocturnal mean growth hormone values and urinary growth hormone in all subjects. Mean (SD) concentrations of urinary growth hormone were similar in groups A (18.0 (9.5) ng/g creatinine) and B (13.6 (5.9) ng/g creatinine), but significantly higher than that of group C (3.4 (3.7) ng/g creatinine). Considering as abnormal urinary growth hormones below the lower limit of the range in group A, specificity and sensitivity of urinary growth hormone was 100% and 35% respectively. Sensitivity for groups B and C were 5% and 78% respectively. When considering only the subjects of group C with pathological magnetic resonance findings, sensitivity increased to 100%. In the four subjects of group A with mean growth hormone concentration < or = 3.3 micrograms/l, specificity decreased to 80%. It is concluded that urinary growth hormone assay is characterised by a sensitivity too low to be regarded as improving the traditional diagnostic approach to define growth hormone deficiency, unless it is used to identify subjects with the most severe deficiencies.

Adolescent↗
PubMed1975

Decrease in serum immunoreactive parathyroid hormone in rats and in parathyroid hormone secretion in vitro by 1,25-dihydroxycholecalciferol.

The present study determined the effects of 1,25-dihydroxycholecalciferol on serum immunoactive parathyroid hormone and on parathyroid hormone secretion in vitro. Rats injected i.p. with 1,25-dihydroxycholecalciferol, 130 pmol (2 U)/140 g body wt, which is probably a physiologic dose, had a significant 43% decrease in serum immunoreactive parathyroid hormone at 4 h. In addition, this dose of 1,25-dihydroxycholecalciferol inhibited the serum immunoreactive parathyroid hormone response to hypocalcemia induced by phosphate injection. Because the increment in serum immunoreactive parathyroid hormone was less but the decrement in serum calcium more in phosphate plus 1,25-dihydroxycholecalciferol-treated than in phosphate plus vehicle-treated rats, the impaired serum immunoreactive parathyroid hormone response to 1,25-dihydroxycholecalciferol could not be attributed to the change in serum calcium. In studies of parathyroid hormone secretion from bovine parathyroid tissue in vitro, the concentration of 1,25-dihydroxycholecalciferol used for most experiments was 1nM, which is in the range found in rat serum. 1,25-Dihydroxycholecalciferol at 1 or 100 nM significantly inhibited parathyroid hormone secretion when medium calcium concentration was normal (1.5 mM), high (3.0 mM), and low (1.0 mM). Maximum inhibition ranged from 19 to 74%; inhibition was generally seen after 2 h of incubation; and inhibition was sustained or progressive thereafter. Vitamin A, 0.1 muM, caused a marked stimulation of parathyroid hormone secretion. 1,25-Dihydroxycholecalciferol at 1 nM markedly reduced (44%) the effect of vitamin A to stimulate parathyroid hormone secretion. This effect of 1,25-dihydroxycholecalciferol was maximal at 1 h and persisted thereafter. Another steroid, hydrocortisone, 10 muM, did not inhibit parathyroid hormone secretion, suggesting that the 1,25-dihydroxycholecalciferol effect was not a nonspecific inhibitory effect on parathyroid cells. Because other workers have shown that parathyroid hormone directly stimulates 1,25-dihydroxycholecalciferol secretion, our results are consistent with the concept that there is a feedback loop where parathyroid hormone directly stimulates secretion of 1,25-dihydroxycholecalciferol, which in turn directly inhibits secretion of parathyroid hormone.

Animals↗
PubMed1977

Reactivity of non-primate growth hormones and prolactins with human growth hormone receptors on cultured human lymphocytes.

Ovine placental lactogen is as reactive as human growth hormone with the human growth hormone receptor of cultured human (IM-9) lymphocytes, which confirms the findings of Carr and Friesen with receptors of human liver. We now also show that bovine and ovine growth hormones and ovine prolactin have reactivity for the human growth hormone receptor on IM-9 lymphocytes that is of the same order of magnitude (0.03%) as that previously reported for human placental lactogen. The binding studies predict that these non-primate hormones will have biological effects on skeletal growth in primates, either as agonists or antagonists. Previous studies have shown that when IM-9 lymphocytes are exposed to human growth hormone for 18 h at 37 C, there is a time and concentration dependent loss of human growth hormone receptors, and the magnitude of the loss of receptors after preincubation for 18 h at 37 C is greater than the average occupancy of receptors under steady state conditions for 90 min at 30 C. In the present study we show that human and ovine placental lactogens, ovine prolactin, and bovine and ovine growth hormones also produce this effect on the human growth hormone receptor. Since the cellular process by which a hormone induces loss of its own receptors appears to require binding of the hormone to its receptor as well as one or more subsequent steps in hormone action, it is likely that all of the preparations that induce receptor loss will be shown to have some agonist activity of human growth hormone in promoting skeletal growth in primates. Further, these studies extend the interrelationships between primate and non-primate pituitary and placental hormones from what has been suggested previously from biological and structural studies.

Animals↗
PubMed1978

Evidence for thyroid hormone-dependent and independent glucocorticoid actions in cultured cells. Studies on the induction of growth hormone and glutamine synthetase in GH1 cells and tyrosine aminotransferase in Reuber H-35 cells.

The induction of growth hormone synthesis and mRNA by thyroid hormone in cultured GH1 cells is mediated by the thyroid hormone nuclear receptor. In addition, the regulation of the growth hormone response by glucocorticoid is highly dependent on the action of thyroid hormone. To clarify whether thyroid hormone has a general influence on glucocorticoid action in GH1 cells, the glucocorticoid induction of growth hormone and glutamine synthetase was simultaneously examined. In contrast to the growth hormone response, the induction of glutamine synthetase by glucocorticoid was not influenced by thyroid hormone. Both responses appear to be modulated by the glucocorticoid receptor, and thyroid hormone had no influence on nuclear-associated glucocorticoid receptor levels. These results suggest that the thyroid hormone control of glucocorticoid induction of growth hormone may be a selective process, and the nuclear associated receptors for both thyroid and glucocorticoid hormones interrelate to control the growth hormone response.

Cell Line↗
PubMed1989

Factors predicting the outcome of varicocele repair for subfertility: the value of the luteinizing hormone-releasing hormone test.

The mechanism by which varicocele caused infertility is not yet clear. Endocrine factors have been suggested to explain impaired spermatogenesis in patients with varicocele. We conducted a prospective study on testosterone and gonadotropin levels and their response to the luteinizing hormone-releasing hormone test to determine the possible role of a hormonal defect in subfertility. Luteinizing hormone-releasing hormone tests were performed on 11 subfertile men with varicocele preoperatively and 3 months postoperatively. The differences in the luteinizing hormone response were statistically significant. The maximal luteinizing hormone levels also were significantly lower in patients whose spermiogram changed postoperatively. No significant changes were noted in testosterone and other gonadotropin levels postoperatively. A prognostic correlation between the change in response of luteinizing hormone to luteinizing hormone-releasing hormone (preoperatively and postoperatively) and improvement in fertility (pregnancy success) was found. We suggest that the luteinizing hormone-releasing hormone test should be considered to estimate the hormonal derangement and also the prognosis of an operation in subfertile men with varicocele.

Adult↗
PubMed2003

Single administration of interleukin-1 increased corticotropin releasing hormone and corticotropin releasing hormone-receptor mRNA in the hypothalamic paraventricular nucleus which paralleled long-lasting (weeks) sensitization to emotional stressors.

Single exposure to the proinflammatory cytokine interleukin-1 induces sensitization of the adrenocorticotropin hormone and corticosterone responses to stressors weeks later (hypothalamus-pituitary-adrenal sensitization). Hypothalamus-pituitary-adrenal responses are controlled by corticotropin-releasing hormone and arginine-vasopressin secreted from parvocellular corticotropin-releasing hormone neurons of the hypothalamic paraventricular nucleus and may involve autoexcitatory feedback mechanisms. Therefore, we studied the temporal relationship between resting levels of corticotropin-releasing hormone, corticotropin-releasing hormone-R1 and arginine-vasopressin receptor (V1a, V1b) mRNAs in the paraventricular nucleus and the development of hypothalamus-pituitary-adrenal sensitization to an emotional stressor (novelty). The adrenocorticotropin hormone precursor molecule proopiomelanocortin hnRNA in the pituitary gland served as an index for acute activation. Single administration of interleukin-1 induced sensitization of the hypothalamus-pituitary-adrenal to novelty from 3 to 22 days later, but not after 42 days. Single administration of interleukin-1 induced biphasic increases in corticotropin-releasing hormone and corticotropin-releasing hormone-R1 mRNAs in the paraventricular nucleus: an early peak within 24 h, followed by a delayed (>7 days) increase that peaked after 22 days. Hypothalamic V1a and V1b mRNA levels were unaffected. In contrast, in the pituitary gland, there was an early decrease in corticotropin-releasing hormone-R1 mRNA (from 10.5 to 3 h after interleukin-1) and V1b receptor mRNA (3 to 6 h), which returned to control levels from 24 h onwards. Thus, interleukin-1-induced long-lasting hypothalamus-pituitary-adrenal sensitizations associated with prolonged activation of corticotropin-releasing hormone and corticotropin-releasing hormone-R1 mRNA expression in the paraventricular nucleus, but not with changes in the expression of proopiomelanocortin hnRNA or V1b receptor or corticotropin-releasing hormone R1 mRNAs in the pituitary gland. We propose that transient exposure to immune events can induce long-lasting hypothalamus-pituitary-adrenal sensitization, which at least in part involves long-term hypothalamic adaptations that enhance central corticotropin-releasing hormone signaling.

Adrenocorticotropic Hormone↗
PubMed1999

Effects of tamoxifen on steroid hormone receptors and hormone concentration and the results of DNA analysis by flow cytometry in endometrial carcinoma.

OBJECTIVES: Tamoxifen is a nonsteroidal triphenylethylene derivate with a predominant antiestrogen activity, used in the endocrine treatment of breast and endometrial cancer. It is not known which endometrial carcinomas will respond favorably to tamoxifen and which ones will not. The aim of this study was to find out whether tamoxifen has an effect on hormone steroid receptors, hormone concentration, DNA content, and proliferative activity in endometrial cancer and to correlate the tamoxifen-induced changes with pathologic parameters such as clinical stage, tumor differentiation, depth of invasion, and histologic type. METHODS: Thirty postmenopausal women with endometrial carcinoma were treated with 30 mg of tamoxifen daily for 7-10 days after curettage. Steroid hormone receptors (estrogen and progesterone receptors), levels of follicle-stimulating hormone, luteinizing hormone, prolactin, estradiol, progesterone, testosterone, dehydroepiandrosterone sulfate, sex hormone binding globulin, and DNA ploidy and proliferative activity were determined before and after therapy. The patients were also divided into favorable and unfavorable prognosis groups according to classical histological parameters. The patients in the favorable group consisted of patients with stage I disease, well and moderately differentiated tumors, favorable histologic type, and a depth of myometrial invasion of less than (1/3). The patients with only one of the unfavorable parameters (clinical stage II or III, poorly differentiated tumors, unfavorable histologic types, and deeper invasion of myometrium) were included in the unfavorable prognosis group. RESULTS: After the treatment, there was a net increase in the progesterone receptors and sex hormone binding globulin and a significant decrease in the estrogen receptors. The increase in progesterone receptors and decrease in estrogen receptors occurred in the patient group with favorable prognosis regarding histologic type, degree of differentiation, and clinical stage, but also in the unfavorable prognosis group regarding the depth of myometrial invasion. Statistically significant decrease in the follicle-stimulating hormone concentration was observed in the groups with favorable prognosis regarding histologic type, depth of myometrial invasion, and grade of differentiation. Concentration of sex hormone binding globulin was significantly increased in groups with favorable prognosis if histologic type and grade of differentiation were taken into account. On the other hand, there was a significant decrease in the concentration of luteinizing hormone in the group with unfavorable histologic type and also a decrease in progesterone concentration in patients with unfavorable prognosis regarding the grade of differentiation. There was no statistical significance either in the concentrations of other hormones measured or in the DNA analysis by flow cytometry. CONCLUSIONS: Our results revealed that tamoxifen can increase progesterone receptors and decrease estrogen receptors in endometrial cancer. The effect was most pronounced in tumors with favorable clinicopathologic parameters. We conclude that tamoxifen therapy can induce progesterone receptor synthesis even in tumors with low initial progesterone receptor levels, making such tumors potentially responsive to additional hormonal therapy with progesterone.

Adenocarcinoma↗
PubMed1992

Attenuated proestrous luteinizing hormone surges in middle-aged rats are associated with decreased pituitary luteinizing hormone-beta messenger ribonucleic acid expression.

OBJECTIVE: This study determined whether attenuated preovulatory luteinizing hormone surges in aging rats are associated with a decrease in pituitary luteinizing hormone content or luteinizing hormone beta-messenger ribonucleic acid expression on proestrus. STUDY DESIGN: Blood samples were taken every 90 minutes from 1:30 to 10:30 PM on proestrus in young (n = 8) and middle-aged (n = 12), regularly cyclic rats for plasma luteinizing hormone determination. On the next proestrus at 12 noon, rats were killed and the pituitaries were removed for luteinizing hormone content determination by radioimmunoassay and luteinizing hormone beta-messenger ribonucleic acid expression by dot blot analysis. Results were analyzed by one-way analysis of variance. RESULTS: Seven of the middle-aged rats had attenuated luteinizing hormone surges while the remaining five females had surges similar to those of young rats. On the next proestrus, all rats had similar quantities of pituitary luteinizing hormone. However, luteinizing hormone beta-messenger ribonucleic acid expression in middle-aged rats with attenuated luteinizing hormone surges was lower (p less than 0.05) than that of middle-aged and young rats with normal surges. CONCLUSION: Decreased luteinizing hormone beta-messenger ribonucleic acid expression, but not pituitary luteinizing hormone content at 12 noon on proestrus is correlated with attenuated luteinizing hormone surges in middle-aged rats.

Aging↗
PubMed1992

Intracellular calcium and the signaling mechanism of luteinizing hormone-releasing hormone in rat granulosa cells.

OBJECTIVE: The purpose of these studies was to determine the source(s) of the increase in intracellular free calcium in response to luteinizing hormone-releasing hormone in ovarian granulosa cells. STUDY DESIGN: Rat granulosa cells were cultured and loaded with fura-2-acetoxy-methyl ester, a fluorescent calcium indicator dye, and intracellular free calcium measured by microspectrofluorometry. The source of the luteinizing hormone-releasing hormone induced increase in intracellular Ca++ was investigated with various calcium channel blockers (verapamil, diltiazem, and nifedipine), high K+ buffer, and perifusion with media lacking Ca++. RESULTS: All three voltage-sensitive calcium channel blockers (10(-5) mol/L) tested were ineffective in blocking the luteinizing hormone-releasing hormone induced intracellular Ca++ increase. Treatment with high K+ buffer also had no effect. Perifusion with media lacking calcium resulted in a gradual loss of the luteinizing hormone-releasing hormone response, an effect that was accelerated by repeated stimulation with hormone. Transient replacement of extracellular Ca++ failed to restore the response but continued perifusion with Ca(++)-replete media allowed a luteinizing hormone-releasing hormone response 10 minutes later. CONCLUSIONS: The luteinizing hormone-releasing hormone induced intracellular Ca++ increase does not appear to result from the opening of voltage-sensitive or K(+)-dependent Ca++ channels. To the contrary, this response likely results from the release of Ca++, primarily from intracellular stores.

Animals↗
PubMed1991

Cardiovascular effects of growth hormone treatment in growth-hormone-deficient adults: stimulation of the renin-aldosterone system.

1. In adult humans with growth hormone deficiency, treatment with growth hormone has recently been shown to have major anabolic effects and to improve exercise performance. The cardiovascular effects of growth hormone in adults with growth hormone deficiency were examined in 24 patients treated with recombinant human growth hormone (0.07 units/kg at night) in a double-blind, placebo-controlled trial lasting 6 months. 2. Compared with placebo, resting M-mode echocardiography showed increases in left ventricular end-diastolic dimension and stroke volume in the group treated with recombinant human growth hormone. No differences were noted between the groups with respect to left ventricular end-systolic dimension, fractional shortening, wall thicknesses or mean arterial blood pressure. Left ventricular myocardial mass increased in the group given recombinant human growth hormone. 3. The supine plasma renin activity was increased and remained elevated over the 6 months, whereas the plasma aldosterone concentration was unchanged, after treatment with recombinant human growth hormone. Clinical signs of sodium retention were evident during the first 3 months of treatment with recombinant human growth hormone. 4. We conclude that treatment with recombinant human growth hormone in adults with growth hormone deficiency resulted in small increases in left ventricular pre-load, due to the sodium-retaining action of growth hormone. Activation of the renin-aldosterone system was involved in such changes. Myocardial hypertrophy was observed without changes in mean arterial pressure, reflecting the anabolic action of growth hormone.

Adult↗
PubMed1977

Regulation of growth hormone messenger RNA by thyroid and glucocorticoid hormones.

Thyroid and glucocorticoid hormones stimulate growth hormone synthesis in cultured rat pituitary cells (GC). We have compared changes in growth hormone production and mRNA in these cells. Triiodothyronine (10 nM) and dexamethasone (1 micron) stimulated increases in growth hormone production by 2.5- and 3.8-fold, respectively. There were corresponding increases in the capacity of RNA from hormone-treated cells to direct synthesis of pregrowth hormone in a wheat germ cell-free translation system, suggesting hormone-regulated increases in growth hormone mRNA. Hormone-induced changes in mRNA were also demonstrated by determining the kinetics of hybridization of a cDNA probe prepared from RNA enriched (about 70%) for growth hormone translational activity with RNA from control and hormone-treated cells. These results suggest that thyroid and glucocorticoid hormones can regulate growth hormone production by influencing the levels of its mRNA.

Antigen-Antibody Reactions↗
PubMed1980

Aggregation of luteinizing hormone receptors in granulosa cells: a possible mechanism of desensitization to the hormone.

The temporal relationship between redistribution of receptors to lutropin (luteinizing hormone)/human chorionic gonadotropin in cultured rat ovarian granulosa cells and the cellular response to hormonal challenge were studied. Visualization of receptor-bound human chorionic gonadotropin by indirect immunofluorescence, with hormone-specific antibodies after fixation with 2% formaldehyde, revealed the existence of small clusters around the entire cell circumference 5--20 min after exposure to the hormone at 37 degrees C. Such small receptor aggregates were also evident if hormone incubation was at 4 degrees C or if cells were fixed with 2% formaldehyde before incubation. Larger clusters were evident after prolonged incubation with the hormone (2--4 hr) at 37 degrees C. The later change coincided with diminished cyclic AMP accumulation in respose to challenge with fresh hormone. When the fixation step was omitted and antibodies to human chorionic gonadotropin were applied after hormonal binding, acceleration of both receptor clustering and the desensitization process was observed. This maneuver also induced capping of the hormone receptors. In contrast, monovalent Fab' fragments of the antibodies were without effect. Internalization of the bound hormone in lysosomes, and subsequent degradation, was evident 8 hr after hormonal application and was not accelerated by the antibodies. It is suggested that clustering of the luteinizing hormone receptors may play a role in cellular responsiveness to the hormone. Massive aggregation of the receptors may desensitize the cell by interferring with coupling to adenylate cyclase.

Adenylyl Cyclases↗
PubMed1978

Effect of adrenocorticotropic hormone on plasma glucocorticoids and antidiuretic hormone of cattle exposed to 20 and 33 C.

Four open, dry Holstein cows in the University of Missouri Climatic Laboratory were used to study the effect of adrenocorticotropic hormone administration on glucocorticoids and antidiuretic hormone of plasma in two reversal trials at thermoneutral (20 C, 50% relative humidity) and heat (33 C, 50% relative humidity) conditions. Average glucocorticoids (saline versus adrenocorticotropic hormone) at thermoneutral were 8.3 and 41.2 ng/ml while values for heat were 6.2 and 40.4 ng/ml. The effect of heat on glucocorticoids of plasma was not significant. Injection of adrenocorticotropic hormone under thermoneutrality and heat caused a marked increase in antidiuretic hormone within 5 min which lasted to 120 min. At thermoneutral average antidiuretic hormone levels (saline versus adrenocorticotropic hormone) were .5 and 1.9 pg/ml while values for heat were 1.8 and 3.6 pg/ml. Antidiuretic hormone concentrations under heat were higher than thermoneutral in cows injected with saline and andrenocorticotropic hormone. The fast response of antidiuretic hormone of plasma to exogenous adrenocorticotropic hormone suggests that adrenocorticotropic hormone might act directly at higher levels of the central nervous system causing release of antidiuretic hormone.

Adrenocorticotropic Hormone↗
PubMed1996

Effects of physiologic growth hormone therapy on bone density and body composition in patients with adult-onset growth hormone deficiency. A randomized, placebo-controlled trial.

BACKGROUND: Patients with adult-onset growth hormone deficiency have reduced bone density and increased fat mass. Growth hormone at high doses may decrease body fat in these patients, but the effects of growth hormone at more physiologic doses on bone density and body composition have not been convincingly shown. OBJECTIVE: To determine whether long-term growth hormone therapy at a dose adjusted to maintain normal insulin-like growth factor 1 (IGF-1) levels has clinical effects in patients with adult-onset growth hormone deficiency. DESIGN: Randomized, placebo-controlled study. SETTING: Tertiary referral center. PATIENTS: 32 men with adult-onset growth hormone deficiency. INTERVENTION: Growth hormone (initial daily dose, 10 micrograms/kg of body weight) or placebo for 18 months. The growth hormone dose was reduced by 25% if IGF-1 levels were elevated. MEASUREMENTS: Body composition and bone mineral density of the lumbar spine, femoral neck, and proximal radius were measured by dual energy x-ray absorptiometry at 6-month intervals. Markers of bone turnover were also measured during the first 12 months of the study. RESULTS: Growth hormone therapy increased bone mineral density in the lumbar spine by a mean (+/- SD) of 5.1% +/- 4.1% and bone mineral density in the femoral neck by 2.4% +/- 3.5%. In the growth hormone group, significant increases were seen in the following markers of bone turnover: osteocalcin (4.4 +/- 3.6 mg/L to 7.2 +/- 4.6 mg/L) and urinary pyridinoline (39.0 +/- 19.8 nmol/mmol of creatinine to 55.7 +/- 25.5 nmol/mmol of creatinine) and deoxypyridinoline (8.4 +/- 7.1 nmol/mmol of creatinine to 14.9 +/- 9.4 nmol/mmol of creatinine). Percentage of body fat in the growth hormone group decreased (from 31.9% +/- 6.5% to 28.3% +/- 7.0%), and lean body mass increased (from 59.0 +/- 8.5 kg to 61.5 +/- 6.9 kg). These changes were significant compared with corresponding changes in the placebo group (P < 0.01 for all comparisons). CONCLUSIONS: Growth hormone administered to men with adult-onset growth hormone deficiency at a dose adjusted according to serum IGF-1 levels increases bone density and stimulates bone turnover, decreases body fat and increases lean mass, and is associated with a low incidence of side effects.

Adult↗