Prolactin and growth hormone synthesis: effects of perphenazine, alpha-methyltyrosine and estrogen in different thyroid states.

The effects of thyroid hormones on prolactin (PRL) and growth hormone (GH) synthesis by the rat anterior pituitary gland were assessed in vitro. A marked reduction (84-87%) in the rate of H3-leucine incorporation into GH was evident 2-4 weeks after thyroidectomy, while incorporation into PRL was 52-71% less than that measured in glands from intact rats. A single injection of T4 (200 mug/kg) administered to thyroidectomized (THX) rats 48 hr before sacrifice significantly increased incorporation into both pituitary hormones, although the stimulation of GH synthesis was much more dramatic. Perphenazine, alpha-methyltyrosine and estrogen enhanced the rate of PRL synthesis in intact rats. Thyroid ablation did not affect the response to perphenazine, but significantly increased the response to alpha-methyltyrosine and estrogen. On the other hand, administration of T4 to THX rats receiving perphenazine, alpha-methyltyrosine or estrogen diminished the stimulatory influence of these treatments on PRL synthesis. Perphenazine, alpha-methyltyrosine and estrogen had no effect on the rate of GH synthesis in THX rats, nor did they alter the ability of T4 to restore GH synthesis in these animals. These results indicate that GH synthesis in the rat is dependent upon thyroid hormones and support the concept that these hormones exert their stimulatory effect directly on pituitary somatotrophs. Pituitary lactotrophs, however, appear to retain much of their capacity to synthesize PRL under conditions of thyroid deficiency. The changes in pituitary PRL levels and synthesis rate induced by thyroid ablation might reflect differences in the number rather than the activity of these cells.     

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.     

Investigations on myelination in vitro. Regulation by thyroid hormone in cultures of dissociated brain cells from embryonic mice.

Cultures of dissociated brain cells from embryonic mice were used to study the influence of thyroid hormone on myelination in vitro. Synthesis of myelin-associated lipids such as cerebrosides and sulfatides was used as an index for myelination. An experimental design, in which the cells were grown on medium containing serum from a thyroidectomized calf, was employed to demonstrate the direct effect of L-3,5,3'-triiodothyronine (T3Y on the biosynthesis of myelin lipids. The cells grown in the presence of hypothyroid calf serum which contained very low levels of thyroid hormones (T4 (thyroxine), 1.2 microgram/ml; T3, less than 25 ng/100 ml) compared to normal serum (T4, 5.8 microgram/ml; T3, 110 ng/100 ml) showed a diminished synthesis of myelin-associated glycolipids. This reduced activity could be restored to normal by including T3 (13 ng/ml) in the medium.     

Tissue-specific regulation of type III iodothyronine 5-deiodinase gene expression mediates the effects of prolactin and growth hormone in Xenopus metamorphosis

Prolactin (PRL) and growth hormone (GH) are known to be able to act as antimetamorphic hormones. From investigations of how PRL inhibits Xenopus tail regression in vitro, it was found that the both hormones could, in addition to their known antimetamorphic actions, upregulate mRNA expression of type III iodothyronine 5-deiodinase (5D), an enzyme that inactivates thyroid hormones (TH). Conversely, both PRL and GH were found to downregulate 5D mRNA expression in the liver. Blockage by PRL of TH-induced tail regression in organ culture was released by treatment with iopanoic acid (IOP, an inhibitor of 5D activity). The IOP-released tail regression displayed a unique morphology of the larger fins retained on the regressing tails, consistent with the finding that mRNA for both PRL receptor and 5D were enriched in the fin. The results suggest that the metamorphosis-modulating actions of PRL and GH are mediated, at least partially, by tissue-specific regulation of 5D mRNA expression.     

Piperine lowers the serum concentrations of thyroid hormones, glucose and hepatic 5'D activity in adult male mice.

Piperine, the main alkaloid of Piper nigrum fruits, was evaluated for its thyroid hormone and glucose regulatory efficacy in adult male Swiss albino mice. Its daily oral administration (2.50 mg/kg) for 15 days lowered the serum levels of both the thyroid hormones, thyroxin (T (4)) and triiodothyronine (T (3)) as well as glucose concentrations with a concomitant decrease in hepatic 5'D enzyme and glucose-6-phospatase (G-6-Pase) activity. However, no significant alterations were observed in animals treated with 0.25 mg/kg of piperine in any of the activities studied except an inhibition in serum T (3) concentration. The decrease in T (4), T (3) concentrations and in G-6-Pase were comparable to that of a standard antithyroid drug, Proylthiouracil (PTU). The hepatic lipid-peroxidation (LPO) and the activity of endogenous antioxidants, superoxide dismutase (SOD), and catalase (CAT) were not significantly altered in either of the doses. It appears that the action of P. nigrum on thyroid functions is mediated through its active alkaloid, piperine. We also suggest that a higher dose of piperine may inhibit thyroid function and serum glucose concentration in euthyroid individuals.     

Pancreatic polypeptides affect luteinizing and growth hormone secretion in rats

We have examined the effects of third cerebroventricular (3V) injections of avian and bovine pancreatic polypeptide (APP and BPP) and the C-terminal hexapeptide amide of human PP (CHPP) on the secretion of anterior pituitary hormones in conscious ovariectomized rats. Injection of APP (2.0 micrograms; 472 pmoles) or BPP (5.0 micrograms; 1191 pmoles) decreased plasma levels of luteinizing hormone (LH) when compared to pre-injection levels in these animals or to saline-injected controls. The lower dose of BPP (0.5 micrograms; 119 pmoles) decreased plasma LH versus pre-injection levels and control animals, however, these effects diminished at later times. Plasma growth hormone (GH) also decreased following 3V injections of APP (2.0 micrograms) or BPP (5.0 micrograms). The lower dose of BPP (0.5 microgram) initially inhibited GH release, however, this effect was rapidly reversed and GH levels were significantly greater than those in controls at 60 and 120 min. Injections of BPP or APP did not alter prolactin (PRL) or thyroid stimulating hormone (TSH) secretion. Administration of 2.0 micrograms and 0.2 microgram of CHPP (2488 and 249 pmoles) produced no significant effects on plasma LH, GH, PRL or TSH. APP and BPP had no consistent effects on hormone secretion from dispersed anterior pituitary cells. The results indicate that APP and BPP exert potent central effects which inhibit LH and GH release from the pituitary gland.     

Hormonal studies in postpartum female camels and their neonates

The expulsion of the fetus from the mother at parturition necessitates reorganization of the endocrine status in both individuals. In this study, the patterns of hormonal changes were investigated in postpartum Dromedary camels and their neonates. Blood samples were recovered within a few hours after calving from 10 female Dromedary camels and their calves, and sampling was continued at varying intervals upto Day 21 post partum. Sera were assayed for progesterone, cortisol and thyroid hormone concentrations by specific radioimmunoassays. Progesterone concentrations in the dams varied between 0.5 and 2.0 ng/ml on the day of calving and declined steadily thereafter to become undetectable by Day 9; progesterone remained undetectable in the neonates. Cortisol concentrations were high (25 to 30 ng/ml) at parturition in both the dams and their calves. They declined to 6 to 7 ng/ml in the dams, but became undetectable in the neonates by Day 14 post partum. The thyroid hormones were low in the dams (T(4) = 70; T(3) = 1.6 ng/ml) on Day 1 post partum but then increased gradually to Day 21 (T(4) = 110; T(3) = 2.2 ng/ml). In contrast, thyroid hormone concentrations in the neonates were 4 to 5 times higher than those of their mothers at birth. They declined thereafter but nevertheless remained at almost double the concentrations found in the dams.     

Effects of TRH on circulating growth hormone, prolactin and triiodothyronine levels in the bovine.

The effects of administration of synthetic thyrotropin-releasing hormone (TRH) on circulating growth hormone (GH), PROLACTIN (PRL) and triiodothyronine (T3) levels of lactating dairy cows, non-lactating dairy heifers, and beef cows were studied. Intravenous administration of 0.1, 1, and 5 microgram of TRH per kg of body weight (bw) elevated plasma GH and PRL levels of lactating cows within 5 min. The plasma GH and PRL levels increased in proportion to the dose of TRH and reached a peak 10 to 30 min after TRH injection. Intravenous administration of 1 microgram of TRH per kg of bw to 7 non-lactating heifers, 14 lactating dairy cows, and 5 non-lactating beef cows elevated plasma GH level to peak values after 15 min, the increase rates being 6.9, 5.6, and 3.8 times as high as those in the pretreatment levels. The mean maximum vale was also in that order. Plasma T3 levels of non lactating dairy heifers at pre- and post-injection of TRH were significantly higher than those of lactating cows. The peak values of plasma PRL were obtained between 5 to 30 min after TRH administration. The increase rates of lactating dairy cows, heifers, and beef cows were 19.2, 13.9, and 20.9 times as high as those in the pretreatment. In contrast to GH and T3, plasma PRL levels of both pre- and post-injection with TRH in lactating cows and heifers were significantly higher in May than in October, though the increase rates were similar. Plasma PRL levels of lactating dairy cows at pre- and post-injection with TRH were significantly higher than those of non-lactating heifers. Subcutaneous administration of TRH was also effective to increase plasma TH, rl, and T3 levels in lactating cows. No significant change of GH or PRL response to TRH was observed after a short-term pretreatment of thyroid hormones.     

Effect of non aromatizable androgens on LHRH and TRH responses in primary testicular failure

We have assessed the gonadotropin, TSH and PRL responses to the non aromatizable androgens, mesterolone and fluoxymestrone, in 27 patients with primary testicular failure. All patients were given a bolus of LHRH (100 micrograms) and TRH (200 micrograms) at zero time. Nine subjects received a further bolus of TRH at 30 mins. The latter were then given mesterolone 150 mg daily for 6 weeks. The remaining subjects received fluoxymesterone 5 mg daily for 4 weeks and 10 mg daily for 2 weeks. On the last day of the androgen administration, the subjects were re-challenged with LHRH and TRH according to the identical protocol. When compared to controls, the patients had normal circulating levels of testosterone, estradiol, PRL and thyroid hormones. However, basal LH, FSH and TSH levels, as well as gonadotropin responses to LHRH and TSH and PRL responses to TRH, were increased. Mesterolone administration produced no changes in steroids, thyroid hormones, gonadotropins nor PRL. There was, however, a reduction in the integrated and incremental TSH secretion after TRH. Fluoxymesterone administration was accompanied by a reduction in thyroid binding globulin (with associated decreases in T3 and increases in T3 resin uptake). The free T4 index was unaltered, which implies that thyroid function was unchanged. In addition, during fluoxymesterone administration, there was a reduction in testosterone, gonadotropins and LH response to LHRH. Basal TSH did not vary, but there was a reduction in the peak and integrated TSH response to TRH. PRL levels were unaltered during fluoxymesterone treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Serum thyroid hormones and reproductive characteristics of Rambouillet ewe lambs treated with propylthiouracil before puberty

Twenty-four Rambouillet ewe lambs (average weight=43.7+/-1.2 kg, approximately 6 months of age) were used to examine the effect of thyroid suppression before the onset of puberty on serum thyroid hormones, body weights (BW), and reproductive performance. Beginning in early September, ewe lambs were randomly assigned to three treatments (n=8 lambs/treatment). All animals remained in a single pen (4 x 12 m) with access to salt, water, shade and alfalfa hay (2.5 kg per animal per day) throughout the experiment. Beginning on Day 0 (first day of treatment), all ewe lambs received daily treatments (gavage) for 15 days consisting of 0, 20, or 40 mg 6-N-propyl-2-thiouracil(PTU)/kg BW per day. Beginning on Day 15, the 20 and 40 mg treatments were lowered to 10 and 20 mg PTU/kg BW, respectively. All animals were treated for 28 days. Ovarian cyclicity was determined by twice weekly progesterone (P(4)) analysis. Thyroxine (T(4)) concentrations were similar on Day 0 (61.6, 54.8 and 56.9+/-2.5 ng/ml, P=0.17) in ewe lambs receiving 0, 20 and 40 mg PTU/kg BW, respectively. By Day 7, both PTU-treated groups had T(4) values less than 20 ng/ml (9.0 and 15.4+/-2.5 ng/ml) compared with 78.5 ng/ml in controls (P<0.01). By 7 days after termination of PTU treatment, serum T(4) had risen to 29.1 and 26.9 (+/-2.9)ng/ml in the 20/10 and 40/20 PTU groups, respectively. On Day 66, control ewes had 55.0 ng T(4)/ml compared with 43.1 and 39.0 (+/-2.6 ng/ml) for ewes in the 20/10 and 40/20 groups, respectively (linear, P<0.01). Serum triiodothyronine (T(3)) followed a similar pattern to that observed for T(4). Ewe lamb BW were similar (P>0.50) among groups throughout the treatment period. However, following the treatment, PTU-treated ewes tended (P<0.10) to weigh less than controls. Average Julian day of puberty was also similar (P>0.50) among treatments (286, 288 and 288+/-5 days; control, 20/10 and 40/20, respectively). Control ewes had a pregnancy rate of 75%, while both PTU-treated groups had pregnancy rates of 88% (P>0.20). The administration of PTU resulted in a rapid decline in serum T(4) and T(3) but neither time of puberty nor pregnancy rates were affected by lowered thyroid hormones.     

Anterior pituitary hormones, stress, and immune system homeostasis

An extensive, and controversial, literature concluding that prolactin (PRL), growth hormone (GH), insulin-like growth factor-I (IGF-I), and thyroid hormones are critical immunoregulatory factors has accumulated. However, recent studies of mice deficient in the production of these hormones or expression of their receptors indicate that there are only a few instances in which these hormones are required for lymphocyte development or antigen responsiveness. Instead, a case is made that their primary role is to counteract the effects of negative immunoregulatory factors, such as glucocorticoids, which are produced when the organism is subjected to major stressors. The immunoprotective actions of PRL, GH, IGF-I, and/or thyroid hormones in these instances may ensure immune system homeostasis and reduce the susceptibility to stress-induced disease. These immuno-enhancing effects could be exploited clinically in instances where the immune system is depressed due to illness or various treatment regimens.     

Low muscle and liver glycogen contents in dogs treated with thyroid hormones

Muscle biopsies for glycogen determinations were taken from dogs before (controls) and after prolonged treatment with thyroid hormones (T4 or T3). The glycogen content in quadriceps femoris was measured before exercise, immediately after its cessation, and during 24h of post-exercise recovery. The effect of thyroxine treatment on the liver glycogen content both at rest and following physical effort was also studied. A marked decrease in the muscle glycogen content determined at rest was found both in T4 and T3-treated dogs in comparison with controls. Physical exercise diminished the muscle glycogen store to similar values in control and thyroid hormone-treated dogs, but the rate of the muscle glycogen utilization during exercise was lower in the latter. The rate of the post-exercise muscle glycogen synthesis was considerably inhibited in thyroid hormone-treated dogs, but 1 hr glucose infusion, applied immediately after cessation of exercise, accelerated the rate of glycogen re-synthesis, so it was close to that in controls without infusion. Thyroxine treatment also affected the liver glycogen store. Both at rest and after physical exercise significantly lower liver glycogen contents were found in T4-treated dogs than in controls.     

Prolactin and thyrotropin response to thyrotropin-releasing hormone in premenopausal women with fibrocystic disease of the breast

Plasma PRL, TSH, total and free T4, total and free T3, and 17 beta-estradiol were evaluated in 29 premenopausal women with well-documented fibrocystic disease of the breast and in 29 healthy matched controls. Plasma PRL and TSH dynamics after acute TRH injection (200 micrograms i.v.) were also determined. All hormonal measurements were performed in the follicular phase of the menstrual cycle. Neither patients nor controls showed any thyroid function impairment. Basal plasma levels of the examined hormones were in the normal range in both groups. When considering data pertinent to PRL and TSH secretory patterns after TRH stimulation, no difference was recorded between patients and controls for TSH secretion, evaluated in terms of maximum peak, net (delta) and percent (delta %) increase above the baseline level and integrated area of response. On the contrary, the response of PRL was significantly higher in patients than controls (maximum peak at 20 min, mean +/- SE, 119.9 +/- 14.1 vs. 60.8 +/- 5.5 ng/ml, p less than 0.001; integrated area of response, 5,725 +/- 908 vs. 3,243 +/- 266 ng/ml/120 min, p less than 0.01). The results are compatible with the view that, in most patients with fibrocystic disease of the breast, there are abnormalities in the control of PRL secretion, which lead to enhanced release of the hormone after stimulation. In such cases the control of TSH appears to be operating normally.     

Effect of growth hormone-releasing factor on plasma growth hormone, prolactin and somatomedin C in hypopituitary and short normal children

We studied the effect of a single intravenous bolus of 0.5 microgram/kg of growth hormone-releasing factor (GRF) on plasma GH, prolactin (PRL) and somatomedin C (SMC) in 12 short normal children and 24 patients with severe GH deficiency (GHD), i.e. GH less than 5 ng/ml after insulin and glucagon tolerance tests. GRF elicited an increase in plasma GH in both short normal and GHD children. The mean GH peak was lower in the GHD than in the short normal children (8.2 +/- 2.5 vs. 39.2 +/- 5.1 ng/ml, p less than 0.001). In the GHD patients (but not in the short normals) there was a negative correlation between bone age and peak GH after GRF (r = -0.58, p less than 0.005); GH peaks within the normal range were seen in 5 out of 8 GHD children with a bone age less than 5 years. In the short normal children, GRF had no effect on plasma PRL, which decreased continuously between 8.30 and 11 a.m. (from 206 +/- 22 to 86 +/- 10 microU/ml, p less than 0.005), a reflection of its circadian rhythm. In the majority of the GHD patients, PRL levels were higher than in the short normal children but had the same circadian rhythm, except that a slight increase in PRL was observed 15 min after GRF; this increase in PRL was seen both in children with isolated GHD and in those with multiple hormone deficiencies; it did occur in some GHD patients who had no GH response to GRF. Serum SMC did not change 24 h after GRF in the short normal children. We conclude that: (1) in short normal children: (a) the mean GH response to a single intravenous bolus of 0.5 microgram/kg of GRF is similar to that reported in young adults and (b) GRF has no effect on PRL secretion; (2) in GHD patients: (a) normal GH responses to GRF are seen in patients with a bone age less than 5 years and establish the integrity of the somatotrophs in those cases; (b) the GH responsiveness to GRF decreases with age, which probably reflects the duration of endogenous GRF deficiency, and (c) although the PRL response to GRF is heterogeneous, it does in some patients provide additional evidence of responsive pituitary tissue.     

Lipid synthesis and lipoprotein secretion by chick liver cells in culture: influence of growth hormone and insulin-like growth factor-I

1. Chick liver cells were incubated in unsupplemented medium (control), or medium supplanted with either 1 microgram/ml pituitary derived chicken growth hormone (GH), 50 ng/ml recombinant human insulin like growth factor-I (IGF-I), or 1 microgram growth hormone/ml and 50 ng insulin like growth factor-I/ml (GH + IGF-I). 2. GH supplementation stimulated acetate incorporation into liver cell lipid. Low density lipoprotein (LDL) lipid secretion was increased quantitatively by GH. 3. Cells incubated with IGF-I incorporated more acetate into lipid and secreted more lipid as VLDL and HDL than controls. 4. A metabolic antagonism between GH and IGF-I was evident with respect to lipogenesis. 5. Neither GH nor IGF-I altered, quantitatively, cell protein synthesis or apoprotein secretion.     

Impairment of cold-induced increase in thyroxine 5'-deiodinase activity in mouse brown adipose tissue by the intracerebroventricular administration of bombesin.

Effects of bombesin on brown adipose tissue (BAT) thyroxine (T4) 5'-deiodinase (5'D) activity and rectal temperature were examined in male mice. Immediately following an intracerebroventricular (ICV) or intravenous (IV) injection of bombesin (0.1-100 ng/animal) or vehicle (20 mM bacitracin dissolved in 0.9% saline), the mice were placed in a room at 4 degrees C or 22 degrees C for 30, 60, 120 or 240 min. The ICV injection of bombesin dose-dependently lessened cold-induced increase in BAT 5'D activity and increased hypothermia determined at 120 min of cold exposure, whereas the IV injection of bombesin was without effect. Bombesin (ICV)-induced hypothermia preceded the inhibition of BAT 5'D activity by at least 30 min at 4 degrees C. BAT 5'D activity was not affected by ICV injection of bombesin in mice kept at 22 degrees C, although the rectal temperature was significantly decreased. Bombesin thus appears to prevent cold-induced increase in T4 5'D activity in mouse BAT by its central effect. Bombesin-induced excessive hypothermia itself and/or the decrease in sympathetic tone of BAT by bombesin might decrease cold-induced increase in BAT 5'D activity.     

Iodothyronine-5'-deiodinase activity in progenies of hypothyroid rats

Iodothyronine-5'-deiodinase activity (I-5'DA) was measured in the progenies of control rats, hypothyroid (Tx) rats, and hypothyroid treated with ovine GH (Tx + GH) during gestation. The enzyme was measured in cerebral cortex and cerebellum at 22 days gestation and at 5, 10, 30 and 60 days postpartum. In addition, the pituitary I-5'-DA was assessed in the postnatal animals. The experiments were undertaken because the tissues of the progenies of rats that were hypothyroid during pregnancy appeared in many ways to resemble those of hypothyroid animals, even at ages when serum thyroxine (T4) and triiodothyronine (T3) levels were normal. It was found that the progenies of Tx mothers had low liver 5'-deiodinase activities. This is a likely cause of the low serum T3 levels with normal T4 levels seen in these progenies in the neonatal period. Cerebral and cerebellar 5'-deiodinase activities were low in these progenies during the thyroid hormone-dependent perinated period of brain development. The progenies of GH-treated Tx dams had higher enzyme activities than the progenies of untreated Tx dams. These pups from GH-treated Tx mothers have been shown previously to have significantly less neurological impairment than the progenies of untreated Tx mothers. As most of the brain intracellular T3 is produced in situ, a functional thyroid deficiency could result from such a 5'-deiodinase deficiency. As the deiodinase deficiency was still seen in the progenies of Tx mothers at 60 days of age, such a deficiency could explain why, even though serum T4 and T3 levels were normal, brain metabolism was in many ways characteristic of hypothyroidism.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prolactin and growth hormone regulate adiponectin secretion and receptor expression in adipose tissue

Adiponectin is a hormone secreted from adipose tissue, and serum levels are decreased with obesity and insulin resistance. Because prolactin (PRL) and growth hormone (GH) can affect insulin sensitivity, we investigated the effects of these hormones on the regulation of adiponectin in human adipose tissue in vitro and in rodents in vivo. Adiponectin secretion was significantly suppressed by PRL and GH in in vitro cultured human adipose tissue. Furthermore, PRL increased adiponectin receptor 1 (AdipoR1) mRNA expression and GH decreased AdipoR2 expression in the cultured human adipose tissue. In transgenic mice expressing GH, and female mice expressing PRL, serum levels of adiponectin were decreased. In contrast, GH receptor deficient mice had elevated adiponectin levels, while PRL receptor deficient mice were unaffected. In conclusion, we demonstrate gene expression of AdipoR1 and AdipoR2 in human adipose tissue for the first time, and show that these are differentially regulated by PRL and GH. Both PRL and GH reduced adiponectin secretion in human adipose tissue in vitro and in mice in vivo. Decreased serum adiponectin levels have been associated with insulin resistance, and our data in human tissue and in transgenic mice suggest a role for adiponectin in PRL and GH induced insulin resistance.     

Paradoxical growth hormone response following thyroid-stimulating hormone administration in the polycystic ovary syndrome

Growth hormone (GH) and prolactin (PRL) responses after TRH administration were studied in 31 women presenting with the clinical, biochemical and ultrasonographic characteristics of the polycystic ovarian (PCO) syndrome; their results were compared with those of 20 normally menstruating women investigated during the early follicular phase of the cycle. Based on the GH responses two PCO subgroups were observed: (a) nonresponders (n = 16) who showed delta max GH responses (0.7 +/- 0.27 ng/ml, x +/- SE) similar to those of the normals (0.97 +/- 0.20 ng/ml), and (b) responders (n = 15), 48.4% of the PCO patients who showed a paradoxical increase in GH levels (delta max GH, 18.0 +/- 1.96 ng/ml) following thyrotropin-releasing hormone (TRH) administration significantly higher than those observed either in nonresponder PCO patients or in normals. Furthermore, basal GH levels were found to be significantly higher in the responder PCO subgroup (5.65 +/- 0.75 ng/ml) compared to either nonresponders (1.58 +/- 0.21 ng/ml) or normals (1.8 +/- 0.18 ng/ml). However, no correlation was found between basal GH levels and delta max GH responses observed. Additionally, basal PRL and delta max PRL levels following TRH administration did not differ either between the two PCO subgroups or those observed in normal controls. delta 4A, T and E2 levels were similar between the two PCO subgroups. No correlation was found between the delta max GH responses to delta max PRL or the post-luteinizing hormone-releasing hormone stimulation test delta max luteinizing hormone:follicle-stimulating hormone ratio observed or to steroid levels.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prenatal androgen exposure and growth and secretion of growth hormone and prolactin in ewes postweaning

Growth and secretion of growth hormone (GH) and prolactin (PRL) in ewe lambs exposed to androgen during fetal development were investigated. Testosterone cypionate was administered to the pregnant dams from approximately Days 28 to 84 of gestation. Ewe lambs from dams that received androgen exhibited masculinized external genitalia and some masculine behavioral characteristics. Intact androgenized ewe lambs grew faster (P less than 0.05) and were more efficient in conversion of food to body gain (P less than 0.05) than ewe lambs born to untreated dams over the period from 70 to 224 days of age. One-half of the ewe lambs in each group was ovariectomized at 58 days of age. Ovariectomy had no effect on subsequent growth or efficiency of growth in the control ewe lambs. However, ovariectomy of androgenized ewe lambs abolished the observed stimulated rate of growth and decreased the improvement in efficiency of food conversion. Blood samples were collected from the lambs at 85 and 136 days of age at 15-min intervals for 8 hr to determine parameters of GH and PRL secretion. Prenatal androgen exposure had no effect on any parameter of GH or PRL secretion. These data indicate that prenatal androgen exposure altered differentiation of growth potential in ewe lambs, but the growth response was not mediated through dramatic changes in secretion of adenohypophysial somatotropic hormones, GH and PRL.