Endocrine Journal (ENDOCR J )

Publisher: Nihon Naibunpi Gakkai


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    Endocrine journal (Online)
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Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: To facilitate personalized health care for multifactorial diseases, risks of genetic and clinical/environmental factors should be assessed together for each individual in an integrated fashion. This approach is possible with the likelihood ratio (LR)-based risk assessment system, as this system can incorporate manifold tests. We examined the usefulness of this system for assessing type 2 diabetes (T2D). Our system employed 29 genetic susceptibility variants, body mass index (BMI), and hypertension as risk factors whose LRs can be estimated from openly available T2D association data for the Japanese population. The pretest probability was set at a sex- and age-appropriate population average of diabetes prevalence. The classification performance of our LR-based risk assessment was compared to that of a non-invasive screening test for diabetes called TOPICS (with score based on age, sex, family history, smoking, BMI, and hypertension) using receiver operating characteristic analysis with a community cohort (n = 1263). The area under the receiver operating characteristic curve (AUC) for the LR-based assessment and TOPICS was 0.707 (95% CI 0.665-0.750) and 0.719 (0.675-0.762), respectively. These AUCs were much higher than that of a genetic risk score constructed using the same genetic susceptibility variants, 0.624 (0.574-0.674). The use of ethnically matched LRs is necessary for proper personal risk assessment. In conclusion, although LR-based integrated risk assessment for T2D still requires additional tests that evaluate other factors, such as risks involved in missing heritability, our results indicate the potential usability of LR-based assessment system and stress the importance of stratified epidemiological investigations in personalized medicine.
    Endocrine Journal 07/2014; 61.
  • Endocrine Journal 10/2011;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Established as a novel subtype of type 1 diabetes in Japan in the year 2000, fulminant type 1 diabetes is characterized by a rapid onset and an absence of diabetes-related antibodies. This disease has been mainly reported in East Asia, especially in Japan. The prevalence of fulminant type 1 diabetes among ketosis-onset type 1 diabetes was 19.4% in a Japanese nationwide survey. Both genetic and environmental factors are involved in the etiology of fulminant type 1 diabetes. The former includes, for example, HLA-DR/DQ or CTLA-4 polymorphisms, and the latter includes viral infection. Fulminant type 1 diabetes is the most severe form of diabetes because of the complete loss of pancreatic beta cells at disease onset, and it is also a high-risk subgroup for diabetic microangiopathy. Key WordsIdiopathic-Epidemiology-HLA-CTLA-4-Virus-Complication
    12/2010: pages 331-342;
  • Endocrine Journal 01/2010; 57(S2):S619.
  • Endocrine Journal 01/2010;
  • Endocrine Journal 01/2010;
  • Endocrine Journal 01/2010; 57:590-591.
  • [Show abstract] [Hide abstract]
    ABSTRACT: We investigated the regulation of each intracellular signal transduction system including cyclic AMP (cAMP)-dependent and calcium (Ca2+) messenger systems in bovine adrenal fasciculo-reticularis cells to clarify the exact mode of action of ACTH. Pretreatment with primaquine and quinacrine, which are phospholipase A2 inhibitors, significantly inhibited cortisol production activated by both low and high concentrations of ACTH. Therefore, it seems that metabolites induced by phospholipase A2 are quite essential for cortisol synthesis induced by ACTH, either at low or high concentrations. At low concentrations of ACTH (10(-13)-10(-12) M), significant increases of cytosolic calcium ([Ca2+]i), but not of cAMP, were observed. Calphostin C, a specific protein kinase C inhibitor, apparently suppressed cortisol production activated by low concentrations of ACTH, while H-89, a specific inhibitor of cAMP-dependent protein kinase, did not. These findings suggest that, at physiologically low concentrations, ACTH activates [Ca2+]i and phospholipase A2 without affecting cAMP formation, resulting in an increased biosynthesis of cortisol, partly via protein kinase C-dependent processes. At high concentrations, ACTH (10(-9)-10(-7) M) induced an increase of cAMP and [Ca2+]i. The cortisol production induced by high concentrations of ACTH was significantly inhibited by pretreatment with calphostin C, H-89 and H-7, suggesting the participation of cAMP-dependent protein kinase and protein kinase C systems in the regulation of cortisol production in the presence of high concentrations of ACTH. In conclusion, cytosolic calcium is biphasically enhanced by ACTH, although cAMP accumulation is increased only by high concentrations of ACTH. A phospholipase A2-dependent process may partly play a crucial role in the regulation of cortisol biosynthesis, when stimulated by low and high concentrations of ACTH.
    Endocrine Journal 09/2007; 54(4):585-92.
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    ABSTRACT: Both increased and decreased fibrinolytic activity have been reported in patients with hyperthyroidism. Elevated levels of plasma plasminogen activator inhibitor-1 (PAI-1) antigen have been found in hyperthyroid patients. Thrombin activatable fibrinolysis inhibitor (TAFI) is a novel plasma protein, which inhibits fibrinolysis through removal of C-terminal lysines from partially degraded fibrin. Previously, we showed that plasma TAFI antigen levels were increased in patients with overt and subclinical hypothyroidism. The aim of this study is to investigate plasma levels of TAFI and PAI-1 antigens in hyperthyroid patients. PAI-1 and TAFI antigen levels were measured in the plasma of 29 patients with hyperthyroidism (14 overt hyperthyroid and 15 subclinical hyperthyroid), and 26 healthy individuals. Although there were increased levels of PAI-1 antigen in hyperthyroid patients, plasma TAFI antigen levels were significantly lower compared to controls (80.79 ng/ml vs. 32.42 ng/ml, p = 0.000 for PAI-1; 10.42 microg/ml vs. 12.24 microg/ml, p = 0.009 for TAFI). Elevated PAI-1 antigen levels were positively correlated with free thyroid hormones, although TAFI antigen levels were in negative correlation with free thyroxine. Furthermore, an inverse correlation between PAI-1 and TAFI antigen levels was found. Our study demonstrated that TAFI antigen levels were decreased in patients with hyperthyroidism. Inverse correlation with PAI-1 suggests that the decrease in TAFI antigen levels may be due to activation of TAFI pathway. Further studies evaluating the underlying mechanisms of low TAFI antigen levels in hyperthyroidism should be undertaken.
    Endocrine Journal 09/2007; 54(4):593-9.
  • Endocrine Journal 09/2007; 54(4):647.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Monocyte adhesion to arterial endothelial cells is the initial step in atherosclerosis. Whereas angiotensin II is known to elicit leukocyte adhesion, it is not clear whether blockade of the angiotensin II receptor signaling reduces monocyte adhesion to endothelial cells beyond its antihypertensive action. This study compared the effect of two different antihypertensive drugs on monocyte adhesion to thoracic aorta endothelium in spontaneously hypertensive rats (SHR): the angiotensin II receptor blocker, valsartan (20 mg . kg(-1) . day(-1)) and the vasodilator, hydralazine (0.75 mg . kg(-1) . day(-1)). The effects were quantitated in vivo using an enface method that optimizes the observation of endothelial surfaces after immunohistochemical staining for CD68. Both agents significantly and comparably reduced blood pressure over 4-week treatment course. Both valsartan and hydralazine profoundly reduced monocyte adhesion compared with nontreated controls, with valsartan having a modestly more reductive effect. Both agents also reduced the intima and medial thickening with valsartan reducing the mean thickness modestly more than hydralazine. Our data confirms that the reduction of blood pressure is effective method to reduce monocyte adhesion. Also, our date demonstrates that valsartan has a modest beneficial effect on monocyte adhesion to endothelial cells and arterial intima-medial vessel thickening beyond its action as an antihypertensive agent.
    Endocrine Journal 09/2007; 54(4):605-12.
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    ABSTRACT: Endothelial dysfunction is an early marker of atherosclerosis. Pioglitazone is commonly used in the treatment of type 2 diabetes and has vascular protective effects beyond its hypoglycemic ones. We investigated the vascular effects of short-term, low-dosage pioglitazone in patients with type 2 diabetes. The study included 15 subjects with type 2 diabetes with normoalbuminuria (age, 60.7 +/- 11.9 years; body mass index [BMI], 23.9 +/- 3.3 kg/m2). The patients received pioglitazone at 15 mg daily for 4 weeks. BMI, systolic and diastolic blood pressure, laboratory parameters (fasting plasma glucose, insulin, lipid profile, high-sensitive C-reactive protein [hsCRP], and adiponectin) were assessed at baseline and after treatment. The forearm blood flow (FBF) was measured during reactive hyperemia by strain-gauge plethysmography. Short-term, low-dosage pioglitazone did not improve glycemic control or insulin sensitivity. However, the peak FBF and flow debt repayment (FDR) were markedly improved. There was no correlation of the improvement of peak FBF and FDR with the observed changes of metabolic parameters. However, the increment of adiponectin and decrement of hsCRP were well correlated with the improvement of peak FBF. These results indicate that short-term low-dosage pioglitazone may improve vascular function via increasing adiponectin expression and decreasing low-grade inflammation in type 2 diabetic patients.
    Endocrine Journal 09/2007; 54(4):613-8.
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    ABSTRACT: A right adrenal tumor was incidentally discovered on abdominal computed tomography performed on a 53-year-old Japanese man, who had been hospitalized with diabetic ketoacidosis. Normal values were obtained for adrenal hormones in the morning after an overnight fast and urinary cortisol excretion after treatment of diabetic ketoacidosis with insulin. However, overnight dexamethasone administration with 1 mg or 8 mg did not completely suppress serum cortisol levels. There were no remarkable physical findings related to Cushing's syndrome. The patient was diagnosed as having preclinical Cushing's syndrome (PCS). Histological examination of the adrenalectomy specimen demonstrated adrenal black adenoma. Blood glucose levels subsequently improved after adrenalectomy, and the patient never developed adrenal insufficiency after hydrocortisone withdrawal. The patient was treated with diet therapy alone, and maintained good glycemic control. However, the patient still showed a diabetic pattern in an oral glucose tolerance test. It seems that the existence of PCS in addition to the underlying type 2 diabetes mellitus contributed to aggravation of blood glucose levels. Although there are many aspects of the natural course of PCS that have not been thoroughly elucidated, it is necessary to remain aware that a PCS patient with abnormal glucose metabolism may develop diabetic ketoacidosis by environmental agents.
    Endocrine Journal 09/2007; 54(4):543-51.
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    ABSTRACT: LIM homeodomain transcription factors regulate many aspects of development in multicellular organisms. LHX4/Lhx4 is a protein that is essential for pituitary development and motor neuron specification in mammals. In human, a heterozygous splicing mutation of the LHX4 gene was reported in a family with combined pituitary hormone deficiencies (CPHD). In addition to CPHD, these patients were characterized by small sella turcica and chiari malformation. Here we report a Japanese patient with CPHD (GH, PRL, TSH, LH, FSH, and ACTH deficiency) due to a novel missense mutation (P366T) of the LHX 4 gene. She showed severe respiratory disease and hypoglycemia soon after birth. Brain MRI demonstrated hypoplastic anterior pituitary, ectopic posterior lobe, a poorly developed sella turcica, and chiari malformation. Sequence analysis of the LHX 4 gene identified a heterozygous missense mutation (P366T) in exon 6, which was present in LIM4 specific domain. Neither of the patient's parents harbored this mutation, indicating de novo mutation.
    Endocrine Journal 09/2007; 54(4):637-41.
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    ABSTRACT: Fructose 2,6-bisphosphate (F2,6BP) is a powerful allosteric activator of 6-phosphofructo-1-kinase, which is the rate-limiting enzyme for glycolysis. Mitogenic stimulation of lymphocytes is related to an enhanced rate of glucose utilization and F2,6BP mediated activation of glycolysis. To determine the effect of hyperglycemia on intracellular glycolysis of lymphocytes, we measured intracellular F2,6BP content in peripheral blood mononuclear cells obtained from patients with diabetes and normal subjects. A total of 62 subjects participated in the present study. Venous blood samples were collected and peripheral blood mononuclear cells were separated by Ficoll gradients. Intracellular F2,6BP levels in peripheral blood mononuclear cells from normal control subjects were significantly lower than age-matched diabetic subjects. We observed a significant positive correlation between intracellular F2,6BP levels and long term glycemic control, as assessed by HbA1c. These data suggest that hyperglycemia increases intracellular F2,6BP in immune cells. These findings may help to clarify the impaired function in immune cells in patients with diabetes.
    Endocrine Journal 09/2007; 54(4):517-20.
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    ABSTRACT: Since the majority of multiple endocrine neoplasia type 2A (MEN 2A) patients have missense mutations at codon 634 and those with the Cys630 RET genotype mutations are extremely rare, limited clinical information is available about this rare type. We report here three members of one Japanese MEN 2A family with the Cys630Tyr genotype. A 67-year-old woman presented a firm thyroid nodule, and preoperative examination revealed medullary thyroid carcinoma with primary hyperparthyoidism and no pheochromocytoma. At surgery, bilateral medullary thyroid carcinomas and parathyroid adenoma were found. No lymph node metastasis was identified. Computed tomography scans and laboratory examination of blood have shown no evidence of tumor recurrence and no abnormality of parathyroid function during the 4 years after surgery. A 40-year-old man, the proband's son, was shown to have the same RET mutation, underwent total thyroidectomy prophylactically, and only microscopic foci of medullary thyroid carcinoma were found. A 10-year-old boy, the proband's grandson also having the same RET mutation, showed normal basal serum calcitonin level and has been followed up conservatively. To our knowledge, 18 patients of 6 families with the Cys630 mutations have been reported so far. This is only the second reported case with primary hyperparathyroidism. RET 630 mutations might be associated with lower penetrance of primary hyperparthyoidism and pheochromocytoma.
    Endocrine Journal 09/2007; 54(4):531-5.
  • [Show abstract] [Hide abstract]
    ABSTRACT: We describe here a case of reversible ampulla (takotsubo) cardiomyopathy caused by secondary adrenal insufficiency in ACTH isolated deficiency. A 53-year-old woman was referred to our department for evaluation and treatment of unconsciousness. On admission, her plasma glucose level was 34 mg/dL, suggesting loss of consciousness due to hypoglycemia. Basal levels of ACTH, cortisol, and dehydroepiandrosterone sulfate in blood, and urinary free cortisol levels were all decreased. ACTH and cortisol levels were not adequately increased in response to CRH administration and the insulin tolerance test. Electrocardiography showed ST segment elevation and T wave inversion in leads V 1-6. The coronary arteries were free of organic stenosis, and a left ventriculogram revealed severe hypokinesis, particularly in the anterior and posterior walls. Based on a diagnosis of adrenocortical insufficiency caused by ACTH isolated deficiency, hydrocortisone was administered. Two weeks after treatment, ultrasound studies of the heart showed recovery of left ventricular wall motion. Activation of the sympathetic nervous system, adrenocortical failure, and hypoglycemic attack were considered to be triggering factors for the takotsubo cardiomyopathy. Careful monitoring of cardiac function and appropriate treatments for both cardiomyopathy and adrenocortical failure are required to recover cardiac dysfunction.
    Endocrine Journal 09/2007; 54(4):631-6.

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