[Factitious and exogenous thyrotoxicosis].
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Anti-Obesity Agents↗
Biomedical subjects
Yoshifumi Hirooka
Publications and source records attributed to Yoshifumi Hirooka.
Multiple endocrine neoplasia type I and Cushing's syndrome due to an aggressive ACTH producing thymic carcinoid.
Thymic carcinoid in multiple endocrine neoplasia type 1 (MEN 1) is previously reported as a non-ACTH producing tumor. The present case is a 39-year-old man with mortal outcome from thymic carcinoid and Cushing's syndrome with high plasma ACTH. The symptom was first observed at age 29 and was relieved after extended thymectomy, with reduction of ACTH level. The tumor was positive for ACTH, Grimelius silver staining and Chromogranin A. The finding of primary hyperparathyroidism, pituitary adenoma, and a novel germline nonsense mutation (W423X) established the diagnosis of MEN 1. Cushing's syndrome due to ACTH producing thymic carcinoid should be also considered as one phenotype of the MEN 1 spectrum.
ACTH Syndrome, Ectopic↗
Hypothalamic monoamine metabolism is different between the diabetic GK (Goto-Kakizaki) rats and streptozotocin-induced diabetic rats.
Hypothalamic neuronal activities of noradrenaline, dopamine and serotonin were investigated in the GK (Goto-Kakizaki) rats, a model for type 2 diabetes, and the streptozotocin (STZ)-induced diabetic rats, a model for type 1 diabetes. Each neuronal activity was assessed from a ratio of the concentrations of the major metabolite to those of its precursor monoamine itself or the metabolite concentrations itself. In the GK rats, hypothalamic noradrenaline and dopamine activities were significantly increased, and serotonin activity was unchanged. In the STZ-induced diabetic rats, hypothalamic dopamine and serotonin activities were significantly decreased, and noradrenaline activity was unchanged. In these two diabetic rats, hypothalamic noradrenaline and dopamine activities correlated significantly with serum insulin concentrations, whereas hypothalamic serotonin activity correlated significantly with serum glucose concentrations. These findings suggest that hypothalamic monoamine metabolism of the GK rats is quite different from that of the STZ-induced diabetic rats, and that not only hyperglycemia but also serum insulin concentrations have an influence on the hypothalamic monoamine metabolism in these diabetic rats.
Animals↗
[Adult-onset hypophosphatemic osteomalacia].
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Humans↗
Serum uric acid concentrations in type 2 diabetes: its significant relationship to serum 1,5-anhydroglucitol concentrations.
OBJECTIVE: Serum uric acid concentrations in diabetics are well known to be significantly lower than those in non-diabetic subjects, due to increased its urinary clearance. Serum 1,5-anhydroglucitol concentrations are also specifically decreased in diabetics through the increased urinary excretion. To gain an insight into the idea that a common mechanism might be possible to work in reducing these serum substances, this study was conducted. METHODS: A total of 121 type 2 diabetic patients, 76 males and 45 females, were studied. Multiple regression analysis was performed to determine the independent association between potential predictor variables (mean blood pressure, body mass index, fasting plasma glucose, glycosylated hemoglobin A1c, serum fructosamine, serum 1,5-anhydroglucitol, serum creatinine, serum total cholesterol, and serum triglycerides) and serum uric acid concentrations as the dependent variable. RESULTS: In the male subjects, serum 1,5-anhydroglucitol, serum creatinine and body mass index were the variables independently related to serum uric acid concentrations. In the female subjects, serum 1,5-anhydroglucitol and serum creatinine were the variables independently related to serum uric acid concentrations. CONCLUSION: Considering the glucosuria-related urinary excretion of 1,5-anhydroglucitol, a close positive association between serum uric acid and 1,5-anhydroglucitol concentrations strongly supports the idea that the reduction in serum uric acid concentrations is mediated by urinary glucose excretion in diabetics.
Adult↗
Distribution of thyrostimulin in the rat: an immunohistochemical study.
OBJECTIVE: To identify the distribution of thyrostimulin, a heterodimer of glycoprotein hormone subunits (A2 and B5) by immunohistochemistry in the rat tissues using specific antipeptide anti-serum which we recently produced. METHOD: Anti-thyrostimulin antibody was raised in New Zealand white rabbits immunized with a conjugate of synthetic A2 or B5 with bovine serum albumin. Immunohistochemical analysis was performed by avidin-biotin complex method. RESULTS: Thyrostimulin immunoreactivity was visualized in the anterior pituitary, central nervous system, adrenal gland, stomach, duodenum, pancreas and testis. When using antiserum pre-incubated with synthetic peptides or rat pituitary homogenate which contains thyrostimulin peptide, no significant stain of the pituitary was detected. CONCLUSION: These findings suggest that thyrostimulin is widely distributed and that the method used is valuable in studying the distribution of thyrostimulin in rats.
Animals↗
Radioimmunoassay for aquaporin-9.
OBJECTIVE: To develop radioimmunoassay for aquaporin-9 (AQP9) and search for its presence in certain rat tissues. METHODS: Anti-AQP9 antiserum has been raised in New Zealand white rabbits immunized with a conjugate of synthetic AQP9 with bovine serum albumin. Radioiodination of AQP9 was performed by chloramin T method followed by purification of radioiodinated material on Sephadex G-25 column. RESULTS: The obtained antibody did not crossreact with other aquaporins, hypothalamic hormones, pituitary hormones, neuropeptides or gut hormones. The assay was performed with a double antibody system. AQP9 was extracted from the tissues with acid acetone. The dilution curve of acid acetone extracts of rat liver in the radioimmunoassay system was parallel to the standard curve. The recovery of tissue AQP9 was about 90%, and the intra-assay and inter-assay variations were 4.8% and 7.9%, respectively. AQP9 was found in the liver, testis and brain. CONCLUSION: These data suggest that this assay system is suitable for the estimation of AQP9 in the tissues.
Animals↗
Enhanced somatostatin secretion into the gastric juice with recovery of basal acid output after Helicobacter pylori eradication in gastric ulcers.
BACKGROUND AND AIM: Antral somatostatin interacts with gastric acid secretion. We aimed to investigate the effect of eradication on gastric acid, somatostatin secretion and mucosal histology in gastric ulcer patients with Helicobacter pylori (H. pylori) infection. METHODS: Twenty-eight patients (21 male, 7 female) with H. pylori-positive gastric ulcer were treated with dual therapy. Before and 4-8 weeks after the therapy, the histology of biopsy specimens, basal acid output (BAO) and maximal acid output (MAO) after stimulation with tetragastrin were assessed. Somatostatin concentration in the gastric juice was measured by radioimmunoassay, and somatostatin output during either the basal or gastrin-stimulated period was also examined. RESULTS: Eradication was successful in 22 patients. Before treatment, the acid and somatostatin output were inversely related to the severity of neutrophil infiltration in the corpus and antrum, respectively. After successful eradication, improvement of histological inflammation and an increase in BAO, basal and gastrin-stimulated somatostatin output were observed. Eradication had no effect on atrophy and MAO. There was a positive correlation between gastric acid and somatostatin output in the basal or stimulated condition, irrespective of H. pylori infection. CONCLUSIONS: The present results suggest that recovery of gastric BAO may be caused by an improvement in corpus neutrophil infiltration, but not by an increase in parietal cell volume or a change in atrophy. Also, there was an increase in basal and gastrin-stimulated somatostatin-containing cell activity accompanied by improved antral neutrophil infiltration in the early phase after H. pylori eradication in gastric ulcers.
Anti-Ulcer Agents↗
Growth hormone insensitivity syndrome associated with syringomyelia and type I Chiari malformation.
A 49-year-old man with syringomyelia and a Type I Arnold-Chiari malformation (Chiari-I) was diagnosed with growth hormone insensitivity syndrome (GHIS). He was short in stature, had high circulating levels of GH, and low circulating levels of insulin-like growth factor-I (IGF-I) and IGF binding protein-3 (IGFBP-3). His GH responses to the administration of growth hormone-releasing hormone (GHRH) and L-DOPA were normal, but his levels of IGF-I and IGFBP-3 did not increase after the administration of exogenous GH. Direct genomic DNA sequencing revealed neither a mutation nor deletion in this patient's GH receptor (GHR) gene, though one polymorphism was detected, indicating that his GHR gene was normal. This is the first reported case of an association of GHIS with syringomyelia and Chiari-I malformation.
Arnold-Chiari Malformation↗