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Biomedical subjects

I Wakabayashi

Publications and source records attributed to I Wakabayashi.

At least 37 records · Page 2Linked to original sources
PubMed2000

Response of leptin mRNA to 24-h food deprivation and refeeding is influenced by age in rats.

To obtain an insight into the influence of aging on leptin gene expression, the responses of leptin mRNA in retroperitoneal and epididymal adipose tissues and plasma leptin concentrations to 24-h food deprivation and refeeding were examined in 2-, 10- and 24-month-old normal rats. The basal level of leptin gene expression in retroperitoneal adipose tissue was significantly higher in 10- and 24-month-old rats than that in 2-month-old rats, while the level in epididymal adipose tissue was highest in 10-month-old rats for all three age groups. The basal concentrations of plasma leptin was significantly higher in 10- and 24-month-old rats than those in 2-month-old rats. The 24-h food deprivation was followed by a significant reduction in leptin mRNA expression in both retorperitoneal and epididymal adipose tissues for all three age groups. The leptin gene expression was restored to control levels 24 h following refeeding in the 2- and 10-month-old rats, but failed to be restored in the 24-month-old rats. In addition, the time course of recovery for leptin mRNA expression by refeeding to the control levels differed between the retroperitoneal and the epididymal adipose tissue in 2- and 10-month-old rats. The concentrations of plasma leptin 24 h following refeeding were compatible with the leptin mRNA levels in adipose tissues in three age groups. These results suggest that the expression of the leptin gene in response to food-deprivation and refeeding is influenced by an animal's age and that this expression is different for different regions of white adipose tissue.

Adipose Tissue↗
PubMed2000

A 6-day intracerebroventricular infusion of the growth hormone-releasing peptide KP-102 stimulates food intake in both non-stressed and intermittently-stressed rats.

The effects of a 6-day intracerebroventricular (i.c.v.) infusion of KP-102, a growth hormone-releasing peptide (GHRP), on food intake and body weight gain were observed in free-feeding rats that were or were not subjected to intermittent electric footshock stress during the 6 days. Food intake and body weight were significantly lower in rats exposed to a 60-min period of footshock twice a day for 6 days compared to non-stressed rats. A 6-day, i.c.v. infusion of KP-102 significantly and steadily increased food intake and body weight in free-feeding non-stressed rats compared to control rats receiving saline i.c.v. In rats exposed to intermittent footshock stress during the 6-day infusion, KP-102 treatment stimulated feeding behavior and resulted in significantly higher body weight compared to stressed rats that received i.c.v. infusion of saline. These results indicate that during a 6-day continuous i.c.v. infusion of GHRP, KP-102, food intake and body weight steadily increased without attenuation of the GHRP effect in both non-stressed rats and those subjected to intermittent stress.

Animals↗
PubMed2000

Inhibitory effects of aclarubicin on nitric oxide production in aortic smooth muscle cells and macrophages.

The effects of aclaruhicin (ACR), an anthracycline antibiotic, on inducible nitric oxide (NO) synthesis was investigated in rat aortic smooth muscle cells (RASMCs) and RAW macrophages. ACR at concentrations as low as 0.1 microM significantly inhibited NO production induced by interleukin-1beta in RASMCs. About 5- to 10-fold higher concentrations of ACR were required for inhibition of interferon-gamma and lipopolipopolysaccharide-induced NO production in RAW cells. When ACR was subsequently administered to inducible NO synthase (iNOS) induction, the NO production was barely suppressed in RASMCs. Moreover, ACR (up to 10 microM) lacked direct inhibitory effects on iNOS activity in homogenates of these cells. ACR (0.1 microM) inhibited the expression of iNOS protein and mRNA in RASMCs without concomitant cytotoxic effects. ACR (>0.5 microM)-induced inhibition of NO production in RAW cells was associated with substantial cytotoxic effects as shown by measurement of lactate dehydrogenase release. These results suggest that ACR is a potent inhibitor of iNOS induction in vascular smooth muscle, but inhibits iNOS induction in macrophage only at high cytotoxic

Aclarubicin↗
PubMed2000

Disturbed expression of the anti-apoptosis gene, survivin, and EPR-1 in hematological malignancies.

Survivin is a newly discovered inhibitor of the apoptosis protein, IAP, expressed during development and in human cancers. The effector cell protease receptor-1 (EPR-1) gene is oriented in the opposite direction on the same DNA double strand. Thus, the Survivin and EPR-1 (Survivin/EPR-1) genes exist in a head-to-head configuration. It is not clear whether mutual expression of the Survivin/EPR-1 genes occurs in both normal cells and cancer cells. Here, we investigated the mutual expression of the Survivin/EPR-1 genes in 12 normal peripheral blood (PB) specimens, seven normal bone marrow (BM) specimens, five lymph node (LN) specimens, and seven leukemic cell lines, and 27 patients with malignant lymphoma (ML), four with acute lymphocytic leukemia (ALL), three with acute myelocytic leukemia (AML), and four with chronic myelocytic leukemia in blastic crisis (CML-BC). Using Northern blot analysis, small amounts of EPR-1 mRNA were detected in normal PB, normal BM and LN specimens, but no Survivin mRNA was detected. However, Survivin mRNA was detected in two of the 12 normal PB, six of the seven normal BM and one of the five LN specimens using reverse transcription and polymerase chain reaction (RT-PCR). Expression of both the Survivin and EPR-1 genes was detected in six of the seven cell line samples by Northern blot, and in all of them by RT-PCR. Mutual expression of the Survivin and EPR-1 genes was detected in three of the four CML-BC samples, 15 of the 27 ML samples, two of the four ALL samples, and all three AML samples using the RT-PCR method. No EPR-1 expression with or without Survivin expression was clearly detected in eight of the nine diffuse large B-cell lymphoma (DLB) specimens, two of the six follicular center lymphoma specimens, one of the four specimens of nodular sclerosis of Hodgkin's lymphoma, two of the four ALL specimens or one of the four CML-BC specimens. The data presented here show that disrupted expression of the Survivin/EPR-1 genes occurred in many kinds of hematologically malignant cells. This may be of biological importance.

Apoptosis↗
PubMed2000

Glucocorticoids regulate pituitary growth hormone secretagogue receptor gene expression.

Glucocorticoids regulate growth hormone (GH) secretion by modulating both hypothalamic and pituitary function. At the level of the pituitary, glucocorticoids increase GH and GH-releasing hormone receptor (GHRH-R) gene expression. To test if glucocorticoids might also regulate the pituitary expression of the recently identified GH secretagogue (GHS) receptor, GHS-R; adult male rats were adrenalectomized or sham operated, and treated with the synthetic glucocorticoid (dexamethasone, 200 microg/day) or vehicle for 8 days. Pituitary GHS-R mRNA levels were assessed by reverse transcriptase polymerase chain reaction (RT-PCR). Adrenalectomy decreased pituitary GHS-R mRNA to 45% of vehicle-treated, sham-operated rats (P < 0.05). Administration of dexamethasone increased GHS-R mRNA levels in sham-operated as well as in adrenalectomized rats (199 +/- 24% (P < 0.05) and 369 +/- 48% (P < 0.01) of vehicle-treated controls). Addition of dexamethasone to primary rat pituitary cell cultures increased GHS-R mRNA levels in a dose- and time-dependent manner while the transcriptional inhibitor, actinomycin D, completely blocked the stimulatory action of dexamethasone. Taken together, these results suggest glucocorticoids directly increase pituitary GHS-R mRNA levels by stimulating GHS-R gene transcription.

Adrenalectomy↗
PubMed2000

Masculinizing effect of dihydrotestosterone on growth hormone secretion is inhibited in ovariectomized rats with anterolateral deafferentation of the medial basal hypothalamus or in intact female rats.

There is a striking sex difference in the pattern of growth hormone (GH) secretion in rats. Our previous studies showed that short-term administration of pharmacological doses of testosterone or dihydrotestosterone (DHT) masculinized the GH secretory pattern in ovariectomized (OVX) rats. The locus where testosterone or DHT interacts with the somatotropic axis is believed to be the hypothalamus. To obtain insights into this phenomenon, we administered a single dose of DHT s.c. to adult OVX rats at 0.01, 0. 1 or 1 mg/rat. Blood GH concentrations were measured in unanaesthetized rats. Six to 12 h after the s.c. administration of all three doses of DHT, the GH secretory pattern revealed a male-like secretory pattern as shown by episodic bursts occurring at 2-3-h intervals with low or undetectable trough levels. When anterolateral deafferentation of the medial basal hypothalamus (ALC) was performed, the blood concentrations revealed irregularly occurring small fluctuations, instead of the usual high bursts, but the basal GH concentration was significantly higher than that of OVX-sham-operated rats. DHT treatment did not elicit pulsatile GH secretion or alter GH concentrations in OVX rats with ALC. When intact adult female rats received DHT at a dose of 1 mg/rat, the male-like GH secretory pattern was not induced. These results suggest that neural inputs from the anterolateral direction to the medial basal hypothalamus are necessary for the masculinizing effect of DHT on the GH secretory pattern in OVX rats, and that oestrogen in intact female rats prevents the masculinizing effect of DHT.

Afferent Pathways↗
PubMed2000

Selective corticotropin-releasing factor type 1 receptor antagonist blocks conditioned fear-induced release of noradrenaline in the hypothalamic paraventricular nucleus of rats.

The effects of conditioned fear on the release of noradrenaline in the hypothalamic paraventricular nucleus (PVN) and the involvement of corticotropin-releasing factor (CRF) receptor type 1 (CRFR1) in conditioned fear-induced changes in noradrenaline release were examined by intracerebral microdialysis in rats. Conditioned fear was produced by placing animals into a box where they had previously been exposed to a 5-min period of electric footshock, 135 min prior to the start of experiment. Conditioned fear for 20 min produced a significant increase in the release of noradrenaline in the PVN. Intraperitoneal preadministration of a selective nonpeptidic CRFR1 antagonist, CRA1000, completely blocked the conditioned fear-induced release of noradrenaline. These results suggest that CRFR1 is involved in the release of noradrenaline in the hypothalamic PVN induced by conditioned fear.

Animals↗
PubMed2000

A subpopulation of fibroblast growth factor-2-binding heparan sulfate is lost in human papillary thyroid carcinomas.

We hypothesized that a change in composition of proteoglycans can regulate the bioactivity of fibroblast growth factor (FGF)-2 in the thyroid. In order to test this hypothesis, we established a simple and sensitive method for detecting FGF-2-binding heparan sulfates and characterized them in papillary thyroid carcinomas and normal thyroids. The thyroid extracts were applied to a Q-Sepharose anion exchange column. After the column was washed with 10 mM of phosphate buffer, 1 microgram of human recombinant FGF-2 was added onto the column. The column was eluted with a gradient of NaCl (0.3-1.5 M). Each fraction was blotted onto nitrocellulose membrane. Immunoreactivity of heparan sulfate and FGF-2 was revealed by the incubation of membranes with the specific antibodies, and quantitatively estimated by measuring the density of the color product. In normal thyroids, immunoreactivity of heparan sulfate was detected as two peaks at 0.7 and 0.9 M of NaCl. Heparan sulfate-containing fractions also showed FGF-2 immunoreactivity, indicating the complex formation of FGF-2 and heparan sulfate. In papillary thyroid carcinomas, immunoreactivity of heparan sulfate showed various elution profiles on Q-Sepharose chromatography, including single peak at 0.7 M of NaCl and the one similar to that of the normal thyroids. However, FGF-2 immunoreactivity was detected only in the fractions eluting at 0.7 M of NaCl. This loss of a subpopulation of FGF-2-binding heparan sulfate in human papillary thyroid carcinomas may lead to the increase of free FGF-2 bioavailable in extracellular matrix.

Anion Exchange Resins↗
PubMed2000

Central effect of ghrelin, an endogenous growth hormone secretagogue, on hypothalamic peptide gene expression.

Ghrelin, an endogenous ligand for the growth hormone secretagogue receptor (GHS-R), was originally purified from the rat stomach. Like the synthetic GHSs, ghrelin specifically releases GH following intravenous administration. Also consistent with the central actions of GHSs, ghrelin-immunoreactive cells were shown to be located in the hypothalamic arcuate nucleus as well as the stomach. However, the central actions of ghrelin have not been elucidated. Here, we used radioactive in situ hybridization histochemistry to examine the effects of central administration of rat ghrelin on neuropeptide genes that are expressed in hypothalamic neurons that were previously shown to express GHS-R. We found that central administration of ghrelin increased both agouti-related protein (AGRP) mRNA levels (245.8 +/- 28.3% of the saline-treated controls; p < 0.01) in the hypothalamus and food intake (5.7 +/- 0.9 g ghrelin vs. 1.9 +/- 0.5 g saline; p < 0.05). On the other hand, 1 microg of rat ghrelin central administration did not alter the episodic GH release of freely moving adult male rats. Thus, ghrelin has an alternative role in stimulating food intake via an increase of AGRP rather than the release of GH from the pituitary.

Agouti-Related Protein↗
PubMed2000

The hexapeptide KP-102 (D-ala-D-beta-Nal-ala-trp-D-phe-lys-NH(2)) stimulates growth hormone release in a cichlid fish (Ooreochromis mossambicus).

Abstract Studies in mammals have shown that synthetic Met-enkephalin derivatives, called growth hormone-releasing peptides (GHRPs), stimulate growth hormone (GH) release. The present study was conducted to determine whether the GHRP, KP-102, specifically stimulates GH release in a teleost. Tilapia (Oreochromis mossambicus) were given a single intraperitoneal injection of KP-102 (D-Ala-D-beta;-Nal-Ala-Trp-D-Phe-Lys-NH(2)) or bovine GHRH(1-29)-amide or vehicle and blood was sampled at 1, 6 and 12 h after injection. KP-102 was administered at two doses of 1 ng/g and 10 ng/g body weight, whereas GHRH (positive control) was administered at a single dose of 10 ng/g body weight. Plasma levels of tilapia GH and prolactins (tPRL(177) and tPRL(188)) were determined by radioimmunoassay. As expected, GHRH injection significantly (P<0.001) elevated plasma GH levels (ng/ml) in tilapia at 6 h post-injection. KP-102 also significantly elevated GH levels (at the low dose) at 6 (P<0.05) and 12 (P<0.01) hours post-injection. There were no significant effects on plasma PRL(s) levels, although mean levels of both PRLs were elevated at 6 h post-injection. These results show for the first time that GHRPs stimulate GH release in teleosts and suggest that the GHRP receptor and possibly a "Ghrelin-like" ligand are also present in lower vertebrates.

Analysis of Variance↗
PubMed2000

Ethanol suppresses L-arginine-induced relaxation response of rat aorta stimulated with bacterial lipopolysaccharide.

Using isolated rat aortic strips without endothelium, we investigated the effect of ethanol on L-arginine-induced relaxation. L-Arginine (10(-5)-10(-3) M) produced a relaxation response in vascular strips incubated for 6 hr with bacterial lipopolysaccharide (1 microgram/ml). The relaxation was either abolished by cycloheximide (10(-5) M) and actinomycin D (10(-5) M) or diminished by polymyxin B (10 micrograms/ml), dexamethasone (10(-5) M) and nitro-L-arginine (10(-4) M) under conditions in which these inhibitors were coincubated with lipopolysaccharide. Also, L-arginine-induced relaxation was significantly inhibited when ethanol (200, 400 mM) was present together with lipopolysaccharide during the 6-hr incubation. However, when ethanol was added to the organ bath after 6-hr incubation with lipopolysaccharide, it did not inhibit the relaxation. These results suggest that the relaxation response to L-arginine is mediated by an inducible type of nitric oxide synthase, which can be induced by lipopolysaccharide, and that ethanol may attenuate this nitric oxide-mediated relaxation by inhibiting expression of inducible nitric oxide synthase.

Animals↗
PubMed2000

Thickening of the roentgenometrical gastric fold in the elderly: relation to peptic ulcer incidence.

Radiographic upper gastrointestinal barium examination is commonly used to diagnose peptic ulcer. However, little attention has been paid to its thickening, except in Ménétrier disease and gastric carcinoma of Borrman type IV. The present study was undertaken to investigate the relation of age to roentgenometrical gastric fold width and history of peptic ulcer. The subjects were 724 men (35-64 years old) who participated in a periodic medical health examination and underwent radiographic upper gastrointestinal barium examination. The gastric fold width of the anterior wall in the body was evaluated by air-contrast examination and expressed in millimeters. In the group with a history of peptic ulcer, the roentgenometrical gastric fold was significantly thicker than that in the group without it. The fold width was significantly greater in the elderly group (55-64 years old) than in the young (35-44 years old) and middle-aged (45-54 years old) groups. The fold width tended to increase with age in persons with peptic ulcer history, but not in those without it. When the subjects were divided into three groups by gastric fold width, the incidence of peptic ulcer was significantly higher in the upper third group compared with the lower third group. This relationship between the gastric fold width and the incidence of peptic ulcer tends to become stronger with aging. In the heavy smoker group (> or = 10 of cigarettes per day), the gastric fold width was significantly thicker than that of non-smokers or those who smoked less. This relationship also tended to grow stronger with aging. The mean incidence of peptic ulcers was significantly higher among the heavy smokers. However, daily alcohol drinkers did not show any significant difference in gastric fold width from the other subjects. The gastric fold seems to be thicker in persons with peptic ulcer history, and the incidence of peptic ulcer is higher in persons with thicker gastric fold. These relationships tend to grow stronger with aging.a

Adult↗
PubMed1999

Psychological stress increased corticotropin-releasing hormone mRNA and content in the central nucleus of the amygdala but not in the hypothalamic paraventricular nucleus in the rat.

The central administration of corticotropin-releasing hormone (CRH) to experimental animals sets into motion a coordinated series of physiological and behavioral events that promote survival during threatening situation. A large body of evidence suggest that CRH in the central nucleus of the amygdala (CEA) induces fear-related behaviors and is essential to fear conditioning; however, evidence of CRH-mediated activation of the amygdala under physiological situation is still limited. We report here a study of the impact of a psychological stressor on hypothalamic and amygdala CRH systems in the rat. Non-footshocked rats placed in a floored compartment surrounded by footshocked rats were defined as the psychological stress group. Rats were exposed to psychological stress for 15 min, and then sacrificed 1.5 and 3 h after cessation of stress. We found that our psychological stressor induced an increase in both CRH mRNA levels, as assessed by in situ hybridization histochemistry, and CRH content, as assessed by micropunch RIA, in the CEA. Exposure to the psychological stressor also caused a significant increase in CRH mRNA levels with a trend for an increase in CRH content in the dorsolateral subdivision of the bed nucleus of the stria terminalis (BNST) which is anatomically associated with the CEA. In contrast, psychological stress induced a small, but significant increase in type-1 CRH receptor (CRHR-1) mRNA in the hypothalamic paraventricular nucleus (PVN), while it failed to elevate either PVN CRH mRNA levels or content, CRH content in the median eminence (ME), or levels of plasma ACTH or corticosterone (CORT). Thus, in the context of a psychological stressor, the activation of the amygdala CRH system can occur without robust activation of the hypothalamic CRH system. In the light of previous data that the psychological stress-induced loss of sleep was reversed by the central administration of a CRH antagonist, these data suggest that CRH in the CEA may contribute to the psychological stress-evoked fear-related behavior such as hyperarousal. These data also indicate that in response to a psychological stressor, the amygdala CRH system is much more sensitive than is the CRH system emanating from the PVN.

Adrenocorticotropic Hormone↗
PubMed1999

Effect of insulin-like growth factor-I on growth hormone-releasing factor receptor expression in primary rat anterior pituitary cell culture.

We examined the effect of insulin-like growth factor-I (IGF-I) on GH-releasing factor (GRF) receptor expression in the primary rat anterior pituitary cell culture. The levels of GRF receptor mRNA were dose-dependently reduced by IGF-I treatment for 24 h. To clarify whether altered levels of GRF receptor mRNA contribute to GRF receptor concentrations, we examined the GH response to GRF in vitro. There was no difference in basal GH secretion between control and IGF-I pretreated cells, while GRF-stimulated GH secretion in cells pretreated with IGF-I for 24 h was significantly lower than that in control cells. Moreover, specific [125I] Tyr10-human GRF binding to pituitary cells was reduced significantly by IGF-I treatment. These results suggest that IGF-I acts directly on the pituitary and participates in the regulation of GRF receptor expression.

Animals↗
PubMed1999

Effects of antitumor agents on inducible prostacyclin production in vascular smooth muscle.

The effects of various antitumor agents were examined on prostacyclin production induced by interleukin-1beta in rat aortic smooth muscle cells. Stimulation of the cells with interleukin-1beta (2.5 ng/ml) resulted in a great increase of prostacyclin production, which was abolished by indomethacin (1 microM) or cycloheximide (2 microM). Daunorubicin at 0.1-1 microM inhibited the inducible prostacyclin production in a concentration-dependent manner. However, other antitumor agents (cyclophosphamide at 1-100 microM, 5-fluorouracil at 1-100 microM and vincristine at 1-100 nM) tested did not significantly affect it. Protein expression of cyclooxygenase-2 induced by interleukin-1beta was inhibited by daunorubicin at 0.1-1 microM, but was not affected by other antitumor agents. These results suggest that daunorubicin inhibits induction of cyclooxygenase-2 and subsequent prostacyclin production in rat aortic smooth muscle cells.

Animals↗
PubMed1999

Low vitamin K intake effects on glucose tolerance in rats.

To investigate the effects of vitamin K (VK) on pancreatic function, intravenous glucose tolerance tests were performed in rats fed with and without low VK diet (including less than 20% required vitamin K1). Plasma glucose and immuno-reactive insulin (IRI) were determined. It was found that at 0 min., plasma glucose and IRI levels in low VK group were slightly less than in the control (glucose, 204.5 +/- 21.7 vs. 229 +/- 19.6 mg/dl, IRI, 6.6 +/- 1.3 vs. 9.3 +/- 1.8 ng/ml mean +/- SEM). At 3 min. after glucose administration, plasma glucose was higher (391.8 +/- 25.6 vs. 371.8 +/- 18.7 mg/dl) and IRI, lower (11.8 +/- 2.1 vs. 18.2 +/- 3.6 ng/ml) in the low VK group. The disappearance rate of plasma glucose in the low VK group at 5-10 min. was significantly less than in the control (6.7 +/- 2.2 vs. 11.9 +/- 1.8 mg/dl/min.). Incremental IRI area at 0 to 5 min. in the low VK group is less than in the control (15.2 +/- 4.4 vs. 25.0 +/- 9.1 ng/ml/min.), but at 5-60 min. and 0-60 min., it was found to be significantly higher compared to the control (210.3 +/- 55.2 vs. 32.5 +/- 47.1 ng/ml/min. at 5-60 min.). Dietary low VK intake would thus appear to induce a tendency of poor early insulin response, and late hyperinsulinemia to the glucose load in rats.

Animals↗
PubMed1999

Growth hormone-releasing hormone receptor (GHRH-R) and growth hormone secretagogue receptor (GHS-R) mRNA levels during postnatal development in male and female rats.

Experimental evidence suggests that differential pituitary sensitivity to hypothalamic signals exerts a role in mediating both age and sex dependent patterns of growth hormone (GH) release and synthesis. One mechanism by which pituitary sensitivity to hypothalamic GH regulators could be modified is by the differential synthesis of their pituitary receptors. In the present report we therefore studied the age and sex dependency of the expression of receptors for two known stimulators of GH release, growth hormone-releasing hormone (GHRH) and the synthetic peptidyl and non-peptidyl GH secretagogues (GHSs). Pituitary GHRH receptor (GHRH-R) and GHS receptor (GHS-R) mRNA levels were measured by reverse transcriptase-polymerase chain reaction (RT-PCR) in male and female rats at postnatal day 1, 10, 30 and 75. We also examined the age- and sex-dependent expression of the GHS-R in whole hypothalamic extracts, since the GHS-R is also expressed in a variety of nuclei within the hypothalamus and has been linked to central regulation of the GH-axis. Pituitary GHRH-R mRNA concentrations were age-dependent; the highest levels were observed in d1 pituitaries and then declined with age, reaching a nadir by d30. These results are in concordance with the age-related decline in pituitary GHRH sensitivity. In contrast, the ontogenic pattern of GHS-R expression was bimodal; GHS-R mRNA concentrations in dl and d30 pituitaries were approximately twice those at d10 and d75. These results mirror the transient increase in GHS sensitivity observed around the onset of puberty, suggesting that gonadal steroids mediate GHS-R expression. GHRH-R mRNA levels were comparable in males and females within each age while GHS-R mRNA levels were gender dependent. At d30, male GHS-R mRNA levels were 30% greater than in their female counterparts. This was reversed at d75, when females had 89% more GHS-R mRNA per pituitary and 65% more per somatotrope than did age-matched males. These sexual differences further support a role for gonadal steroids in the modulation of pituitary GHS-R synthesis. The ontogenic and gender-specific pattern of hypothalamic GHS-R expression differed from that observed for the pituitary. Hypothalamic GHS-R mRNA levels increased with age but exhibited no significant sex difference at each age tested. Taken together, these data demonstrate that changes in the levels of pituitary GHS-R mRNA, but not GHRH-R mRNA, are associated with changes in the gonadal steroid environment, thereby implicating the GHS/GHS-R signalling system as a control point in the establishment and maintenance of sexually dimorphic patterns of GH secretion.

Animals↗