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Biomedical subjects

M Matsubara

Publications and source records attributed to M Matsubara.

At least 181 records · Page 10Linked to original sources
PubMed1987

[The clinical significance of the measurement of plasma transferrin as a growth factor. II. The changes in various endocrine status].

The clinical significance of the measurement of plasma transferrin (Tf) in patients with hypophysial disorders was reported in our previous papers. In the present study, we determined plasma Tf levels in 55 patients with various endocrine states and considered their clinical significance compared with plasma somatomedin-C (SM-C) levels. Plasma Tf levels decreased significantly in patients with anorexia nervosa (p less than 0.02), hyperthyroidism (p less than 0.05), primary hypothyroidism (p less than 0.05) and Cushing's syndrome (p less than 0.05), while they were elevated significantly in pregnancy (p less than 0.01) or females using estrogens (p less than 0.05). The former two declines were considered a reflection of the malnutritional state of the patients since a significant negative correlation was observed between plasma Tf levels and the percentile deficit from the ideal body weight in patients with anorexia nervosa (p less than 0.01), or between plasma Tf levels and elevated T3 levels which induce hypermetabolism in patients with hyperthyroidism (p less than 0.01). A significant correlation was observed between the SM-C and Tf levels in these subjects (including normal controls and patients with hypophysial disorders) as a whole (r = 0.79, p less than 0.001). These data indicate that plasma Tf is changeable according to the endocrinological and nutritional conditions with good correlation to the SM-C, and it is suggested that Tf also operates as a growth factor in vivo.

Adolescent↗
PubMed1987

[Suppression by dopamine of GH release induced by GRF in a case of acromegaly].

Inhibition of plasma GH by dopaminergic agonists is one of the characteristics of the GH secretion in acromegaly. GRF is known to stimulate GH secretion in most patients with acromegaly. In order to elucidate the relationship between GRF and dopamine in regulating the secretion of GH in this disease, we examined plasma GH responses to dopamine (DA) infusion (4 micrograms/kg/min), GRF injection (100 micrograms i.v.), sulpiride (SP) injection (200 mg i.v.), a DA blocker, DA plus GRF and SP plus GRF in a 51-year-old male patient with acromegaly. Plasma GH was reduced to 14% of the initial level by iv infusion of DA, and was elevated to 158% by iv injection of GRF. No considerable change was observed in plasma GH by iv infusion of SP (114% of the initial level). GH release induced by GRF was remarkably reduced by simultaneous administration of DA (28% of the initial level), whereas SP administration did not affect GRF-induced GH release (154%). The marked reduction of GH release after DA plus GRF seems to suggest that the effect of DA on the GH regulation is stronger than that of GRF in this acromegalic patient. It is suggested also that endogenous DA may not play an inhibitory role in GH secretion in this case since DA blockade by SP did not raise basal GH levels and the GH response to GRF.

Acromegaly↗
PubMed1987

Effects of dopaminergic agonists on plasma luteinizing hormone-releasing hormone (LRH) and gonadotropins in man.

To try to determine the site and mode of action of dopamine (DA) on the secretion of gonadotropins in humans, 4 series of studies were performed in 19 healthy volunteers (7 healthy males, 5 females in follicular phase and 7 postmenopausal females). The intravenous infusion of DA at the rate of 4 micrograms/kg/min decreased plasma LH levels to 75.9 +/- 3.7 (mean +/- SE)% of the initial levels. The oral administration of 500 mg of levodopa (Dopa) also suppressed the concentration of plasma LH to 73.0 +/- 3.5%, but the pretreatment with two doses of 100 mg each of carbidopa (CD), a peripheral dopa decarboxylase inhibitor, attenuated this suppressing effect of Dopa on LH levels (nadir 82.4 +/- 4.1). Plasma FSH were not significantly altered by these drugs. On the other hand, the concentration of endogenous LRH in peripheral blood remained unchanged throughout the studies. The administration of CD alone had no effect on any of these 3 parameters. These results would suggest the direct suppressing effect of DA on pituitary gonadotrophs, although the modulation at the level of the hypothalamus also cannot be ruled out.

Administration, Oral↗
PubMed1987

Beta-adrenergic receptor in heart of starved rats.

Female Wistar-strain rats were starved for 14-19 days by feeding approximately 1/4 of the amount consumed by ad libitum fed controls. The body weight was reduced by 41% and the heart weight by 38% in these starving periods. The 125I-iodocyanopindrol (ICYP) binding capacity of heart preparations from the starved rats was 35.3 +/- 11.1 (mean +/- SD) fmol/mg protein in comparison with 69.3 +/- 14.9 for the controls. Serum 3,5,3'-triiodothyronine (T3), thyroxine and TSH levels as well as pituitary TSH contents were markedly lower in the starved rats. One group of them further received 20 ng of T3 daily after the 8th day of the experiment. The body weight decreased by 47% of the controls but the ICYP binding capacity recovered to 56.3 +/- 10.9 fmol/mg protein. There was no difference in association constants of the receptors in these three groups. It was concluded that quasi-chronic starvation in rats caused a remarkable decrease in the number of beta-adrenergic receptors in heart and this was partly offset by the substitution of T3.

Animals↗
PubMed1987

Biphasic effects of dexamethasone on growth hormone release in vitro.

The effect of dexamethasone (Dex) on growth hormone (GH) release was examined in vitro in monolayer culture of normal rat pituitary cells and human somatotropinoma cells from patients with acromegaly. In either cell strain, Dex, at a concentration of 50 nM initially inhibited, but later (48 less than or equal to h) potentiated, the release of GH into the medium, with or without growth hormone releasing hormone (GHRH). The intracellular GH was significantly increased by 4-hour incubation with Dex in rat cell cultures. These results indicate a biphasic effect of glucocorticoids on GH release, irrespective of the origin of somatotrophs, and that the initial inhibitory effect is probably caused by inhibition of the release.

Acromegaly↗
PubMed1987

Dichotomic action of glucocorticoids on growth hormone secretion.

The mechanism of apparently discrepant actions of glucocorticoids (GC) on GH secretion, in vivo suppression and in vitro potentiation, was studied in rats. Dexamethasone (Dex), at the concentration of 50 nmol/l, potentiated basal and GHRH-stimulated GH release from monolayer culture of normal rat pituitary cells in 48 h. On the other hand, in vivo administration of Dex, 165 micrograms daily for 3 days, consistently suppressed serum GH levels in female rats. In these rats, the hypothalamic content of immunoreactive (IR) SRIH was significantly increased, whereas that of IR-GHRH was significantly decreased in comparison with the untreated rats. Bioassayable GH-releasing activity was also lower in Dex-treated rats. These findings indicate that the suppressing effect of GC on GH release in vivo is, at least partially, due to the increase in hypothalamic SRIH release and probably also to the decrease in GHRH release, and these effects surpass the potentiating effect of GC on GH release at the pituitary level, resulting in a net inhibitory effect in vivo.

Animals↗
PubMed1986

[The significance of the measurement of plasma transferrin as a growth factor. I. The changes in hypophysial diseases before and after treatment].

The concentrations of plasma transferrin (Tf), which has been described as possessing growth promoting activity in vitro, were determined in patients with various endocrine diseases before and after treatment. Plasma Tf levels in 74 healthy subjects were 269 +/- 3 (mean +/- SE) mg/dl. In 11 patients with active acromegaly, they were elevated to 353 +/- 11 mg/dl (p less than 0.001), while they were reduced to 168 +/- 14 mg/dl in 8 patients with hypopituitarism (p less than 0.001). They were normalized after treatment. These data indicate that plasma Tf varies according to the endocrine conditions with good correlation of the status of plasma somatomedin C, and therefore its measurement may be useful clinically for the evaluation of the status of growth factors. However, the values should be assessed carefully in cases with proper Tf abnormalities, such as hematological, hepatic, or renal disorders.

Acromegaly↗
PubMed1986

[Effects of intranasal administration of LHRH superanalogue on endogenous LHRH and gonadotropins in humans].

Plasma LH, FSH and endogenous LHRH were determined by radioimmunoassay (RIA) when 100 micrograms of LHRH superanalogue, des-Gly10-[D-Leu6]-LHRH ethylamide (leuprolide) was intranasally administered to both 7 healthy subjects aged 22 to 63 years and 6 patients with various hypogonadism aged 22 to 43 years [2 with anorexia nervosa, 3 with hypophysial hypogonadism and 1 with isolated gonadotropin (Gn) deficiency]. The response of plasma LH after the intranasal administration of leuprolide was observed to be 814 +/- 236 (mean +/- SE)% in the healthy subjects at 2 to 10 hours, and 528 +/- 183% in the patients with hypogonadism at 2 to 4 hours. These elevations were observed until 24 hours after administration in both groups. The response of plasma FSH was observed to be 449 +/- 99% in the healthy subjects at 3 to 8 hours, and 593 +/- 238% in the patients with hypogonadism at 2 to 6 hours. These elevations were observed until 24 hours in the healthy subjects and until 12 hours in the patients with hypogonadism. Furthermore, these responses tended to be higher than those after 100 micrograms intravenous administration of LHRH; LH responded up to 386 +/- 50% in the healthy subjects and up to 390 +/- 91% in the patients with hypogonadism, and FSH up to 282 +/- 38%, 343 +/- 90%, respectively. The elevation of plasma immunoreactive LHRH which was determined using RIA having no immunocrossreactivity with leuprolide (less than 0.01%) was observed at 6 hours after the administration of leuprolide in the healthy subjects (789 +/- 497%).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Intranasal↗
PubMed1986

Immunoreactive LHRH in chronic starved rats.

The effects of chronic starvation (1/4 of ad libitum food intake) for 21 or 30 days were studied on the hypothalamic and serum concentrations of LHRH, the pituitary and serum concentrations of LH, and the weights of the anterior pituitary, ovary and uterus in adult female Wistar rats (chronic starved group, CSG). Control female rats were fed ad lib. for the same periods (control group, CG). On day 22 or 31, half of the rats of each group were weighed and sacrificed by decapitation. Since there were no difference on above parameters between the experiments on 22nd and 31st day, the results were combined for each parameters. At the time of sacrifice, the body weight of CSG was on the average 44% lower than that of CG rats, and also marked reduction in anterior pituitary (44%), ovarian (61%) and uterine weights (69%) was observed. Serum LH concentrations (mean +/- SE; 5.67 +/- 0.67 versus 33.30 +/- 6.00 ng/ml, P less than 0.001) and pituitary LH content (286.7 +/- 19.4 vs 451.0 +/- 32.8 micrograms, P less than 0.001) were significantly decreased in CSG than in CG rats. However, pituitary LH concentration was not reduced because of the proportional reduction to the pituitary weight of CSG rats. Hypothalamic immunoreactive LHRH (IR-LHRH) content in CSG showed a significant increase as compared to CG rats (5.77 +/- 0.52 vs 4.41 +/- 0.27 ng/hypothalamic extract, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗