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Volume 88, Issue 10
Displaying 1-9 of 9 articles from this issue
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Eiji Takeda, Hisami Okumura, Yutaka Taketani, Hironori YamamotoArticle type: Article
2014 Volume 88 Issue 10 Pages 499-506
Published: October 25, 2014
Released on J-STAGE: August 10, 2017
JOURNAL FREE ACCESSNutritional science of vitamin D in pediatric and adult diseases was summarized. Vitamin D-dependency type II is a rare disease caused by a disorder of the human vitamin D receptor (VDR). Except for the alopecia, severe rickets and other biochemical abnormalities of 6 patients were reversed by treatment with 3 μg/kg/d of 1α-hydroxyvitamin D_3. A polymorphism at the translation initiation codon of the human VDR gene also affects the bone mineral density (BMD) in Japanese. Attention to phosphorus intake is important because both phosphorus deficiency and overloading impair bone health and quality of life (QOL). Elevation of extracellular phosphorus level causes endothelial dysfunction and medial calcification, which are closely associated with the development of cardiovascular disease (CVD). A dietary approach to limit phosphorus intake is particularly important to prevent bone impairment and CVD in patients with chronic kidney disease (CKD). Increased serum fibroblast growth factor 23 (FGF23)level is an early finding of abnormal mineral metabolism in CKD which causes secondary hyperparathyroidism and resistance of the parathyroid gland to the action of FGF23. In order to improve bone health and QOL in the general population, it should be important that attention to phosphorous intake from processed foods containing phosphorus additive is paied.View full abstractDownload PDF (1076K) -
[in Japanese]Article type: Article
2014 Volume 88 Issue 10 Pages 507-
Published: October 25, 2014
Released on J-STAGE: August 10, 2017
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Toru NishikawaArticle type: Article
2014 Volume 88 Issue 10 Pages 508-514
Published: October 25, 2014
Released on J-STAGE: August 10, 2017
JOURNAL FREE ACCESSA body of evidence indicates that D-serine is an intrinsic co-agonist for the N-methyl-D-aspartate (NMDA) type glutamate receptor. Thus, the author and collaborators have demonstrated that D-serine is present at high concentrations in mammals throughout the life with brain-preferring and NMDA receptor GRIN2B subunit-like distribution, although D-amino acids had long been believed to be uncommon in mammalian tissues. D-serine alone fails to activate the NMDA receptor but is required for activation of the receptor in vitro, suggesting that the D-amino acid could be a co-agonist for the receptor. The author's research group has also reported the biochemical processes of the synthesis, extracellular release, uptake and degradation of D-serine in mammalian brain tissues. Among these processes, D-serine biosynthesis is catalyzed by, at least, a vitamin B_6-dependent enzyme, serine racemase, and its degradation is mediated by a vitamin B_2-dependent enzyme, D-amino acid oxidase. The NMDA receptor plays pivotal roles in expression and regulation of a wide variety of higher order brain functions. Therefore, disturbed D-serine metabolism has been considered to be involved in the pathophysiology of neuropsychiatric disorders including schizophrenia. It is also hypothesized that, in the brain of patients with schizophrenia, hypofunction of the NMDA receptor occurs due to deficit in the extracellular D-serine signaling or other mechanisms based on the facts that NMDA receptor antagonists and anti-NMDA receptor antibodies cause schizophrenia-like positive, negative and cognitive symptomatologies.View full abstractDownload PDF (923K) -
Yurika Miyoshi, Ryuichi Konno, Masashi Mita, Kenji HamaseArticle type: Article
2014 Volume 88 Issue 10 Pages 515-523
Published: October 25, 2014
Released on J-STAGE: August 10, 2017
JOURNAL FREE ACCESSD-Amino-acid oxidase (DAO), which metabolizes neutral and basic D-amino acids including D-serine and D-alanine, and serine racemase (SRR), which catalyzes racemization of L-serine to D-serine, are regulatory factors of the intrinsic amounts of D-amino acids in mammals. Both enzymes have been demonstrated to have relation to neuronal diseases such as schizophrenia and amyotrophic lateral sclerosis via the regulation of the intrinsic amounts of neuromodulators of N-methyl-D-aspartate receptors, D-serine and D-alanine. Therefore, the regulators of DAO and SRR are proposed to become novel targets of drugs for changing the intrinsic amounts of D-serine and D-alanine, and the alterations of D-serine and D-alanine amounts following the changes of DAO and SRR activities are expected to be clarified. In this review, we have summarized recent works on the changes of D-serine and D-alanine amounts in mammalian brain tissues and physiological fluids with the decrease of activities of DAO and SRR. The highly sensitive and selective two-dimensional high-performance liquid chromatographic system for the determination of small amounts of D-amino acids in mammals has also been introduced.View full abstractDownload PDF (893K) -
Kiyoshi FukuiArticle type: Article
2014 Volume 88 Issue 10 Pages 524-529
Published: October 25, 2014
Released on J-STAGE: August 10, 2017
JOURNAL FREE ACCESSD-Amino acid oxidase (DAO) is a flavoenzyme that catalyses the oxidative deamination of D-amino acids. D-Serine, one of the physiological substrates for DAO, is an endogenous co-agonist for N-methyl D-aspartate (NMDA) receptor and plays important roles in glutamate receptor-mediated neurotransmission. Based on the enzymatic activity of DAO in D-serine catabolism, the enzyme has been proposed to be involved in the decreased glutamatergic neurotransmission in schizophrenia. Therefore, the modulation of DAO activity is expected to be useful for the therapy of schizophrenia. We examined the inhibitory effect of antipsychotic drugs, chlorpromazine and risperidone, on human DAO activity and demonstrated that chlorpromazine and risperidone inhibited the enzyme activity. Moreover, we examined the distribution of DAO in brain to clarify its pathophysiological role in the regulation of neurotransmission. Immunohistochemcal analyses revealed that DAO was present in glial cells and choroid plexus (CP) in human brain. The level of DAO expression in CP epithelial cells in schizophrenic patients was also found to be significantly higher than the normal control. These results indicate the possibility that a decrease in D-serine concentration due to an increase in DAO expressed in CP epithelial cells in brain is involved in the pathophysiology of schizophrenia which is caused by dysfunction of NMDA receptor. From these findings, it can be thought that DAO expressed in CP is regarded as a potential therapeutic target for schizophrenia and also it can be expected that a new therapeutic agent for schizophrenia will be developed.View full abstractDownload PDF (3420K) -
Hiroko Horiuchi, Naoki Harada, Ryoichi YamajiArticle type: Article
2014 Volume 88 Issue 10 Pages 530-534
Published: October 25, 2014
Released on J-STAGE: August 10, 2017
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Kazuya Yoshimura, Takahiro IshikawaArticle type: Article
2014 Volume 88 Issue 10 Pages 535-537
Published: October 25, 2014
Released on J-STAGE: August 10, 2017
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Shoji Yamada, Keiko YamadaArticle type: Article
2014 Volume 88 Issue 10 Pages 538-542
Published: October 25, 2014
Released on J-STAGE: August 10, 2017
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Article type: Bibliography
2014 Volume 88 Issue 10 Pages 543-547
Published: October 25, 2014
Released on J-STAGE: August 10, 2017
JOURNAL FREE ACCESSDownload PDF (544K)
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