[Imaging diagnosis of adrenal gland diseases].
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Adrenal Gland Diseases↗
Biomedical subjects
Y Oki
Publications and source records attributed to Y Oki.
Changes in hepatic lipogenic enzyme activities in voles and mice treated with monosodium aspartate.
Changes in activities of hepatic lipogenic enzymes, ATP citrate lyase and acetyl-CoA carboxylase, were measured in voles and C57BL mice following neonatal administration of monosodium aspartate (MSA). Hepatic lipogenic enzyme activities in voles were considerably lower than those in mice; these low activities were considered to be one of the characteristics of voles as a herbivore. In the MSA-treated voles and mice, the plasma insulin concentrations increased significantly. The MSA-treated mice showed remarkable obesity and increased lipogenic enzyme activities. In the MSA-treated voles, signs of obesity were not observed and hepatic ATP citrate lyase activity increased significantly; acetyl-CoA carboxylase activity did not increase.
ATP Citrate (pro-S)-Lyase↗
Alterations in acetyl coenzyme A carboxylase activities in voles and mice treated with monosodium aspartate.
Changes of body weights and hepatic acetyl-CoA carboxylase activities were measured in voles and mice treated with monosodium-L-aspartate (MSA). MSA was administrated subcutaneously to neonates at 4 mg/g. The MSA-treated mice showed remarkable obesity, associated with the increase in the plasma insulin concentrations and acetyl-CoA carboxylase activities. The activity of acetyl-CoA carboxylase of control voles was very low; under half that of mice. In the MSA-treated voles, although the plasma insulin concentrations also increased, acetyl-CoA carboxylase activities were not elevated and signs of obesity were not observed.
Acetyl-CoA Carboxylase↗
Interleukin-1 (IL-1) stimulates arginine vasopressin (AVP) release from superfused rat hypothalamo-neurohypophyseal complexes independently of cholinergic mechanism.
We studied whether interleukin-1 (IL-1) affects the release of arginine vasopressin (AVP) from the superfused hypothalamo-neurohypophyseal complex (HNC) of rats. Involvement of the cholinergic system in the mediation of IL-1 on AVP release from HNC was also examined. Both human recombinant IL-1 alpha and -1 beta elicited a rapid increase of AVP from HNC in a dose-dependent manner at concentrations ranging from 0.1 to 10 nM. However, neither IL-1 alpha nor -1 beta at concentrations of 100 nM increased AVP, and even suppressed the stimulatory effect of 10 nM IL-1 alpha and -1 beta added later. Acetylcholine at concentrations of 1 to 100 nM caused a dose-dependent, rapid increase in AVP, whereas AVP release induced by 10 nM acetylcholine was completely suppressed by the combined presence of 10 microM hexamethonium, a nicotinic receptor antagonist, and 50 microM atropine, a muscarinic receptor antagonist. On the other hand, AVP release induced by 10 nM IL-1 alpha and -1 beta was not affected by the combination of the two antagonists. These results suggest that both IL-1 alpha and -1 beta may stimulate AVP release by acting directly on the hypothalamo-neurohypophyseal system, and that the stimulatory effect of IL-1 on AVP release may be independent of the cholinergic system.
Acetylcholine↗
Stimulation by interleukin-1 (IL-1) of the release of rat corticotropin-releasing factor (CRF), which is independent of the cholinergic mechanism, from superfused rat hypothalamo-neurohypophysial complexes.
The effects of interleukin-1 (IL-1) and interferon-gamma (Ifn-gamma) on the release of corticotropin-releasing factor (CRF) from superfused hypothalamo-neurohypophysial complexes (HNC) of rats were examined in the present study. In this in vitro system, the release of CRF from HNC was not affected by any dose of human recombinant Ifn-gamma tested (0.1, 1 and 10 nM). In contrast, a rapid increase of CRF from HNC was elicited in a dose-dependent manner by human recombinant IL-1 alpha and -1 beta in concentrations of 0.1-10 nM. The involvement of the cholinergic system in the mediation of the stimulatory effect of IL-1 on CRF release was evaluated. Acetylcholine in concentrations of 1-100 nM also elicited a rapid increase of CRF. The increase in CRF release induced by 10 nM of acetylcholine was completely suppressed in the presence of both hexamethonium (10 microM) and atropine (50 microM), a nicotinic and a muscarinic receptor antagonist, respectively. On the other hand, the increase in CRF release induced by 10 nM IL-1 alpha or -1 beta was not affected by these two antagonists. These results indicate that IL-1 stimulates CRF release through an action on the hypothalamo-neurohypophysial system, most likely on the hypothalamus, and that the stimulatory effect of IL-1 is probably independent of the cholinergic system.
Acetylcholine↗
An ultrastructural study on the pancreatic islet B cells in diabetic herbivorous voles.
An ultrastructural study was performed on the pancreatic islet cells of normal herbivorous voles and of voles in which diet-induced diabetes had been induced by feeding a low-fibre, high-concentrate diet. Examination of the pancreatic islet cells revealed degranulation and a well-developed Golgi apparatus and rough endoplasmic reticulum in the B cells of the slightly diabetic voles showing moderate hyperglycaemia and hyperinsulinaemia, and markedly degenerative B cells with almost complete absence of secretory granules in the severely diabetic voles showing marked hyperglycaemia and hypoinsulinaemia. These results indicate that the pancreatic B cells had become hyperfunctional so that insulin secretion was increased in the slightly diabetic voles; thereafter the B cells degenerated rapidly and the voles fell into insulin deficiency.
Animals↗
A case of primary malignant lymphoma of the liver.
Primary lymphoma of the liver is extremely rare, and its preoperative or premortem diagnosis is still difficult. The author report here a case of primary malignant lymphoma of the liver diagnosed on a basis of ultrasonically guided biopsy of the tumor. A 51-year-old man was found to have a relatively large tumor in the right lobe of the liver as well as elevated serum LDH with abnormal isoenzyme pattern. Immunohistological studies of both biopsy and postmortem specimens of the tumor indicated T cell malignant lymphoma of the liver. The present case appears to be the second case of T cell origin of the disease.
Humans↗
A case of cervical carcinoma of the uterus presenting with hyperosmolar non-ketotic coma as a manifestation of ectopic adrenocorticotropic hormone syndrome.
A case of advanced cervical carcinoma of the uterus with ectopic adrenocorticotrophic hormone (ACTH) syndrome is described. The patient was seen for general malaise 21 months after surgical treatment of the primary lesion whose histology was undifferentiated small cell carcinoma of the uterine cervix. She had extensive metastases in the liver and the abdominal wall. In addition to the typical clinical manifestations of Cushing's syndrome such as moon face, central obesity and acne vulgaris, hyperglycemia was so severe that she was in a hyperosmolar non-ketotic coma. Endocrinological examinations revealed elevated plasma ACTH and cortisol, and urinary excretion of 17-hydroxycorticosteroids and 17-ketosteroids, which were not suppressed by high-dose dexamethasone administration. Based on these clinical and laboratory findings, a diagnosis of ectopic ACTH syndrome was made. Among the results of other endocrinological examinations conducted to find the etiological cause of the hyperglycemic coma, which seemed to be unusual for ectopic ACTH syndrome, the plasma somatostatin level was abnormally high. Metastatic tumors in the liver obtained at the time of autopsy contained large amounts of both ACTH and somatostatin, and gel filtration studies revealed that the peptides produced by the tumor had the molecular sizes of the biologically active forms of the respective peptides. These observations suggest possible involvement of the somatostatin in deteriorating glucose intolerance to develop hyperglycemic hyperosmolar non-ketotic coma as a drastic disturbance of metabolism.
Adrenocorticotropic Hormone↗
Immunohistochemical, ultrastructural, and hormonal studies on the endocrine pancreas of voles (Microtus arvalis) with monosodium aspartate-induced diabetes.
A single subcutaneous administration of monosodium aspartate (MSA) to 30 neonatal voles, Microtus arvalis Pallas, induced a diabetes mellitus in 50% of the treated animals in early adulthood. The voles (18 males and 12 females) were weaned at 3 weeks of age and fed pellets for Herbivora and cubed hay. Diabetic voles with glycosuria (nine males and six females) were classified into two groups according to the duration and grade of glycosuria. One group had slight diabetes with glycosuria (+: 0.1%) for 1 week and the other severe diabetes with marked glycosuria ( : greater than or equal to 0.5%) for over 4 weeks. Pancreatic islets of diabetic voles (n = 7) were examined immunohistochemically, light microscopically, and electron microscopically. Blood glucose concentration and tissue content of insulin, glucagon, and somatostatin were also measured. Slightly diabetic voles (n = 3) had enlarged islets, that, viewed by light microscopy, were characterized by hypertrophy and hyperplasia of beta cells with moderate degranulation. No changes were observed in the peripherally located alpha and delta cells; the voles were moderately hyperglycemic, and they had decreased pancreatic insulin content. Severely diabetic voles (n = 4) that had marked hyperglycemia and almost complete loss of insulin content showed marked vacuolation and degranulation of beta cells. In addition, altered distribution of alpha and delta cells from the periphery of the islets to their interior was noted. Ultrastructural examination revealed features compatible with those of hyperfunction of beta cells in the slightly diabetic voles and marked degeneration of beta cells with glycogen accumulation in the severely diabetic voles.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effects of intracellular Ca2+ depletion and glucocorticoid on stimulated adrenocorticotropin release by rat anterior pituitary cells in a microperifusion system.
Arginine vasopressin (AVP), oxytocin (OT), and angiotensin-II (AII) elicit a biphasic ACTH secretory response by perifused anterior pituitary cells consisting of an initial transient (less than 3-min) spike phase and a subsequent sustained plateau phase. In contrast, CRF produces a monophasic sustained plateau type of ACTH secretory response. We have previously demonstrated that 1) influx of extracellular Ca2+ (Cae2+) via L-type voltage-sensitive Ca2+ channels is involved in both the response to CRF and the sustained phase of the response to AVP and OT; 2) release of intracellular Ca2+ (Cai2+) is involved in the spike phase of the response to AVP, OT, and AII; and 3) activation of protein kinase-C is required for the sustained phase, but not for the spike phase, of the response to AVP. CRF action is mediated by activation of protein kinase-A. In this study we further examined the role of Cai2+ by exploiting the fact that a low concentration (1 microM) of ionomycin, a potent Ca2+ ionophore, releases Cai2+ from nonmitochondrial inositol-1,4,5-trisphosphate (IP3)-sensitive Cai2+ stores without causing Cae2+ influx. Pretreatment with ionomycin for 10 min decreased the spike phase of the response to 100 nM AVP, OT, and AII, but had no effect on the response to 10 nM CRF or the sustained phase of the responses to the other agonists. The combination of CRF plus AVP induced a biphasic and synergistic release of ACTH. Ionomycin pretreatment reduced the spike phase, especially the first 1 min, without any effect on the sustained phase. These results indicate that Cai2+ release, but not Cae2+ influx, is involved in the spike phase of the response to AVP, OT, and AII and that Cai2+ is not involved in the synergistic effect of the combination of CRF plus AVP. Having established these relationships, we examined the effect of 2-h perifusion with 100 nM dexamethasone (DEX) on stimulated ACTH release. DEX pretreatment reduced the total response to CRF, the sustained phase of the responses to AVP and OT, and the sustained phase of the synergistic response to CRF plus AVP. However, DEX had no effect on the spike phase of the responses to AVP, OT, or AII or the spike phase of the response to CRF plus AVP. These results indicate that DEX inhibits ACTH release mediated by activation of either protein kinase-A or protein kinase-C, but does not affect inositol-1,4,5-trisphosphate/Cai2(+)-mediated ACTH release.(ABSTRACT TRUNCATED AT 400 WORDS)
Adrenocorticotropic Hormone↗
Changes in plasma insulin and glucagon concentrations and hepatic enzyme activities in diabetic voles treated with monosodium aspartate.
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Animals↗
[Activities of hepatic ATP-citrate lyase and acetyl CoA carboxylase in herbivorous voles and C57BL/6J mice].
Activities of hepatic ATP-citrate lyase and acetyl CoA carboxylase, lipogenetic key enzymes, were measured in herbivorous voles and C57BL/6J mice. Hepatic ATP citrate lyase and acetyl CoA carboxylase activities in voles were very low, under one fifth and one half of those in C57BL/6J mice, respectively. It is considered to be one of characteristics as a herbivore that hepatic lipogenetic ability in voles is considerably low as compared to that in mice.
ATP Citrate (pro-S)-Lyase↗
Characteristics of the neutron field in the KEK counter hall.
We have measured the neutron leakage spectra outside the shielding in the KEK counter hall using a multisphere technique supplemented by the 12C(n, 2n)11C reaction in a carbon activation detector. The neutron spectra were derived from the measurements using the LOUHI78 unfolding code. The shape of these unfolded neutron spectra matched very closely that of spectra calculated by O'Brien and McLaughlin. A comparison of the dose equivalent as derived from the spectra with that measured by a neutron dose equivalent meter confirmed that the dose equivalent meter measurements usually underestimate the dose equivalent by at least 30%.
Methods↗
Roles of intracellular and extracellular calcium in the kinetic profile of adrenocorticotropin secretion by perifused rat anterior pituitary cells. II. Arginine vasopressin, oxytocin, and angiotensin-II stimulation.
We examined the effects of removing extracellular Ca2+ (Ca2+e), depleting intracellular Ca2+ (Ca2+i), inhibiting cAMP-dependent calmodulin, and blocking voltage-sensitive Ca2+ channels on the secretion of ACTH by perifused dispersed rat anterior pituitary cells. The cells were stimulated with synthetic arginine vasopressin (AVP), oxytocin (OT), and angiotensin-II (AII), all of which are thought to act via the Ca2+/inositol phosphate-dependent protein kinase-C pathway, with synthetic ovine CRF, which acts via the cAMP-dependent protein kinase-A pathway, and with dioctanoylglycerol, which directly activates protein kinase-C. All three secretagogues elicited an initial spike phase ACTH secretory response that peaked within 1 or 2 min and ended within 6 min. AVP and OT also elicited a sustained plateau phase response that lasted for as long as the cells were exposed to the secretagogue, but AII did not. Removal of Ca2+e diminished the initial spike phase by 30-50%, but depletion of Ca2+i virtually abolished it. In contrast, the sustained phase of the response to AVP and OT was abolished by removal of Ca2+e. The effect of dioctanoylglycerol, which elicits a sustained progressive increase in ACTH release, but no initial spike phase, was also greatly inhibited by Ca2+e removal; no greater effect was observed when Ca2+i was depleted. Blockade of L-type voltage-sensitive Ca2+ channels with nimodipine, a dihydropyridine drug, had the same effect as Ca2+e removal on both the initial spike and sustained plateau phases of the response to AVP. Inhibiting cAMP-dependent calmodulin with penfluridol had no effect on the initial spike phase, but reduced the sustained plateau phase of the response to AVP. Removal of Ca2+e or depletion of Ca2+i did not abolish the synergistic ACTH secretory response to the combination of AVP and CRF.(ABSTRACT TRUNCATED AT 400 WORDS)
Adrenocorticotropic Hormone↗
Role of protein kinase-C in the adrenocorticotropin secretory response to arginine vasopressin (AVP) and the synergistic response to AVP and corticotropin-releasing factor by perifused rat anterior pituitary cells.
Arginine vasopressin (AVP) stimulates biphasic release of ACTH from anterior pituitary corticotrophs. The response consists of an initial transient spike phase lasting less than 3 min and a subsequent sustained plateau phase that persists for as long as AVP is present. AVP also acts synergistically with CRF on ACTH release. We have previously shown that the initial spike phase of the response mainly requires release of intracellular Ca2+ and is independent of calmodulin, whereas the sustained plateau phase, like the monophasic sustained response elicited by CRF, involves the influx of extracellular Ca2+ via L-type voltage-sensitive Ca2+ channels and activation of calmodulin. We have also shown that the synergism between AVP and CRF does not require extracellular Ca2+ influx. In this study we examined the role of Ca2+/phospholipid-dependent protein kinase-C (PKC) in the two phases of the response to AVP and in the synergism between AVP and CRF. We exploited the observation that prolonged exposure to phorbol esters down-regulates PKC. Dispersed adult male rat anterior pituitary cells were incubated in static suspension culture for 4-5 days, 0.5 microM phorbol 12-myristate 13-acetate (PMA) or 0.0005% dimethylsulfoxide vehicle alone was added, and the incubation was continued for 24 h. The cells were preperifused with PMA-free perifusion medium for 3 h and then perifused with various agents for 10-20 min. Effluent fractions were collected every 30 sec or 1 min and subjected to ACTH RIA. Pretreatment with PMA inhibited the subsequent response to 100 nM PMA and 100 microM dioctanoylglycerol, but not to 5 microM forskolin or to depolarization with 56 mM KCl, demonstrating specific down-regulation of PKC. PMA pretreatment had no effect on the initial spike phase of the response to AVP, but inhibited the sustained plateau phase by 57% (P less than 0.005) and, consequently, the integrated total response by 33% (P less than 0.05). Pretreatment had no effect on the response to CRF. However, pretreatment with PMA completely blocked both phases of the synergistic response to the combination of AVP and CRF. These results indicate that activation of PKC is required for the sustained phase of the response to AVP and both phases of its synergistic interaction with the protein kinase-A pathway, but is not involved in the initial spike phase of the response to AVP, which presumably is mediated by inositol 1,4,5-trisphosphate-stimulated mobilization of intracellular Ca2+, or in the independent activation of the protein kinase-A pathway by CRF.
Adrenocorticotropic Hormone↗
[Composition of milk and electrophoretic analysis of milk casein in herbivorous voles (Microtus montebelli)].
Milk samples were collected from herbivorous voles (Microtus montebelli) and their compositions were analyzed. Total solids, fat, protein and ash concentrations of vole's milk were very higher than those of cow's milk. The lactose concentration was very lower than that of milk of cow or mouse. The electrophoretic patterns of milk casein of vole were different markedly from those of bovine, but resembled to those of mouse.
Animals↗
Hepatic enzyme activities and plasma insulin concentrations in diabetic herbivorous voles.
The activities of the hepatic glycolytic enzymes glucokinase (GKase) and hexokinase (HKase) in herbivorous Microtus arvalis were very low and the hepatic fructose-1,6-diphosphatase (FDPase) activities were almost the same as those in C57BL/6J mice. Glycosuria was observed in over 50% of voles fed on a low fibre, high concentrate diet. Voles with a high incidence of glycosuria for over 6 weeks became insulin deficient. In these diabetic voles, the hepatic GKase, HKase and FDPase activities decreased considerably as a result of diminished insulin secretion and fatty degeneration of the hepatic cells. It was considered that M. arvalis would be a useful animal model in which to study disorders of glucose utilization in herbivora.
Animals↗
Kinetic actions and interactions of arginine vasopressin, angiotensin-II, and oxytocin on adrenocorticotropin secretion by rat anterior pituitary cells in the microperifusion system.
We have examined the actions and interactions of arginine vasopressin (AVP), angiotensin-II (AII), and oxytocin (OT) on the ACTH secretory response of dispersed rat anterior pituitary cells in a microperifusion system. There was a dose-dependent ACTH secretory response to a 3-min perifusion of AII which reached its maximum 10 sec after the cells were exposed to AII and fell rapidly to baseline within 2 min, despite continued infusion of AII. This brief spike type of pattern is similar to that produced by AVP, but different from the sustained plateau response induced by CRF. The threshold stimulating concentration of AII was about 10(-9) M; the maximally stimulating concentration was not defined, but was 10(-6) M or more. The initial ACTH response to OT was similar, but fell to a plateau 2 min after the cells were exposed to OT and remained constant until perifusion with OT was stopped, after which it fell rapidly to baseline. The threshold stimulating concentration of OT was 10(-8) M; the maximally stimulating concentration was not defined, but was 10(-6) M or more. The ACTH secretory response to 10(-8) M AII was greatly diminished when cells were exposed to 10(-6) AVP or 10(-6) M OT before AII infusion. However, prior exposure to AII had no effect on the magnitude of the ACTH secretory response to either AVP or OT. The effects of simultaneous perifusion of AII and AVP and of AII and OT were additive. When AVP and OT were perifused sequentially, the ACTH secretory response to the peptide that was infused second was completely abolished. Furthermore, the combination of AVP and OT stimulated no greater response than either agent alone. When cells were perifused with the combination of 10(-7) M OT and 10(-7)- to 10(-5)-M concentrations of two potent AVP V1 receptor antagonists, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine]-Arg8-vasopressin and [1-deaminopenicillamine-2-(O-methyl)tyrosine]-Arg8-vasopressin, both phases of the response to OT were progressively and almost completely inhibited. The initial spike phase was inhibited at lower antagonist concentrations than the sustained plateau phase.(ABSTRACT TRUNCATED AT 400 WORDS)
Adrenocorticotropic Hormone↗