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PubMed1988

Anthropometric relevance on sublabial transseptal transsphenoidal hypophysectomy in the Asiatic type of skull.

In order to preoperatively estimate the width of the operating field during transphenoidal hypophysectomy, we measured the distance between the right and left medial pterygoid plates in 27 normal adults and 11 patients with pituitary adenoma from anteroposterior tomograms. In normal subjects, the mean distance was about 3.2 cm. The distance in patients with acromegaly was not wider than that in normal subjects, but 1 case with giantism showed a much wider distance of 4.1 cm. The measurement of the actual operating field was 2.0 cm in width, about 1.0 cm narrower than the preparative tomogram calculations.

Adenoma↗
PubMed1985

Long-term follow up of trans-sphenoidal hypophysectomy for Cushing's disease.

Fourteen patients with Cushing's disease treated by trans-sphenoidal hypophysectomy between 1962 and 1975 were reviewed in 1983. Complete ablation had been attempted. There were no surgical deaths and one episode of bacterial meningitis. Two patients required a second operation for a cerebrospinal fluid leak. There have been three late deaths from unrelated causes. All patients had a biochemical remission of their Cushing's disease postoperatively and no relapse has been recorded. Most patients need some hormone replacement but residual pituitary function and sella radiography have remained stable. This treatment seems satisfactory and the evidence implies a pituitary aetiology of the syndrome.

Adult↗
PubMedDate not supplied

Transseptal transsphenoidal hypophysectomy.

The usual surgical approach to the sella turcica is via a labial sulcus incision over the nasal spine with continuation backward to the nasal septum and sphenoid sinus. In our series of 25 transsphenoidal hypophysectomies, a primary transseptal approach was used, avoiding the oral incision. The operating time was reduced, and the visualization was adequate. The morbidity associated with the labial sulcus incision was also avoided. The surgical approach and results are discussed.

Humans↗
PubMed1977

Corticotropin releasing factor distribution in normal and Brattleboro rat brain, and effect of deafferentation, hypophysectomy and steroid treatment in normal animals.

Corticotropin-Releasing Factor (CRF) activity was determined (dispersed pituitary cell assay) in rat median eminence (ME), various hypothalamic nuclei, as well as in entire median basal hypothalamus (MBH) and extra-hypothalamic areas. Highest concentrations were seen in ME, with decreased concentrations noted proceeding dorsally and cephalad from ME. Potency (NIAMDD HE-RP-1, ME reference extract, equivalent to 1.0) estimates were: ME-2.2; arcuate n.-0.88; dorsomedial n.-041; ventromedial n.-0.35; periventricular n.-0.24; hypothalamus-0.05; thalamus-0.01; cortex-0.005. Measurable, but lesser amounts, than in the above cited nuclei, were present in supraoptic and paraventricular nuclei. CRF activity was not measurable in preoptic area, septum, olfactory bulb, striatum, mesencephalon, pons, medulla or cerebellum. Complete hypothalamic deafferentation was accompanied by an increase in CRF activity/mug protein in ME and MBH, associated with decreased AM plasma ACTH and corticosterone concentrations. CRF-like activity in ME and MBH increased following hypophysectomy and after dexamethasone pretreatment. These findings indicate that CRF is mainly synthesized in the ME and surrounding area, and this source of CRF is sensitive to feedback effects and that extrahypothalamic inputs affect CRF release. Female animals had higher ME CRF content than did male animals. Homozygous and heterozygous Brattleboro rats had significantly less CRF in ME and MBH than did control animals, with significant differences also noted between homozygous and heterozygous animals.

Adrenal Cortex Hormones↗
PubMed1978

The effect of hypophysectomy on the quail's oviduct response to low and high doses of estradiol benzoate.

The response of the quail's (Coturnix coturnix Japonica) oviduct to different doses of estradiol benzoate (EB) was explored in ovariectomized and ovariectomized-hypophysectomized animals. Doses of EB ranged from 10 microgram to 1 mg/animal daily for 6 consecutive days; animals were sacrificed 24 h after the last injection. Controls were injected with olive oil. Parameters thought to reflect stimulation of the oviduct were 1) wet and dry weight, 2) DNA, 3) RNA, 4) soluble proteins, 5) ovalbumin, and 6) morphological changes at the level of magnum's mucosa. A statistical significant difference in several of the parameters listed was found between the effect of different doses of EB and whether the injection was done in ovariectomized or in ovariectomized-hypophysectomized animals. The dose response with EB for cell proliferation and induced proteins accumulation (ovalbumin) show that it takes considerably more EB to maximally stimulate ovalbumin accumulation when compared with cell proliferation. Hypophysectomy decreases the oviduct responses to high EB doses. Ultrastructural studies of the magnum mucosa confirm these biochemical results. The evidence presented suggesting an EB dose-dependent difference induction of specific cellular responses in the presence and absence of the pituitary in quails are the basis to postulate the contributing role of the pituitary in the parameters measured.

Animals↗
PubMed1979

Effects of hypophysectomy, thyroidectomy, and thyroxine on specific prolactin receptor sites in kidneys and adrenals of male rats.

The effect of T4 on specific PRL binding in the kidneys and adrenals was measured in intact, hypophysectomized, and thyroidectomized male rats. PRL binding in the kidneys was reduced from 12.1 +/- 1.1% in the intact group to 4.5 +/- 0.5% after hypophysectomy; 4-day replacement with T4 returned PRL binding to intact values. T4 administered to intact rats significantly increased PRL binding above intact values. Thyroidectomy reduced PRL binding in the kidneys from 14.9 +/- 1.2% to 7.0 +/- 0.6%, and T4 treatment restored PRL binding to intact values. PRL binding was measured at 2, 3, 5, 7, and 10 days after thyroidectomy in kidneys and found to decrease progressively from 8.2+/-0.5% in the intact rats to 2.3+/-0.3% on day 10. A single injection of T4 doubled PRL recetor binding in kidneys of thyroidectomized rats at 12 h and returned binding to intact levels at 24 h. In contrast to the effects of T4 on kidney PRL binding, adrenal PRL binding was only slightly altered by thyroidectomy and T4. These results suggest that T4 has a specific role in regulating PRL receptors in the kidneys but not in the adrenals. Since PRL receptors in the adrenals were only slightly altered by thyroid status, it is believed that the changes in kidney receptors represent a specific rather than a general metabolic effect of T4.

Adrenal Glands↗
PubMed1980

Matrix-induced endochondral bone differentiation: influence of hypophysectomy, growth hormone, and thyroid-stimulating hormone.

The influence of hypophysectomy (hypox), GH, and TSH on the discrete phases of matrix-induced endochondral bone differentiation was investigated. [3H]Thymidine incorporation by proliferating mesenchymal cells on day 3 was inhibited by hypox, but was corrected by GH administration. On day 7, 35SO4 incorporation into cartilage proteoglycans was reduced by hypox, but was restored to values higher than controls by GH. Calcification of cartilage and bone was monitored by alkaline phosphatase activity. 45Ca incorporation into bone mineral, and total calcium. Alkaline phosphatase levels were maximal on day 11 in the controls and declined thereafter; however, the activity of alkaline phosphatase remained elevated in hypox recipients. Hypox reduced and delayed the rate and extent of calcification, as reflected by 45Ca incorporation and total calcium, respectively. The administration of GH and TSH alone and in combination restored 45Ca incorporation to control values in tibial metaphyses but not in the matrix-induced osteogenic plaques on day 10. These findings imply that the hormonal requirements for initiation of de novo mineralization of bone may be different from those required for the maintenance of mineralization that was initiated in early fetal life, as in the case of metaphyses. Hypox resulted in a delayed and reduced bone formation due to 1) inhibition of mesenchymal cell proliferation, 2) decreased and delayed chondrogenesis, 3) delayed and reduced vascular invasion, and 4) impaired bone formation.

Acid Phosphatase↗
PubMed1980

The effect of hypophysectomy on somatostatin-like immunoreactivity in discrete hypothalamic and extrahypothalamic nuclei.

Several hypothalamic and extrahypothalamic sites that have high concentrations of somatostatin-positive nerve terminals and/or cell bodies are important in the regulation of GH secretion. GH is capable of inhibiting its own secretion under certain prescribed conditions, and a short loop feedback regulatory mechanism may involve somatostatinergic pathways. The purpose of this investigation was to determine the effect of removal of GH by hypophysectomy on the content of somatostatin-like immunoreactivity (SLI) in discrete hypothalamic and extrahypothalamic nuclei. Individual nuclei were removed from frozen brain sections of hypophysectomized and sham-operated male rats. The tissue content of somatostatin was determined by a specific RIA. The content of SLI in the median eminence of hypophysectomized animals was significantly reduced by 38%, compared to sham-operated controls (278 +/- 53.2 vs. 447.0 +/- 57.4 pg/microgram protein, respectively). Significant reductions of SLI in the medial preoptic (50%), arcuate (33%), and periventricular (30%) nuclei were also observed in hypophysectomized animals when compared to controls (10.2 +/- 1.6 vs. 20.0 +/- 3.0; 60.2 +/- 8.2 vs. 89.8 +/- 13.3; and 19.4 +/- 1.8 vs. 27.8 +/- 3.1 pg/microgram protein, respectively). No significant changes were detected in the ventromedial, suprachiasmatic, medial, central, or cortical a mygdaloid nuclei nor in the nucleus interstitialis striae terminalis. These data suggest that GH may exert a feedback effect on specific hypothalamic nuclei that involves somatostatin-containing systems.

Animals↗
PubMed1981

Diabetes, hypophysectomy, or thyroidectomy reduces nuclear L-triiodothyronine-binding capacity of rat lung.

L-T3 (T3) receptors of the lungs of rats were found to be under hormonal control. The apparent binding capacity of T3 receptors of lungs of diabetic, hypophysectomized, and thyroidectomized rats were 0.224 +/- 0.009, 0.195 +/- 0.007, and 0.102 +/- 0.008 pmol/mg DNA, as compared to 0.0321 +/- 0.014 pmol/mg DNA for normal animals. The binding affinities for T3 in normal, diabetic, hypophysectomized, and thyroidectomized rats were 256 +/- 3.24, 270 +/- 3.81, 249 +/- 4.03, and 260 +/- 8.2 pM, respectively. The magnitude of the maximum binding capacity in these cases was apparently not due to the loss of either T3 receptors or DNA during the incubation. Serum T3 and T4 concentrations in normal rats were 120.0 +/- 7.2 ng/dl and 5.9 +/- 0.5 micrograms/dl, respectively. Diabetes, hypophysectomy, and thyroidectomy lowered these values to 79 +/- 5.4, 60 +/- 5.8, and 30 +/- 1.6 ng/dl for T3 and 3.5 +/- 0.3, 2.7 +/- 0.4, and 1.9 +/- 0.2 micrograms/dl for T4, respectively.

Animals↗
PubMed1986

Differential endocrine regulation of alpha 2U-globulin messenger ribonucleic acid activity: effect of age at hypophysectomy.

Three alpha 2U-globulin products were identified on two-dimensional gel electrophoretograms of the [35S]methionine-labeled products formed in response to total hepatic RNA by the reticulocyte lysate translational assay. These products, arbitrarily designated A, B, and C, were quantified by video-imaging of two-dimensional electrophoretograms. At both 65 and 85 days, they represent approximately 13%, 10%, and 77%, respectively, of the total translational products coding for alpha 2U-globulin. Hypophysectomy at either 30 or 55 days resulted in a marked decrease in all three products when measured at 60 and 85 days. Products A and B were not induced in animals hypophysectomized (hypox) at 30 days and subsequently reinjected for 10 days beginning on day 50 with GH alone; with T4, corticosterone, and dihydrotestosterone (three hormones); or with a four-hormone combination. Product C was significantly induced by the four-hormone combination. In animals hypox at 55 days and reinjected for 10 days beginning on day 75, GH alone and the three-hormone combination failed to increase product A. In contrast to the observations in animals hypox at 30 days, the four-hormone combination induced a significant increase in products A and B in animals hypox at 55 days, and product C was induced by the three-hormone as well as the four-hormone combination. Measurement of total alpha 2U-globulin mRNA by cDNA hybridization indicated that animals hypox at 30 days achieved only 33.8% of age-matched normal levels, whereas animals hypox at 55 days achieved 69% (P less than 0.05) when injected with all four hormones. Furthermore, the three-hormone combination increased total alpha 2U-globulin mRNA in animals hypox at 55 days, but not in animals hypox at 30 days. The observations on the individual alpha 2U-globulin products suggest that endocrine regulation of individual alpha 2U sequences is not identical. The different magnitude of response observed in the animals hypox at different ages suggests that exposure of the liver to a pituitary-dependent factor between 30 and 55 days modifies the ability of the liver to regulate alpha 2U-globulin mRNA levels.

Aging↗
PubMed1987

Effect of hypophysectomy on hypothalamic growth hormone-releasing factor content and release in the rat.

The possible regulation of hypothalamic GH-releasing factor (GRF) by GH was studied in untreated and GH-treated hypophysectomized rats by measurement of rat hypothalamic GRF content and release in vitro with a specific GRF RIA. Two weeks after hypophysectomy, animals not receiving hormone replacement showed a marked reduction in hypothalamic GRF content (to 28% of sham-operated control values; P less than 0.001). Replacement therapy with T4, cortisone, and testosterone for 9 days did not correct the decrease in hypothalamic GRF content in hypophysectomized rats, though the addition of GH therapy partially restored GRF levels (to 55% of control values; P less than 0.001). GRF release from incubated mediobasal hypothalamic fragments of hypophysectomized rats was decreased both basally and in response to 30 mM K+. This defect was completely corrected by prior GH treatment. The results suggest an impairment of GRF synthesis and release in the presence of GH deficiency.

Animals↗
PubMed1988

The effect of hypophysectomy and growth hormone administration on pre-prosomatostatin messenger ribonucleic acid in the periventricular nucleus of the rat hypothalamus.

Physiological evidence suggests that hypothalamic somatostatin (SS) inhibits pituitary GH release and that GH acts through a short-loop feedback mechanism to stimulate SS secretion. The feedback action of GH could be mediated by an effect on SS synthesis, secretion, or both. We hypothesized that GH acts to regulate the expression of the SS gene and that changes in the level of circulating GH would result in corresponding changes in SS mRNA in cells of the periventricular nucleus (PeN) of the hypothalamus. To test this hypothesis we measured the effect of hypophysectomy (HPX) and HPX with bovine GH (bGH) replacement on SS mRNA signal levels in cells of the PeN of the rat brain. We report that HPX male rats treated with bGH have significantly higher PeN SS mRNA signal than their vehicle-treated controls (P less than 0.05) and that bGH administration to sham-HPX rats results in elevated PeN SS mRNA signal levels compared to those in sham-HPX rats treated with vehicle (P less than 0.05). These observations suggest that GH participates in the regulation of its own secretion by influencing the expression of the SS gene and that one mechanism of short-loop pituitary feedback may involve the modulation of neuropeptide gene expression.

Animals↗
PubMed1990

Restoration of spermatogenesis by exogenously administered testosterone in rats made azoospermic by hypophysectomy or withdrawal of luteinizing hormone alone.

The major objective of the studies presented herein was to compare the extent to which exogenously administered testosterone is able to restore spermatogenesis in adult rats made azoospermic by withdrawal of all pituitary hormones (hypophysectomy for 4 weeks) vs. withdrawal of LH alone [testosterone- and estradiol-filled (TE) polydimethylsiloxane implants of 2.5 and 0.1 cm, respectively, for 8 weeks]. In hypophysectornized (Hypox) rats, serum LH and FSH were both undetectable; in the rats that received TE implants, serum LH was undetectable, but FSH was unaffected compared to control values. Seminiferous tubule fluid testosterone concentrations were reduced significantly from their control values of 60-65 to 1.4-1.7 ng/ml in the azoospermic Hypox and TE rats. These rats then received testosterone-filled implants of 4, 12, 18, or 24 cm and were killed 2 months later. In both the Hypox and TE rats, seminiferous tubule fluid testosterone concentrations rose linearly with increasing capsule sizes, and with each of the implant sizes, these concentrations did not differ significantly between the Hypox and TE rats. This made it possible for the first time to examine the effects of comparable intratesticular testosterone concentrations on the numbers of advanced spermatids per testis that could be restored in the azoospermic testes of rats lacking all pituitary factors vs. those lacking only LH. The results that we present demonstrate that the numbers of restored advanced spermatids were consistently and significantly lower in Hypox than in TE rats despite equivalent seminiferous tubule fluid testosterone concentrations. These results provide quantitative conclusive evidence to support the contention that pituitary factors in addition to LH are required for the quantitative restoration of spermatogenesis in the adult rat testis.

Animals↗
PubMed1990

Characterization of insulin-like growth factor binding proteins (IGFBPs) during gestation in mice: effects of hypophysectomy and an IGFBP-specific serum protease activity.

Characterization of insulin-like growth factor binding proteins (IGFBPs) and their pituitary regulation were investigated in intact and hypophysectomized (HX) pregnant and nonpregnant mice. Serum samples were obtained from pregnant mice killed on days 5, 8, 10, 12, 14, and 18 of gestation and fetal mice killed on day 18 of gestation. Some animals were HX or sham operated (SH) on days 9, 11, and 14 of gestation; HX and SH control animals were killed 3 days post surgery. Identification and relative quantities of IGFBPs were determined by Western ligand blotting (WLB) of whole serum, or immunoprecipitated and/or deglycosylated serum, using [125I]IGF-II as the ligand. Serum IGF-I and -II concentrations were determined in both HX and SH day 14 pregnant, nonpregnant, and day 18 fetal mouse sera. WLB analysis of nonpregnant mouse serum demonstrated IGFBPs with apparent Mr of approximately 45-40, 31-27, and 24 K. The 45-40 K IGFBPs appeared to be the mouse equivalent of IGFBP-3, and one of the 31-27 K IGFBPs appeared to be IGFBP-2. The other IGFBPs present are not yet fully identified. During pregnancy, the amount of IGFBP-3 present in serum (as measured by WLB) gradually decreased to 42%, 17%, and 10% of virgin levels on days 5, 8, and 10 of gestation. The amount of IGFBP-3 present in pregnant serum after day 10 of gestation was not measurable by scanning laser densitometry. Additionally, an IGFBP of approximately 27 K appeared during gestation; after treatment with Endoglycosidase F, this IGFBP decreased to 24 K. The major IGFBP in fetal serum appeared to be IGFBP-2, with lesser amounts of IGFBP-3 and the 27 and 24 K IGFBPs. Hypophysectomy significantly decreased IGFBP-3, IGF-I, and IGF-II in nonpregnant mouse serum, increased the amount of IGFBP2 found in pregnant mouse serum, and had no effect on IGF-I or -II concentration in day 14 pregnant mouse serum. Incubation of nonpregnant serum with late (day 17) pregnant serum for 5 h at 37 C, decreased the amount of IGFBP-3 (as measured by WLB) in the mixed sample to 93% of the amount present in the nonmixed sample. Iodinated recombinant IGFBP-3 ([125I]human (h)IGFBP-3) was incubated with different mouse serum samples, and proteolytic fragments were visualized after separation by sodium dodecyl sulfate polyacrylamide gel electrophoresis and autoradiography.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Ontogeny of pituitary regulation of growth in the developing rat: comparison of effects of hypophysectomy and hormone replacement on somatic and organ growth, serum insulin-like growth factor-I (IGF-I) and IGF-II levels, and IGF-binding protein levels in the neonatal and juvenile rat.

We investigated pituitary regulation of growth during two critical stages of development in the rat, using hypophysectomy (Hx) with replacement of GH and/or T4. In the neonatal period (Hx on day 6), body weight and tail length were inhibited by 60% and 50%, respectively, while these parameters were inhibited by 80% and 85% by Hx in the juvenile period (Hx on day 45). Administration of T4 alone significantly increased skeletal growth (tail length) in neonatal Hx rats, while T4 alone proved ineffective in promoting somatic growth in juvenile Hx rats. GH effects were greater on body weight than on tail length at both stages of development. Replacement of both GH and T4 restored somatic growth to normal values during both time periods. The brain was the sole organ whose growth appeared to be independent of the pituitary. Hx reduced serum insulin-like growth factor-I (IGF-I) and -II in both age groups, and GH alone restored IGF-I and -II levels to the control range. The major IGF-binding proteins (IGFBPs) were analyzed by Western ligand blots. The effect of Hx on the predominant IGFBP was greater in the juvenile rat. T4 replacement in the neonate and GH replacement in the juvenile rat restored IGFBPs to control levels. We conclude that somatic growth in the rat is less pituitary dependent in the neonatal period. There are also important age-specific differences in organ response to GH and T4. Serum IGFs and their binding proteins are pituitary dependent even in infancy, and GH is their primary regulator. The neonatal Hx rat is an important model for the study of the dynamic development of the pituitary-dependent growth.

Aging↗
PubMed1991

Pituitary-placental interaction: hypophysectomy modulates the secretion of mouse placental lactogen-I.

To determine whether the pituitary gland influences the concentration of mouse placental lactogen-I (mPL-I) in maternal serum, pregnant Swiss Webster mice were hypophysectomized or sham-operated on day 9 of gestation. Blood was collected on days 10-13 and 18, and the mPL-I concentration of the serum was measured by RIA. The serum mPL-I concentration of hypophysectomized mice was significantly higher than that of sham-operated and intact mice on days 10-13. There was no difference in mPL-I concentration on day 18 of pregnancy among the groups. Similar elevations in serum mPL-I concentration were observed when hypophysectomy was performed on day 10 of pregnancy. Steady state levels of placental mPL-I messenger RNA (mRNA) were analyzed by Northern hybridization. No differences were observed in the amount of mPL-I mRNA among hypophysectomized, sham-operated, and intact mice. These results demonstrate that the pituitary gland exerts inhibitory control over the maternal serum mPL-I concentration. This control does not appear to be affected at the level of steady state amounts of mPL-I mRNA.

Animals↗
PubMed1975

Changes of endocrine properties of a transplantable, multihormonal, pituitary tumor (MtT-F4) after hypophysectomy of host rats.

The transplantable rat pituitary tumor MtT-F4 failed to grow in rats hypophysectomized at the time of transplantation, but did grow in thyroxine-treated hypophysectomized rats. In the latter rats, the tumor did not stimulate the adrenals to the same extent as in control rats. When the tumor did not stimulate the adrenals to the same extent as in control rats. When the tumor cells were isolated and incubated in vitro, those from hypophysectomized thyroxine-treated rats released much less ACTH into the incubation medium than the tumor cells from control rats. They also released significantly less growth hormone than tumor cells from intact, intact thyroxine-treated, and thyroidectomized thyroxine-treated rats. Prolactin release by the isolated tumor cells in vitro was the same in all groups studied. The results suggest that the hypophysectomy and thyroxine treatment of the host rat might selectively influence the production of hormones by the MtT-F4 transplantable rat pituitary tumor.

Adrenal Glands↗
PubMed1996

The effect of hypophysectomy and growth hormone replacement on sst1 and sst2 somatostatin receptor subtype messenger ribonucleic acids in the arcuate nucleus.

Although considerable evidence indicates that somatostatin (SRIF) exerts direct actions on GH-releasing hormone-containing arcuate neurons within the hypothalamus to modulate hypophyseal GH secretion, the underlying mechanism(s) remains to be elucidated. We recently demonstrated high levels of expression of the messenger RNAs (mRNAs) coding for two prototypic receptors of the recently cloned SRIF receptor (sst) family, sst1 and sst2, in the arcuate nucleus of the rat hypothalamus. However, information on the biological roles of these receptor subtypes and the factors regulating their expression is lacking. In the present study, we hypothesized that perturbations in GH would influence sst mRNA levels in cells of the arcuate nucleus in vivo. To test this hypothesis, we examined the effects of hypophysectomy (HPX) and HPX with GH replacement, on sst1 and sst2 mRNA levels in the brains of adult male rats by in situ hybridization using 35S-labeled antisense riboprobes. The number of labeled cells and the density of silver grains per cell were quantified using a computer-assisted image analysis system. Two weeks after HPX, there was a 50-60% reduction in both the number and labeling density of sst1 and sst2 mRNA-expressing cells in the arcuate nucleus compared to those in sham-operated control rats. Administration of recombinant human GH (200 micrograms/day for 7 days by continuous sc infusion using osmotic minipumps) to HPX rats augmented both the cell number (P < 0.05) and labeling density (P < 0.01) of sst1 mRNA in the arcuate nucleus, but did not significantly alter sst2 mRNA levels compared to those in HPX rats infused with H2O. There were no significant changes in sst1 and sst2 mRNA levels in extra-arcuate areas, including the cerebral cortex and medial habenula, or in suprachiasmatic, medial preoptic, and magnocellular preoptic nuclei after either HPX or GH replacement. These results indicate that the expression of both sst1 and sst2 SRIF receptor subtypes in brain is under the regulatory influence of pituitary hormones. They further suggest that GH may participate in the regulation of its own secretion by influencing the expression of the sst1 receptor gene on arcuate neurons. Such a mechanism may be important in the feedback regulation of GH secretion by the arcuate nucleus.

Animals↗