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H Watanobe

Publications and source records attributed to H Watanobe.

88 records · Page 5Linked to original sources
PubMed1988

Ectopic ACTH syndrome due to Grawitz tumor.

An extremely unusual case of adrenocorticotropin (ACTH)-producing Grawitz tumor is reported in a 56-year-old female. The clinical feature of the patient was compatible with Cushing's syndrome. The plasma levels of ACTH and cortisol were markedly elevated. At autopsy, a left renal tumor was demonstrated and its histopathological diagnosis was renal cell carcinoma (Grawitz tumor). The adrenal gland was bilaterally enlarged with diffuse hyperplasia of the fasciculate zone. The adenohypophyseal cells were atrophic and showed Crooke's degeneration. The tumor contained extremely high levels of ACTH, beta-lipotropin and beta-endorphin. The presence of large molecular weight forms of ACTH has also been demonstrated by a Sephadex G-50 gel filtration of the tumor extract. We authors believe that this is the first documented case of ACTH-producing Grawitz tumor in the literature.

ACTH Syndrome, Ectopic↗
PubMed1988

Hepatocellular carcinoma associated with a rare combination of polycythemia and chronic thyroiditis.

A case of hepatocellular carcinoma associated with polycythemia and chronic thyroiditis, is reported in a 76-year-old female. At autopsy, the liver tumor was shown to be co-existent with liver cirrhosis. A series of hematological studies including the determination of plasma erythropoietin levels, led to the conclusion that this patient's polycythemia was most likely due to an excessive production of erythropoietin by the liver tumor. Chronic thyroiditis, another combined disease, might be related to liver cirrhosis, if the formerly advocated "hepato-thyroidal syndrome" is accepted. The author reports on this patient, since prior to this case there has been no documented case report of hepatocellular carcinoma accompanying both polycythemia and chronic thyroiditis.

Aged↗
PubMed1987

Postnatal ovary is necessary for the maturation of estradiol-induced luteinizing hormone and prolactin surges in female rats.

The role of postnatal ovary in the maturation of estradiol (E2)-induced luteinizing hormone (LH) and prolactin (PRL) surges was examined in female rats of Wistar-Imamichi strain. Animals were bilaterally ovariectomized at 24 h after birth, 1 week (w), 2 w, 3 w, 4 w or 6 w of age. At about 10 w of age, every group was primed with estradiol benzoate (E2B) for two days, and on the third day was decapitated at either 0900 h or 1900 h. Anterior pituitary (AP) LH and PRL content was determined in every group of no E2B treatment. Surge-like secretions of LH and PRL were observed at 1900 h, only in rats ovariectomized on or after 4 w of age. AP LH and PRL content was the higher, as ovariectomy was delayed. These results indicate that postnatal ovary is necessary for the maturation of E2-induced LH and PRL surges. Such an effect of ovary is mediated at least by its stimulation of AP LH and PRL content.

Animals↗
PubMed1987

Role of postnatal gonadal function in the determination of thyrotropin (TSH) releasing hormone-induced TSH response in adult male and female rats.

Permanent effects of postnatal gonadal function on the hypothalamo-pituitary-thyroid axis were examined in male and female rats of the Wistar-Imamichi strain. Animals were used at the age of about 10 weeks. Neonatally castrated (NC) males showed a significantly higher plasma TSH response to TRH (10 micrograms/kg BW, ip) than males castrated at 1, 2, 3, 4, or 6 weeks of age. The TSH response in intact males was similar to that seen in NC males. Neonatal androgenization of NC males with 100 micrograms/rat of testosterone propionate decreased the TSH response in the group. The anterior pituitary (AP) TSH content was similar among all male groups. The number of AP TRH receptors was significantly higher in both NC males and intact males than in both NC + neonatal androgenization males and 6-week-castrated males. In female rats, TRH-induced TSH response, AP TSH content, and AP TRH receptor number were all unaffected by the age of castration, whereas intact females significantly exceeded 6-week-castrated females in these three variables. The circulating levels of T3 and T4 and hypothalamic TRH content were similar in all groups in each sex. These results indicate biphasic effects of postnatal testosterone on the TSH response to TRH, that is, a permanent inhibition in early postnatal days and a transient stimulation in adult age. The effects occurred not via changes in AP TSH content but via changes in AP TRH receptor number. In females, however, postnatal gonads did not exert any permanent effects on the TRH-TSH system.

Aging↗
PubMed1987

Involvement of postnatal gonads in the maturation of dopaminergic regulation of prolactin secretion in male rats.

Permanent effects of postnatal gonads on dopamine (DA)-mediated regulation of PRL secretion were examined in adult male rats of the Wistar-Imamichi strain. Rats were bilaterally orchidectomized at varying postnatal days, i.e. 8 h after birth [neonatal castration (NC)] or at 1, 2, 3, 4, or 6 weeks of age, and subjected to experiments at the age of about 10 weeks. Ten-week-old intact adults were also examined. All groups were injected ip with saline or sulpiride (1 mg/kg BW), and blood samples were collected by rapid decapitation 20 min later. Anterior pituitaries (AP) thus obtained were subjected to determination of PRL content. The circulating level of testosterone was similar among all castrated groups. Rats castrated on or after 3 weeks of age showed a significantly smaller PRL response to sulpiride than intact adults. In turn, sulpiride-induced PRL release in rats castrated on or before 2 weeks of age was similar to that in intact adults. However, the AP PRL content of saline control was uniformly lower in castrated males than in intact adults regardless of age at castration (P less than 0.01). The value in males castrated at 1 week was 2.0-fold higher than that in NC males, but a decreasing trend was observed in groups castrated at 2 or 3 weeks. That such a stimulation of AP PRL content by the neonatal testis is not mediated by an action of estradiol converted from testosterone has been suggested by the failure of daily neonatal tamoxifen (estrogen antagonist) treatment of intact males, before castration at 1 week, to decrease AP PRL content during adulthood. Sulpiride-induced reduction of the AP PRL content was significant only in males castrated at 6 weeks and intact adults. Characteristics of AP DA receptors labeled by [3H]spiperone were not different between males castrated at 6 weeks and intact adults. However, a heterogeneity was observed between NC males and a set of males castrated at 6 weeks and intact adults. The Kd was significantly (P less than 0.05) greater in NC males (mean +/- SE, 1.19 +/- 0.22 nM) than in males castrated at 6 weeks (0.52 +/- 0.08 nM), and the number of binding sites was significantly (P less than 0.05) larger in NC males (20.4 +/- 1.6 fmol/pituitary) than in both males castrated at 6 weeks and intact adults (12.6 +/- 2.0 and 13.1 +/- 1.9 fmol/pituitary, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗
PubMed1987

Involvement of postnatal gonads in the maturation of dopaminergic regulation of prolactin secretion in female rats.

Permanent effects of postnatal gonads on dopamine (DA)-mediated regulation of PRL secretion were examined in adult female rats of the Wistar-Imamichi strain. Experiments were uniformly done at the age of about 10 weeks. First, rats were bilaterally ovariectomized on varying postnatal days, i.e. 24 h after birth [neonatal castration (NC)] or at 1, 2, 3, 4, or 6 weeks of age. Intact diestrous females were also examined. All groups were injected ip with saline or sulpiride (1 mg/kg BW), and blood samples were collected by rapid decapitation 20 min later. Also, in saline control groups, the anterior pituitary (AP) PRL content was determined. In NC females, significant PRL release was not observed by either sulpiride or saline. However, stimulation of PRL release by sulpiride was observed consistently in rats ovariectomized on or after 1 week of age. Although there was not a complete correlation between the plasma PRL level attained after sulpiride treatment and the AP PRL content, the general trend was that the AP PRL content was increased as the postnatal age of the ovariectomy was delayed. Values in intact adult females exceeded those in all of the castrated groups in both parameters. Second, daily sc injection for 7 days with estradiol benzoate (E2; 2.5 micrograms/kg BW) and/or progesterone (P; 5 mg/kg BW) was given after NC to determine which ovarian secretion(s) is involved in the aforementioned findings. Sulpiride stimulated PRL release in NC females that had been treated neonatally (postnatal days 3-9) with either E2 or P. This effect was accompanied by an increase in the AP PRL content. An enhancement of both parameters was also observed when the same dose of E2 or P was given in the fourth week (postnatal days 22-28). However, neither parameter was further augmented by concurrent administration of E2 and P at either postnatal time. Characteristics of AP DA receptors were subsequently analyzed in some of the foregoing groups using [3H]spiperone. The number of binding sites, when expressed as femtomoles per pituitary, did not differ among all groups examined. However, a significant difference in the dissociation constant (Kd) was observed between NC females and females castrated at 6 weeks of age. The Kd in NC females was not altered by subsequent neonatal treatment with E2 and/or P. Nonetheless, the E2 effect on Kd was dependent on when E2 was given after NC.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗
PubMed1987

Cimetidine-induced prolactin release in rats. The effect of sex and gonadal steroids.

The cimetidine-induced plasma Prl response was examined in rats of both sexes. First, 10 week old intact adult males and females (dioestrous) were compared. There was no significant difference in the Prl response to cimetidine between the two groups, despite the fact that in adult females the anterior pituitary Prl content was 4 times greater than in males. Second, the effect of gonadal state in adult age on the Prl response to cimetidine was examined in both sexes. In male rats, gonadectomy at the age of 6 weeks significantly reduced the plasma Prl response as well as the pituitary Prl content, both of which were sufficiently restored by testosterone replacement. However, in females, neither gonadectomy at the age of 6 weeks nor subsequent oestradiol replacement affected the Prl response to cimetidine, despite the fact that gonadectomy significantly reduced and oestradiol treatment significantly enhanced the pituitary Prl content. Third, possible permanent effects of the postnatal gonadal milieu on the cimetidine-induced Prl response and the pituitary Prl content were examined in both sexes by castration at varying postnatal ages. The ratio of plasma Prl response to pituitary Prl content was similar in all castrated males. In females, however, the ratio decreased with increasing castration age. In conclusion, the mechanism of cimetidine-induced Prl release is less sex-dependent than are the mechanisms of Prl release by other Prl secretagogues. First, this may be due to a minor role of oestrogen in females in determining the Prl response to cimetidine. Second, the postnatal ovarian secretions may exert a permanent inhibition of the development of the cimetidine-mobilized anterior pituitary Prl pool.

Age Factors↗
PubMed1985

Adrenocortical carcinoma with Cushing's syndrome presenting unusual urinary 17-ketosteroid fractionation.

A case of adrenal carcinoma with Cushing's syndrome was presented. Endocrinological and morphological investigations disclosed the presence of a functional adrenal carcinoma. This case was characterized by its unusual urinary 17-ketosteroid (17-KS) fractionation, i.e. a marked elevation of 17-KS was accompanied by the increments of etiocholanolone, but not of dehydroepiandrosterone (DHEA) or androsterone. Measurements of the plasma adrenocorticosteroids revealed normal DHEA and DHEA-S (sulfate) levels, moderately increased 17-OH-pregnenolone, and markedly increased (less than 100 times the normal) 11-deoxycortisol (cpd S). Therefore, it seems plausible that the normal urinary DHEA level in this patient would have occurred as a result of remarkably low C17-20 lyase activity sufficient to hamper DHEA production, and that markedly increased etiocholanolone might possibly have been converted from cpd S as well as from DHEA and androstenedione through 5 beta-reduction.

17-Ketosteroids↗
PubMed1985

Sexual differentiation of prolactin responsiveness to thyrotropin releasing hormone (TRH) in the rat. Effects of postnatal testosterone on adenohypophyseal TRH receptor ontogenesis in male rats.

The influence of postnatal testosterone on thyrotropin releasing hormone (TRH)-induced prolactin (PRL) response was tested in male rats. Under urethane anesthesia following estradiol pretreatment, neonatally castrated males showed a female-like plasma PRL response 4-fold greater than in adult-castrated males. Substitution of testosterone reversed the NC effect. However, postnatal age-dependent difference was observed in the effect of testosterone. Testosterone produced a marked inhibition on PRL response when given at 2 or 4 weeks of life but not at earlier days. Determinations of adenohypophyseal PRL concentration and TRH receptor density revealed that testosterone inhibition occurred via its detrimental influence not on PRL concentration but on TRH receptor density. These results indicate that the sex-related difference in the rat PRL response to TRH ensues at least partially through inhibition by postnatal testosterone on the adenohypophyseal TRH receptor ontogenesis in male rats, and that there might be a functional dissociation in testosterone-dependent temporal development between two hypothalamic centers which independently regulate cyclic secretability and secretory reserve of PRL.

Animals↗
PubMed1985

Cushing's syndrome presenting the coexistence of a pituitary corticotrophic cell hyperplasia and a unilateral functional adrenal adenoma.

A very unusual case of Cushing's syndrome is presented. Most of the preoperative biochemical and radiological examinations were compatible with Cushing's syndrome owing to a right adrenal adenoma. Exceptional findings include normal concentrations of adrenocorticotrophin (ACTH) in plasma as well as a disturbance of its circadian rhythmicity and a significant adrenocortical responsiveness to exogenous ACTH. Secretory patterns of ACTH did not change even after right adrenalectomy. Studies in vitro revealed that the adenoma itself, but not the surrounding normal adrenal, was the source of cortisol secreted in response to ACTH. Post mortem examinations disclosed unexpectedly a hormonally inactive left adrenal adenoma and a focal hyperplastic lesion of the anterior pituitary with an ACTH concentration 53 times higher than that of the remaining tissue of the gland. It is a possibility that this case may have represented a transition between pituitary-dependent adrenocortical hyperplasia and adrenal adenoma to this date reported in only one similar case.

Adenoma↗
PubMed1984

[A case of adrenocortical carcinoma with Cushing's syndrome presenting unusual urinary 17-ketosteroid fractionation].

A patient with adrenocortical carcinoma with Cushing's syndrome is presented. This case seems to be most characterized by its very unusual urinary 17-ketosteroid (KS) fractionation, since markedly increased etiocholanolone was not accompanied by increments of either DHEA or androsterone. Determination of the plasma adrenocorticosteroids of the patient revealed normal DHEA and DHEA-S levels, moderately increased 17-OH-pregnenolone, and markedly increased 11-deoxycortisol. Therefore, it seems plausible that the unique 17-KS fractionation of this patient would have ensued as a result of remarkably decreased C17-20 lyase activity sufficient to nullify the increased 17-OH-pregnenolone and that markedly increased etiocholanolone might have been converted from 11-deoxycortisol.

17-Hydroxycorticosteroids↗
PubMedDate not supplied

Involvement of oxytocin and cholecystokinin-8 in interleukin-1 beta-induced adrenocorticotropin secretion in the rat.

It is well established that corticotropin-releasing hormone (CRH) is a principal neuropeptide which mediates the adrenocorticotropic hormone (ACTH) secretory response to interleukin (IL)-1 in the rat. It has recently been suggested that besides CRH, arginine vasopressin may also play a stimulatory role in IL-1 induced ACTH secretion. However, it remains to be elucidated whether other neuropeptides possessing an ACTH-releasing activity are involved in this neuroendocrine event. Therefore, in this study, we examined possible roles for oxytocin (OT) and cholecystokinin (CCK)-8 in the IL-1-induced ACTH response, utilizing the technique of immunoneutralization of these peptides. For comparison, we examined the effect of CRH immunoneutralization as well. Human recombinant IL-1 beta (50 ng) was given intracerebroventricularly (to the 3rd ventricle) to freely moving male rats 15 min after injecting specific antiserum against CRH, OT, or CCK-8, or normal rabbit serum (control) via the same route. As expected, anti-CRH antibody significantly suppressed the ACTH response to IL-1 beta. Interestingly, anti-OT antibody acted in the same manner, whereas anti-CCK-8 antibody did not. These results suggest that in addition to CRH and arginine vasopressin, OT may also play a significant role in mediating the IL-1 beta-induced ACTH secretion in the rat.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

The role of arginine vasopressin in interleukin-1 beta-induced adrenocorticotropin secretion in the rat.

In this study we examined whether arginine vasopressin (AVP) in the brain is involved in the adrenocorticotropin (ACTH) secretion induced by interleukin (IL)-1 beta in the rat. Human recombinant IL-1 beta (50 ng) was given intracerebroventricularly to freely moving male rats with or without a prior (15 min before) administration of anticorticotropin releasing hormone (CRH) or AVP antibody via the same route. The ACTH response to IL-1 beta was significantly reduced by both anti-CRH and anti-AVP antisera compared to the levels after normal rabbit serum. These results suggest that not only CRH but also AVP may mediate the IL-1 beta stimulation of ACTH secretion in the rat.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

In vivo evidence that arginine vasopressin is involved in the adrenocorticotropin response induced by interleukin-6 but not by tumor necrosis factor-alpha in the rat.

We examined whether arginine vasopressin (AVP) is involved in the adrenocorticotropin (ACTH) response induced by interleukin (IL)-6 or tumor necrosis factor (TNF)-alpha in the rat. To accomplish this, we employed immunoneutralization of brain AVP by injecting anti-AVP antiserum intracerebroventricularly (i.c.v., 3rd ventricle). For comparison, we also tested the effect of immunoneutralization of corticotropin-releasing hormone (CRH) in the brain. Anti-CRH antibody, anti-AVP antibody, or normal rabbit serum (control) was given i.c.v. 15 min before an i.c.v. administration of human recombinant IL-6 (100 ng) or TNF-alpha (100 ng). Both IL-6 and TNF-alpha significantly elevated plasma ACTH levels. The IL-6-induced ACTH response was significantly suppressed by both anti-CRH and anti-AVP antibodies. On the other hand, the TNF-alpha-induced ACTH response was not significantly affected by anti-AVP antibody, although anti-CRH antibody could suppress the response. These results suggest that the IL-6-induced ACTH response may be mediated by both CRH and AVP, whereas the ACTH response to TNF-alpha is only via CRH.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Effects of gender and gonadectomy on ACTH response to interleukin-1beta in the rat: comparison with the modulation of ACTH response to immobilization stress.

We examined the influence of gender and gonadectomy on the plasma adrenocorticotropin (ACTH) response to intravenous administration of human recombinant interleukin (IL)-1beta (3 microg/kg) in the rat. For comparison, we also examined whether gender and gonadectomy affect ACTH secretion after immobilization stress (a 30-min period), which is a nonimmunological stressor. IL-1beta induced a significantly higher ACTH response in females than in males, and this sexual difference was abolished by gonadectomy in both sexes. By contrast, ACTH secretion after immobilization was statistically the same in males and females, but tended to be higher in gonadectomized males than in gonadectomized females. These results may suggest a dissociative regulation by gonadal steroids of IL-1beta- and immobilization-induced ACTH responses in the rat. The sexual difference in ACTH response to IL-1beta may represent another example of the sexually dimorphic immunological activity, which is known to be higher in females than in males.

Adrenocorticotropic Hormone↗