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Biomedical subjects

K Fujieda

Publications and source records attributed to K Fujieda.

At least 109 records · Page 6Linked to original sources
PubMed1985

[Insulin, glucagon and growth hormone responses during glucose, arginine and insulin tolerance tests in children with hyperthyroidism].

There are many reports of glucose intolerance in adult patients with hyperthyroidism but few reports of glucose intolerance in hyperthyroid children. In this study, we measured plasma levels of glucose, insulin, glucagon and growth hormone in hyperthyroid children and control subjects by the use of three kinds of tolerance tests: an oral glucose tolerance test, an arginine tolerance test and an insulin tolerance test. In the oral glucose tolerance test, mean fasting glucose levels (79.6 +/- 1.4 mg/dl) rose to maximum levels (157.3 +/- 4.3 mg/dl) at 30 min in hyperthyroid children which were significantly higher than the levels in control subjects (p less than 0.01). The maximum levels of glucose fell slowly and returned to fasting levels at 180 min. In this test, plasma insulin levels increased from basal levels (12.7 +/- 1.9 microU/ml) to maximum levels (120.8 +/- 22.1 microU/ml) at 30 min in the prepubertal age group of hyperthyroidism. On the other hand, in the pubertal age group of hyperthyroidism, maximum levels of insulin were observed at 60 min, but not at 30 min. These maximum levels of insulin of both hyperthyroid age groups were significantly higher than those in the control subjects (p less than 0.05, p less than 0.01 respectively). There was no difference in insulin-glucose ratio at 30 min (delta IRI/delta BG) and insulinogenic index (I.I.) at 0 to 60 min between these two groups of hyperthyroid children and control subjects. However, I.I. at 0 to 120 min and 0 to 180 min decreased significantly in the pubertal age group of hyperthyroidism as compared with those in the control group (p less than 0.05, p less than 0.02 respectively). In the oral glucose tolerance test, plasma glucagon levels decreased from basal levels (74.1 +/- 4.3 pg/ml) to minimum levels (36.4 +/- 4.7 pg/ml) at 90 min in hyperthyroidism, which were significantly lower than those in the controls (p less than 0.05). However, there was no difference in -epsilon delta IRG/epsilon delta BG (cumulative glucagon response/cumulative glucose response) between the subjects with hyperthyroidism and the controls. On the other hand, lower responses of blood glucose, insulin, glucagon and growth hormone to arginine were observed in subjects with hyperthyroidism than in the controls. Moreover in the insulin tolerance test, there was no difference in glucagon and growth hormone response between the subjects with hyperthyroidism and the controls. Thus our conclusions are as follows: A marked increase in blood glucose after oral glucose load was observed in spite of normal insulin-glucose ratio in hyperthyroid children, suggesting the existence of peripheral insulin resistance.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1984

Pituitary and gonadal function in prepubertal boys with hypospadias.

Luteinizing hormone releasing hormone and human chorionic gonadotropin tests were performed to examine the pituitary gonadal axis in 31 prepubertal boys with hypospadias. Luteinizing hormone and follicle stimulating hormone responses to luteinizing hormone releasing hormone in these boys with hypospadias were significantly higher than those in prepubertal control subjects (luteinizing hormone, p less than 0.01). follicle stimulating hormone, p less than 0.05). Prepubertal boys with hypospadias had remarkably reduced testosterone responses to human chorionic gonadotropin stimulation compared to controls (p less than 0.01). Hormonal milieus were further analyzed in the subtypes of hypospadias depending on their severity (distal vs. proximal). Nine of the 31 boys with hypospadias were classified as the proximal type. Basal luteinizing hormone levels in the proximal type were significantly higher than in the distal type (p less than 0.05). Luteinizing hormone and follicle stimulating hormone responses to luteinizing hormone releasing hormone and responses of testosterone to human chorionic gonadotropin were not significantly different in the 2 types. Seven of the 31 boys with hypospadias had a history of maternal progestin ingestion. Basal luteinizing hormone levels and responses of luteinizing hormone and follicle stimulating hormone to luteinizing hormone releasing hormone were also significantly higher in these subjects than in controls (p less than 0.005), though basal levels and responses of testosterone to human chorionic gonadotropin were not different from those of controls. Tests conducted to determine luteinizing hormone and follicle stimulating hormone and testosterone levels using luteinizing hormone releasing hormone and human chorionic gonadotropin stimulation revealed no statistical differences between the boys with hypospadias who had a history of maternal progestin ingestion and those without such a history. The majority of prepubertal boys with hypospadias had varying degrees of deficient testicular activity. The testicular function of these patients should be evaluated longitudinally at puberty and thereafter in order to insure the completion of secondary sexual development.

Child↗
PubMed1984

Prolactin response to thyrotropin-releasing hormone in children with gynecomastia, premature thelarche and idiopathic precocious puberty.

Plasma prolactin (PRL) response to synthetic thyrotropin-releasing hormone (TRH) was studied in six patients with pubertal gynecomastia, five patients with premature thelarche and nine female patients with idiopathic precocious puberty. The basal concentration of plasma PRL was higher (p less than 0.01) in pubertal gynecomastia as compared to control, while baseline plasma PRL levels in premature thelarche and idiopathic precocious puberty were similar to those in controls. Plasma PRL level after TRH in patients with pubertal gynecomastia was higher (p less than 0.01) than that in control, while plasma PRL responses to TRH in idiopathic precocious puberty and premature thelarche were comparable to those controls. The TRH-induced PRL release was more enhanced during treatment with cyproterone acetate (CA) than before CA therapy in four of five patients with idiopathic precocious puberty. These data suggest that the enhanced release of PRL may, at least in part, contribute to breast enlargement in pubertal gynecomastia and that seen in idiopathic precocious puberty and premature thelarche may not depend on the PRL secretion. The prolonged administration of CA enhances the PRL responsiveness to TRH.

Adolescent↗
PubMed1983

Plasma prolactin response to thyrotropin releasing hormone in children with newly diagnosed insulin dependent diabetes.

The basal and TRH-induced prolactin (PRL) and TSH secretions were examined in 14 children aged 4 to 13 years with newly diagnosed insulin dependent diabetes (IDD) within three weeks after diagnosis. Basal PRL levels did not differ from the values of control. In response to TRH, 6 out of 14 patients showed an exaggerated PRL response and 8 a normal PRL response. The basal and TRH-induced TSH secretions were normal, while plasma triiodothyronine (T3) and thyroxine (T4) concentrations were significantly (p less than 0.001, p less than 0.02) lower in patients than in controls. These findings suggest that a significant proportion of children with newly diagnosed IDD has an exaggerated PRL response to TRH, and TSH secretion remains unchanged despite significant decreases of circulating thyroid hormone levels.

Adolescent↗
PubMed1983

Epidemiologic survey of juvenile-onset insulin dependent diabetes mellitus (IDDM) in Hokkaido, Japan, 1973-1981.

An epidemiological survey of juvenile-onset insulin dependent diabetes mellitus (0-15 years) was performed in Hokkaido, Japan, during 1973-1981. The mean annual incidence during the nine year period was 1.26 per 100,000 and showed a significant increasing trend. The prevalence of IDDM at the ages of 0-15 and 6-15 were 7.7 and 11.7 per 100,000 respectively. These figures were much lower than those previously reported in Caucasians. Peaks in incidence were seen from February to April, and a reduction in incidence from July to September. The females showed a bimodal distribution with the peak incidence at 10 to 12 years and with a smaller peak at about 7 years. The males showed a broad single peak at about 10 to 13 years.

Adolescent↗
PubMed1982

Prolactin response to arginine in children with hyperthyroidism and primary hypothyroidism.

Plasma prolactin (PRL) response to arginine was examined in 16 prepubertal and 18 pubertal children with constitutional short stature, 5 patients with hyperthyroidism and 4 patients with primary hypothyroidism. The mean basal concentration of plasma PRL was significantly higher (P less than 0.01) in primary hypothyroidism than in other groups. Arginine infusion elicited significant (P less than 0.05) rises in plasma PRL in all groups. The maximal increment of plasma PRL above the baseline level after arginine stimulation was significantly larger (P less than 0.05) in pubertal than in prepubertal females and was significantly smaller (P less than 0.05) in patients with hyperthyroidism than in age- and sex-matched controls. There was no sex difference in arginine-stimulated PRL secretion. These data suggest that arginine produces a significant increase in plasma PRL and the PRL response to arginine was greater in pubertal than in prepubertal children. Plasma PRL response to arginine is suppressed in children with hyperthyroidism and the basal plasma PRL is markedly elevated in primary hypothyroidism.

Adolescent↗
PubMed1982

Regulation of the pituitary-adrenal axis and corticosteroid-binding globulin-cortisol interaction in the guinea pig.

Adult male guinea pigs were used to examine pituitary-adrenal function and corticosteroid-binding globulin (CBG)-cortisol interaction. A biphasic pattern in the circadian rhythm of plasma cortisol was observed, with nadirs occurring at 0800 and 2400 h and peaks and 1600 and 0400 h. An excellent correlation was noted between total and free plasma cortisol levels. In contrast, no correlation was noted between CBG binding capacity and either the total or free plasma cortisol level. The free plasma cortisol concentration ranged from 0.6-5.8 micrograms/dl, representing 6.1-14.5% of the total cortisol concentration. The CBG binding capacity ranged from 12.2-161.7 micrograms/dl, and the binding affinity was 1.3-2.2 x 10(7) M-1 at 22 C, which is 20-fold lower than that of human CBG. These results suggest that CBG in the guinea pig has a relatively minor effect on the plasma distribution of cortisol, and that free plasma cortisol is dependent on cortisol binding to nonspecific plasma proteins as well as on the total plasma cortisol concentration. It was found that the guinea pig was relatively resistant to dexamethasone suppression, requiring at least 1 mg/kg BW to obtain essentially complete suppression of the pituitary-adrenal axis. In addition, it was found that administering dexamethasone 6 h before the time that the animals were killed led to suppression, whereas giving the steroid 12 h before killing the animals was totally ineffective. Stress induced by both ether vapor and histamine injection significantly increased plasma cortisol levels. When the guinea pigs were treated with a 1 mg/kg BW dose of dexamethasone 6 h before the stimulus, however, a marked suppression of the plasma cortisol increment secondary to application of the stressful stimulus occurred.

Animals↗
PubMed1982

The control of steroidogenesis by human fetal adrenal cells in tissue culture. IV. The effect of exposure to placental steroids.

The effect upon steroidogenesis of adding various steroids produced by the placenta was studied in short term cultures of human fetal adrenal cells. The addition of high concentrations (10(3) ng/ml) of estrone or estriol inhibited the production of cortisol, but only the former elicited a parallel increase in dehydroepiandrosterone (DHA) production. Estradiol was effective in inhibiting delta-4-3-ketosteroid production at concentrations of 10-100 ng/ml, levels which approach those found in the fetal circulation, while DHA production was increased at concentrations of 1 microgram/ml. The addition of progesterone (4 microgram/ml) to the medium caused increased production of cortisol and corticosterone, but had no effect on DHA production. Pregnenolone (4 microgram/ml) increased the basal production of DHA and slightly impaired both basal and ACTH-stimulated aldosterone production, but had no effect on cortisol production. The data demonstrate that the many fetal and placental factors which have been studied to date, only ACTH and estrogens can interact to produce the characteristic fetal pattern of steroidogenesis. Preliminary studies indicate that this effect-stimulated aldosterone production, but had no effect on cortisol production. The data demonstrate that the many fetal and placental factors which have been studied to date, only ACTH and estrogens can interact to produce the characteristic fetal pattern of steroidogenesis. Preliminary studies indicate that this effect-stimulated aldosterone production, but had no effect on cortisol production. The data demonstrate that the many fetal and placental factors which have been studied to date, only ACTH and estrogens can interact to produce the characteristic fetal pattern of steroidogenesis. Preliminary studies indicate that this effect of estrogen is not influenced by other peptide hormones such as hCG, human prl, beta-lipotropin, corticotropin-like intermediate lobe peptide, or beta-endorphin. A revised model of the fetoplacental steroidogenic unit is presented which may explain both normal and fetal hyperplasia and postnatal involution of the adrenal cortex and the variations from this pattern seen in apituitary children.

Adrenal Cortex Hormones↗
PubMed1981

The control of steroidogenesis by human fetal adrenal cells in tissue culture. I. Responses to adrenocorticotropin.

A technique of monolayer tissue culture of human fetal adrenal cells was developed in order to study steroidogenic responses to factors such as ACTH. The daily production of 12 steroids [pregnenolone, 17-hydroxy pregnenolone, dehydroepiandrosterone (DHA), DHA sulfate, progesterone, 17-hydroxyprogesterone, androstenedione, testosterone, corticosterone, 11-desoxycortisol, cortisol, and aldosterone) was measured by RIA. Initially, fresh fetal adrenal cells produced DHA, DHA sulfate, 17-hydroxypregnenolone, and small amounts of cortisol, but in the absence of ACTH, the production of all steroids declined during culture to low levels. The addition of physiological amounts (1-10(4) pg/ml) of either alpha ACTH-1(1-24) or alpha ACTH-(1-39) or coculture with fetal pituitary cells elicited a progressive rise in steroid production during the first 4-6 days of incubation. The lowest ACTH doses elicited a proportionately greater adrenal androgen response (as reflected in the DHA to cortisol ratio), but with increasing ACTH dosage, there was greater stimulation of cortisol production, which equalled or exceeded that of DHA. The data demonstrate that fetal adrenal cells may be maintained in short term culture and can respond to physiological amounts of ACTH. The progressive increase in the production of cortisol and other delta 4, 3-ketosteroids in vitro suggests that the characteristic fetal pattern of steroidogenesis may result from the interaction of ACTH with some circulating inhibitor of adrenal 3 beta-hydroxysteroid dehydrogenase.

17-alpha-Hydroxypregnenolone↗
PubMed1981

The control of steroidogenesis by human fetal adrenal cells in tissue culture. II. Comparison of morphology and steroid production in cells of the fetal and definitive zones.

Preparations of dispersed human fetal adrenal cells from the inner third of the gland and from the subcapsular area were maintained in culture, and their ultrastructure and steroid production were studied. The former type of preparation contained only fetal zone cells, while the latter contained definitive zone cells together with varying numbers of fetal zone cells. Both types could be cultured with equal ease, but during short term culture, fetal and definitive zone cells became morphologically indistinguishable. The patterns of steroid production and, in particular, the relative production of delta 4,3-ketosteroids and delta 5,3 beta-hydroxysteroids were similar in both preparations, as were their dose-response relationships during incubation with alpha ACTH-(1-24). Although considerable variability in total steroid production was observed between cells from different adrenal glands, in no specimen was any evidence for functional zonation of the fetal adrenal cortex observed in vitro. The results suggest that the apparently unique histological appearance and function of the fetal adrenal cortex may only reflect intense stimulation by ACTH secondary to the combined influences of a rapid cortisol MCR and of some inhibitor of fetal adrenal 3 beta-hydroxysteroid dehydrogenase activity.

Adrenal Cortex↗
PubMed1981

The control of steroidogenesis by human fetal adrenal cells in tissue culture. III. The effects of various hormonal peptides.

The effects upon production of cortisol and dehydroepiandrosterone (DHA) by human fetal adrenal cells in tissue culture were studied using commercial hCG (0.5 and 5 IU/ml), purified hCG (0.7-6.7 IU/ml), the alpha-subunit of hCG (200 and 1000 ng/ml), human GH (50 and 200 ng/ml), human PRL (0.1-100 ng/ml), alpha-MSH (0.1-10 ng/ml), corticotropin-like intermediate lobe peptide (200 ng/ml), human beta-lipotropin (0.1 and 0.2 ng/ml), and beta-endorphin (100 ng/ml). Although each peptide was added to the culture medium in a concentration either similar to that observed in the fetal circulation or (where such information was not available) in amounts several times greater than those effective for ACTH in this system, none demonstrated any significant stimulation of steroid production. In particular, repeated studies with hCG showed that this hormone had no stimulating effect upon DHA production, neither in cultures of whole adrenals nor in cultures of separated fetal zone and definitive zone cells. Furthermore, none of these peptides showed a synergistic effect upon DHA production when they were added to cultures together with concentrations of alpha-ACTH-(1-24) (10(2)-10(3) pg/ml) previously demonstrated to represent the middle of the dose-response curve. Indeed, the only significant interactions with alpha-ACTH-(1-24) observed in these studies were a slight reduction in cortisol production produced by corticotropin-like intermediate lobe peptide and apparent inhibition of DHA production by beta-lipotropin and GH. The data do not lend credence to the suggestion that any of these peptides plays an important role in vivo in stimulating fetal adrenal steroidogenesis.

Adrenal Glands↗