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Biomedical subjects

E Ubukata

Publications and source records attributed to E Ubukata.

14 recordsLinked to original sources
PubMed1997

Glucocorticoids potentiate effect of ACTH on cortisol secretion in isolated perfused guinea pig adrenal glands.

To clearly understand the autoregulation of glucocorticoid secretion by the glucocorticoid level, we studied the effects of cortisol and dexamethasone on the cortisol secretion in the perfused guinea pig adrenal glands. The basal cortisol secretion was suppressed by cortisol infusion at 0.1 microgram/ml, but not affected by dexamethasone infusion at 1 microgram/ml. The cortisol response to ACTH after pre-perfusion for 35 min was much quicker and larger in the presence of 0.1 microgram/ml cortisol, and was quicker in the presence of 1 microgram/ml dexamethasone than in the absence of glucocorticoid. It is considered that glucocorticoids play a permissive role in the action of ACTH on the adrenal gland.

Adrenal Glands↗
PubMed1996

Effect of various glucagon/insulin molar ratios on blood ketone body levels in rats by use of osmotic minipumps.

The bihormonal control by insulin and glucagon of blood ketone body level was studied. Mixed solutions with various molar ratios of glucagon and insulin (G/I) were subcutaneously infused continuously for five days by use of the osmotic minipump in the normal rats. The concentrations of insulin and glucagon solution were set at the high G/I molar ratio, the moderate G/I molar ratio and the low G/I molar ratio. In addition, the moderate G/I molar ratio group was divided into three sub-groups: low glucagon and low insulin, moderate glucagon and moderate insulin, and high glucagon and high insulin. After five days, the rats were decapitated to measure plasma ketone body, free fatty acid (FFA), glucose, insulin and glucagon. The FFA level was not significantly different among three groups. The glucose level was not different between the high and moderate G/I molar ratio groups, and decreased in the low G/I molar ratio group. 3-beta-hydroxybutyrate (3-OHBA) and acetoacetate (AcAc) levels in the high G/I molar ratio group were elevated, and 3-OHBA level in the low G/I molar ratio group was lowered compared to those in the moderate G/I molar ratio group. Among three moderate G/I molar ratio sub-groups, there was no difference in 3-OHBA and AcAc levels. These results demonstrate that plasma ketone body levels are controlled by the plasma G/I molar ratio.

3-Hydroxybutyric Acid↗
PubMed1996

Captopril increases renin release stimulated by furosemide and hypotension in isolated perfused guinea pig kidneys.

To clearly understand the feedback mechanism of renin secretion by intrarenal angiotensin II synthesis, we studied the stimulatory effect of captopril, an angiotensin converting enzyme inhibitor, on renin release from the isolated perfused guinea pig kidneys. Captopril did not affect the basal renin secretion. Captopril increased on a dose dependent basis renin release induced by 0.1 mg/ml furosemide; 5.8 +/- 1.3 ng/ml/hr at 0 mg/ml of captopril vs. 8.8 +/- 1.6 ng/ml/hr at 0.01 mg/ml (p < 0.05) and 11.8 +/- 2.4 ng/ml/hr at 0.1 mg/ml (p < 0.01), 15-20 min after furosemide infusion. After lowering the flow rates from 10 to 5 ml/min, renin secretion was not altered during the first 12 minutes. However, after adding 0.1 mg/ml captopril, renin secretion was enhanced within the following 8 minutes (8.3 +/- 1.5 vs. 3.7 +/- 0.5 ng/ml/hr at the end of low flow rate period, p < 0.01). Lowering the perfusion flow of the guinea pig kidneys decreases the NaCl flux at the macula densa and also seems to have a similar effect to furosemide. Therefore, these effects of captopril suggest that intrarenal angiotensin II production has an important role in the regulation of renin secretion, probably via effects on the macula densa function.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Isolation and characterization of Marek's disease virus (MDV) cDNAs mapping to the BamHI-I2, BamHI-Q2, and BamHI-L fragments of the MDV genome from lymphoblastoid cells transformed and persistently infected with MDV.

We have isolated and sequenced two cDNAs of sizes 2674 and 677 bp from a cDNA library derived from MKT-1, a lymphoblastoid cell line transformed and latently infected with Marek's disease virus (MDV) using probes corresponding to the right-hand end of the BamHI-I2 fragment of the MDV genome. The larger cDNA clone represents an abundant transcript, which extends from the right-hand end of BamHI-I2 to the adjacent BamHI-Q2 and BamHI-L fragments of the MDV genome and contains the Meq (MDV Eco-Q) open reading frame. The smaller cDNA clone represents a spliced transcript containing the putative DNA binding domain of Meq as well as sequences in the BamHI-L region. We prepared a polyclonal antibody against part of the protein sequence of Meq and detected a 44-kDa protein in MKT-1 cells and in cells lytically infected with MDV. In addition, riboprobes corresponding to sequences specific to each cDNA as well as shared sequences between cDNAs detected a number of transcripts in cells either lytically or latently infected with MDV. Our results indicate that the Meq transcriptional unit extends to the BamHI-L fragment and that the transcripts mapping to the right-hand end of the BamHI-I2 and adjacent BamHI-Q2 and BamHI-L fragments are not preferentially expressed during latency.

Amino Acid Sequence↗
PubMed1995

Impaired glucose uptake and intact gluconeogenesis in perfused rat liver after carbon tetrachloride injury.

The dynamics of glucose movement across perfused livers were assessed in carbon tetrachloride (CCl4)-injured rats. Rats were given CCl4 for 8 weeks and became glucose intolerant and hyperinsulinemic. The fasted rat liver was cyclically perfused with 4 mM lactate and various concentrations (0-20 mM) of glucose for 20 min. In the CCl4-injured liver, net glucose output was less suppressed at high glucose levels than in the normal liver (147 +/- 70 vs 18 +/- 10 mumol at 20 mM glucose, P < 0.05). Deposition of the carbon from [14C] glucose into glycogen was stimulated at high glucose levels and was markedly reduced in the CCl4-injured liver compared to the normal liver (0.58 +/- 0.33 mumol vs 1.44 +/- 0.20 mumol at 20 mM, P < 0.01). Conversion of [14C] lactate to [14C] glucose was not different between the CCl4-injured and the normal liver at each glucose level. Deposition of the carbon from [14C] acetate into glycogen in the CCl4-injured liver was larger than that in the normal liver at 0 mM glucose (0.81 +/- 0.15 mumol vs 0.32 +/- 0.06 mumol, P < 0.01), but was similar to the normal at 20 mM glucose. In the CCl4-injured liver, utilization of exogenous glucose was impaired at high glucose levels, and gluconeogenetic activity was not impaired at low glucose levels. These changes in the hepatic glucose metabolism seem to account for postprandial hyperglycemia without fasting hypoglycemia associated with liver diseases.

Animals↗
PubMed1995

The transcripts from the sequences flanking the short component of Marek's disease virus during latent infection form a unique family of 3'-coterminal RNAs.

We have constructed a cDNA library using poly(A)+ RNA from the stably transformed Marek's disease virus cell line MKT-1 and isolated cDNAs specific to the short internal repeat region of the BamHI-A fragment of the viral genome. Four distinct classes of cDNA were identified through sequence analysis of the 5' and 3' termini of each clone isolated, and a representative of each class was chosen for complete sequencing. These cDNAs were mapped on the basis of the genomic nucleotide sequence of this region, and a family of 3'-coterminal overlapping transcripts consisting of several highly spliced species, was identified. PCR was used to amplify specific regions of each cDNA, which were subcloned and used to generate riboprobes. These riboprobes hybridized to a variety of transcripts in poly(A)+ RNA fractions isolated from cells either lytically or latently infected with Marek's disease virus.

Base Sequence↗
PubMed1992

Epinephrine augments cortisol secretion from isolated perfused adrenal glands of guinea pigs.

To determine direct effects of epinephrine on adrenal cortisol secretion, bilateral adrenal glands were isolated from guinea pigs, together with bilateral kidneys, aorta, and inferior caval vein for influent and effluent routes. The preparation was perfused with oxygenated Krebs-Ringer bicarbonate solution (pH 7.4) containing 10 mM glucose, 0.2% bovine serum albumin, and 4.6% dextran. The perfusate cortisol level was elevated by the addition of epinephrine in a dose-dependent manner at concentrations greater than 100 pg/ml and increased eightfold as high as the basal level at 1 micrograms/ml epinephrine. The stimulatory effect of epinephrine on cortisol secretion was completely abolished by phentolamine, an alpha-adrenergic antagonist but was not affected by propranolol, a beta-adrenergic antagonist. These results demonstrate that epinephrine has a direct stimulatory effect on adrenal cortisol secretion via an alpha-adrenergic mechanism and also suggest that not only adrenocorticotropin but also epinephrine is a most important factor for the regulation of cortisol secretion.

Adrenal Glands↗
PubMed1990

Diurnal variation of blood ketone bodies in insulin-dependent diabetes mellitus and noninsulin-dependent diabetes mellitus patients: the relationship to serum C-peptide immunoreactivity and free insulin.

We examined whether the rise in ketone body concentration around midnight and in the early morning was due to the lack of free insulin (IRI) or excess of insulin counterregulatory hormones such as human growth hormone (hGH), cortisol and glucagon in noninsulin-dependent diabetes mellitus (NIDDM) and insulin-dependent diabetes mellitus (IDDM) patients and whether the monitoring of blood ketone body concentration was clinically useful as an index of metabolic control for deciding to increase or decrease the insulin dose in the treatment of diabetes mellitus. Serum levels of 3-hydroxybutyrate (3-OHBA), acetoacetate (AcAc) and 3-OHBA/AcAc ratio before breakfast were significantly increased in insulin-treated NIDDM patients with well-controlled fasting plasma glucose levels and IDDM patients compared to those in normal subjects. Mirror image diurnal changes were found between serum concentrations of 3-OHBA and serum C-peptide or free IRI in normal subjects and NIDDM patients treated with diet alone or sulfonylurea during the 24-hour daily profiles. However, there were no correlations between 3-OHBA and free IRI in the NIDDM patients treated with insulin and IDDM patients who had a much larger increase in the mean concentration of serum 3-OHBA at 6 a.m. caused by a low concentration of free IRI. Counterregulatory hormones were not increased in IDDM patients compared to normal subjects in the early morning. Cortisol/free IRI and hGH/free IRI molar ratios were significantly increased in NIDDM and IDDM patients compared to normal subjects in the early morning, but glucagon/free IRI molar ratio was not changed between IDDM and normal subjects. In conclusion, the early morning rising of ketone body concentration in insulin-treated diabetic patients, particularly IDDM patients, is due to the absolute lack of free IRI and/or the relative lack of free IRI to the levels of hGH or cortisol, and the monitoring of 3-OHBA is clinically useful as a more sensitive index of metabolic control.

3-Hydroxybutyric Acid↗
PubMed1988

Role of endogenous arginine vasopressin in potentiating corticotropin-releasing hormone-stimulated corticotropin secretion in man.

Exogenously administered vasopressin (VP) augments ACTH secretion stimulated by CRH. This study was performed to elucidate the role of endogenous VP in potentiating CRH-induced ACTH secretion in man. Synthetic human CRH (100 micrograms) was injected iv into seven normal men after they had been water loaded (20 mL/kg; 60 and 30 min before CRH injection; WL-CRH test) and water deprived (water restriction for 18 h before CRH injection; WD-CRH test). Blood samples were obtained before and 5, 15, 30, 60, 90, and 120 min after CRH injection at 0900 h for determination of plasma ACTH, cortisol, arginine vasopressin (AVP), CRH, and catecholamine levels and osmolality. Urine was obtained immediately before and 120 min after CRH injection for determination of osmolality. The mean plasma AVP levels were significantly higher during the WD-CRH test [1.8 +/- 0.4 (+/- SE) to 1.9 +/- 0.4 pmol/L] than during the WL-CRH test (0.6 +/- 0.1 to 0.9 +/- 0.1 pmol/L). The mean plasma ACTH and cortisol levels rose significantly from basal (4.5 +/- 0.6 pmol/L and 320 +/- 20 nmol/L, respectively) to peak values of 14.0 +/- 2.1 pmol/L at 30 min and 700 +/- 50 nmol/L at 60 min, respectively, during the WD-CRH test. During the WL-CRH test, mean basal plasma ACTH and cortisol levels were 3.5 +/- 0.7 pmol/L and 420 +/- 50 nmol/L, respectively, and reached peak values of 7.7 +/- 1.1 pmol/L at 60 min and 550 +/- 40 nmol/L at 30 min, respectively. Both the mean peak levels and integrated ACTH and cortisol responses were significantly higher during the WD-CRH than during the WL-CRH test. There was no significant difference between the plasma CRH and catecholamine concentrations in both tests. These results suggest that endogenous AVP potentiates CRH-stimulated ACTH secretion and, thus, plays a physiologically significant role in regulating CRH-stimulated ACTH and cortisol secretion in man.

Adrenocorticotropic Hormone↗
PubMed1987

[Trials for simplified hypertonic saline test].

Hypertonic saline test is indispensable for the evaluation of posterior pituitary function. However the test is not simple, including water loading, urine sampling and at least 45 min of hypertonic saline infusion, mostly because the test relies on urinary osmolality as an index of ADH secretion. The object of this study is try to simplify the test by directly measuring plasma ADH concentration before and after 10 min of hypertonic saline infusion. Intravenous infusion of hypertonic saline (5% NaCl, 0.24 ml/kg/min, for 10 min) was performed on normal subjects, patients with diabetes insipidus and patients with renal failure under chronic hemodialysis. Venous blood samples were obtained seriously including just before and after 10 min of the infusion. ADH was extracted from plasma using Sep-Pak C18 column and assayed by specific RIA. Minimum sensitivity of the assay was 0.25 pg/ml. The hypertonic saline infusion resulted in an increase of plasma osmolality by about 8 mOsm/kg H2O and plasma sodium concentration by 4 mEq/l. Plasma ADH increased from 0.77 +/- 0.09 to 3.42 +/- 0.73 pg/ml (m +/- SE, n = 8, p less than 0.01) in normal subjects of ad lib. water drinking and from 0.55 +/- 0.33 to 2.34 +/- 0.33 (m +/- SE, n = 4, p less than 0.05) in water loaded normal subjects (20 ml/kg of water, 60 min before hypertonic saline infusion).(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnosis, Differential↗
PubMedDate not supplied

A case of a gallbladder cancer with marked hypercalcemia and leukocytosis.

Hypercalcemia and leukocytosis of malignancy have been highlighted over a decade. We report a case of a gallbladder cancer with marked hypercalcemia and leukocytosis. A 54-year-old woman was admitted to the hospital because of remittent fever and left hypochondric pain. The computed tomographic scan of the abdomen revealed the cancer of the gallbladder with liver metastases. The patient's medical condition deteriorated as the tumor was rapidly growing up. Her medical course was marked by hypercalcemia and an increase in mature neutrophils. Medical therapy with normal saline, furosemide, indomethacin, prednisolone, and calcitonin failed to ameliorate hypercalcemia. On the twenty-ninth hospital day the serum calcium was elevated to 17.6 mg/dl which responded to 1000 micrograms of mithramycin while leucocytosis continued. Despite the chemotherapy with doxorubicin and tegafur, the tumor continued to grow. Leukocytosis was attributed to the elevated colony-stimulating factor activity which was two-fold of control. The parathyroid hormone and nephrogeneous cyclic AMP levels were normal with low vitamin D levels. Hypercalcemia was attributed to a parathyroid hormone-like substance because of a decrease in %TRP in the presence of normal renal function and the normal parathyroid hormone level. Autopsy revealed an undifferentiated adenocarcinoma of the gallbladder with multiple liver metastases, and bone resorption in the vertebral column and sternum without evident bone metastasis.

Adenocarcinoma↗