研究者詳細 - 辰巳佐和子

論文 - 辰巳佐和子

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Effect of Npt2b deletion on intestinal and renal inorganic phosphate (Pi) handling. 国際誌

Ikuta K, Segawa H, Sasaki S, Hanazaki A, Fujii T, Kushi A, Kawabata Y, Kirino R, Sasaki S, Noguchi M, Kaneko I, Tatsumi S, Ueda O, Wada NA, Tateishi H, Kakefuda M, Kawase Y, Ohtomo S, Ichida Y, Maeda A, Jishage KI, Horiba N, Miyamoto KI.

Clin Exp Nephrol. 2017年11月

Control of phosphate balance by the kidney and intestine. 招待国際誌

Kaneko I, Tatsumi S, Segawa H, Miyamoto KI.

Clin Exp Nephrol. 21 ( Supplement 1 ) 21 - 26 2017年3月

Control of phosphate balance by the kidney and intestine 査読

Ichiro Kaneko, Sawako Tatsumi, Hiroko Segawa, Ken-ichi Miyamoto

CLINICAL AND EXPERIMENTAL NEPHROLOGY 21 ( 1 ) 21 - 26 2017年3月

記述言語：英語出版者・発行元：SPRINGER

The prevention and correction of hyperphosphatemia are major goals of the treatment of chronic kidney disease (CKD)-bone mineral disorders, and thus, Pi balance requires special attention. Pi balance is maintained by intestinal absorption, renal excretion, and bone accretion. The kidney is mainly responsible for the plasma Pi concentration. In CKD, reduced glomerular filtration rate leads to various Pi metabolism abnormalities, and Pi absorption in the small intestine also has an important role in Pi metabolism. Disturbances in Pi metabolism are mediated by a series of complex changes in regulatory hormones originating from the skeleton, intestine, parathyroid gland, and kidney. In this review, we describe the regulation of type II sodium-dependent Pi co-transporters by the kidney and intestine, including the regulation of Pi transport, circadian rhythm, and the vicious circle between salivary Pi secretion and intestinal Pi absorption in animals with and without CKD.

DOI： 10.1007/s10157-016-1359-4

Web of Science

PubMed

Transcriptional Regulation of Sodium-Phosphate Cotransporter Gene Expression 査読

Ichiro Kaneko, Hironori Yamamoto, Kayo Ikuta, Sawako Tatsumi, Hiroko Segawa, Ken-Ichi Miyamoto

Molecular, Genetic, and Nutritional Aspects of Major and Trace Minerals 437 - 445 2016年9月

記述言語：英語掲載種別：論文集(書籍)内論文出版者・発行元：Elsevier Inc.

The sodium-dependent phosphate cotransporter (NaPi) family plays a critical role in Pi homeostasis in mammals via several mechanisms, including renal tubular reabsorption, intestinal absorption, and exchange with intracellular or bone storage. The type II NaPi transport family (SLC34) is especially important for renal and intestinal Pi handling. SLC34 protein dysfunction causes several abnormalities, such as hypophosphatemic hereditary rickets/osteomalacia and hyperphosphatemia-induced vascular disease. Expression of SLC34 family members is regulated at several steps, including transcription, translation, protein degradation, and cellular trafficking. Both hormonal (1,25-dihydroxyvitamin D3, fibroblast growth factor 23, estrogen, T3, and epidermal growth factor) and nonhormonal (dietary Pi, Ca, and vitamin A) factors regulate the transcriptional step. Here, we describe the transcriptional regulation of the SLC34 genes in the small intestine and kidney.

DOI： 10.1016/B978-0-12-802168-2.00036-1

Scopus

Regulation of inorganic phosphate ion homeostasis: crosstalk kidney and other organs. 査読

Tatsumi S, Miyamoto K

Nihon yakurigaku zasshi. Folia pharmacologica Japonica 147 ( 2 ) 84 - 88 2016年2月

記述言語：日本語出版者・発行元：公益社団法人日本薬理学会

無機リン酸（Pi）は生体にとって必須のイオンであり，エネルギーの中間代謝，糖，タンパク質，脂質，核酸代謝，酵素活性の調節，細胞内シグナル伝達，骨格形成の基質など多数の生理機能を有している．血中リン濃度は，おもに腸管吸収，骨代謝（骨形成・吸収），腎臓における排泄と再吸収により維持されている．腎臓からの再吸収能は，リン恒常性維持に重要な役割を果たしているため，その調節は生体内リン恒常性維持の中核と考えられている．これまでの研究から，腎臓尿細管におけるリン再吸収・排泄を制御する巧妙な調節系が存在し，複数の臓器と相互作用していることが分かってきた．とくに，慢性腎臓病（CKD）では，骨と腎臓を結ぶリン代謝系に異常が観察され，CKD早期から骨細胞における線維芽細胞様増殖因子23（FGF23）の発現は亢進し，リン過剰を呈していることが報告されている．また古くより，肝臓がん患者や生体肝移植のドナーに肝臓切除手術を施すと，術後急激に，腎臓によるリン排泄亢進に起因して低リン血症を呈することが知られていた．最近，これらの原因が検討され，肝臓と腎臓を結ぶリン代謝系が明らかにされた．肝臓切除後の尿中リン排泄亢進の原因は，何らかの因子によるNamptの活性化を介した腎臓内ニコチンアミド代謝促進である可能性がわかった．本稿では，新しいリン調節経路を加えて，腎臓を中心とした多臓器にわたるリン恒常性維持機構について概説する．

DOI： 10.1254/fpj.147.84

PubMed

CiNii Books

その他リンク： https://jlc.jst.go.jp/DN/JLC/20020492838?from=CiNii

Regulation of renal phosphate handling: inter-organ communication in health and disease 査読

Sawako Tatsumi, Atsumi Miyagawa, Ichiro Kaneko, Yuji Shiozaki, Hiroko Segawa, Ken-ichi Miyamoto

JOURNAL OF BONE AND MINERAL METABOLISM 34 ( 1 ) 1 - 10 2016年1月

記述言語：英語出版者・発行元：SPRINGER JAPAN KK

In this review, we focus on the interconnection of inorganic phosphate (Pi) homeostasis in the network of the bone-kidney, parathyroid-kidney, intestine-kidney, and liver-kidney axes. Such a network of organ communication is important for body Pi homeostasis. Normalization of serum Pi levels is a clinical target in patients with chronic kidney disease (CKD). Particularly, disorders of the fibroblast growth factor 23/klotho system are observed in early CKD. Identification of phosphaturic factors from the intestine and liver may enhance our understanding of body Pi homeostasis and Pi metabolism disturbances in CKD patients.

DOI： 10.1007/s00774-015-0705-z

Web of Science

PubMed

Niacin and Chronic Kidney Disease. 招待国際誌

Taketani Y, Masuda M, Yamanaka-Okumura H, Tatsumi S, Segawa H, Miyamoto K, Takeda E, Yamamoto H.

J Nutr Sci Vitaminol (Tokyo). 61 ( Supplement ) 173 - 175 2015年11月

Relationship between sodium-dependent phosphate transporter (NaPi-IIc) function and cellular vacuole formation in opossum kidney cells 査読

Yuji Shiozaki, Hiroko Segawa, Saori Ohnishi, Akiko Ohi, Mikiko Ito, Ichiro Kaneko, Shinsuke Kido, Sawako Tatsumi, Ken-ichi Miyamoto

Journal of Medical Investigation 62 ( 3 ) 209 - 218 2015年9月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：University of Tokushima

NaPi-IIc/SLC34A3 is a sodium-dependent inorganic phosphate (Pi) transporter in the renal proximal tubules and its mutations cause hereditary hypophosphatemic rickets with hypercalciuria (HHRH). In the present study, we created a specific antibody for opossum SLC34A3, NaPi-IIc (oNaPi-IIc), and analyzed its localization and regulation in opossum kidney cells (a tissue culture model of proximal tubular cells). Immunoreactive oNaPi-IIc protein levels increased during the proliferative phase and decreased during differentiation. Moreover, stimulating cell growth upregulated oNaPi-IIc protein levels, whereas suppressing cell proliferation downregulated oNaPi-IIc protein levels. Immunocytochemistry revealed that endogenous and exogenous oNaPi-IIc proteins localized at the protrusion of the plasma membrane, which is a phosphatidylinositol 4,5-bisphosphate (PIP2) rich-membrane, and at the intracellular vacuolar membrane. Exogenous NaPi-IIc also induced cellular vacuoles and localized in the plasma membrane. The ability to form vacuoles is specific to electroneutral NaPi-IIc, and not electrogenic NaPi-IIa or NaPi-IIb. In addition, mutations of NaPi-IIc (S138F and R468W) in HHRH did not cause cellular PIP2-rich vacuoles. In conclusion, our data anticipate that NaPi-IIc may regulate PIP2 production at the plasma membrane and cellular vesicle formation.

DOI： 10.2152/jmi.62.209

Scopus

PubMed

Regulation of renal phosphate handling: inter-organ communication in health and disease. 招待国際誌

Tatsumi S*, Miyagawa A, Kaneko I, Shiozaki Y, Segawa H, Miyamoto K.

J Bone Miner Metab. 34 ( 1 ) 1 - 10 2015年8月

Relationship between sodium-dependent phosphate transporter (NaPi-IIc) function and cellular vacuole formation in opossum kidney cells. 国際誌

Shiozaki Y, Segawa H, Ohnishi S, Ohi A, Ito M, Kaneko I, Kido S, Tatsumi S, Miyamoto K.

J Med Invest. 62 ( 3.4 ) 209 - 218 2015年8月

[Bone and Nutrition. Sclerostin and bone metabolism]. 査読

Tatsumi S, Nagamoto K, Ogata M, Miyamoto K

Clinical calcium 25 ( 7 ) 1043 - 1047 2015年7月

Niacin and Chronic Kidney Disease 査読

Yutaka Taketani, Masashi Masuda, Hisami Yamanaka-Okumura, Sawako Tatsumi, Hiroko Segawa, Ken-ichi Miyamoto, Eiji Takeda, Hironori Yamamoto

JOURNAL OF NUTRITIONAL SCIENCE AND VITAMINOLOGY 61 S173 - S175 2015年5月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：CENTER ACADEMIC PUBL JAPAN

Chronic kidney disease (CKD) is an increasing problem worldwide. The number of end-stage renal disease patients requiring treatment by dialysis is estimated to be increasing by 10,000 patients per year in Japan. Furthermore, an estimated 13 million people are living with CKD in Japan. Various complications are associated with CKD, including cardiovascular disease (CVD). More than one-third of CKD patients die from CVD. Thus, prevention of CVD is a primary concern for the treatment of CKD patients. CKD-mineral and bone disorder (CKD-MBD) is a serious complication that typically leads to CVD. Hyperphosphatemia is thought to be a central-risk factor for CKD-MBD. Therefore, managing hyperphosphatemia is crucial to prevent CKD-MBD and CVD. It is difficult to achieve the target serum phosphate level through dietary modifications alone in patients with hyperphosphatemia, because most foods contain phosphate. Thus, phosphate binders such as calcium carbonate are commonly prescribed to CKD patients with hyperphosphatemia, but these have undesirable side effects. Inhibition of intestinal phosphate transport activity has also been investigated as an alternative approach for controlling serum phosphate levels in CKD patients. Nicotinamide, which is the amide of niacin, can inhibit intestinal phosphate transport. Niacin and related compounds have also been developed as drugs for hyperlipidemia conditions, especially hypertriglyceridemia with low high-density lipoprotein. This type of dyslipidemia is frequently observed in CKD patients and is a modifiable risk factor for CVD. Thus, niacin and related compounds may have utility for the treatment of both hyperphosphatemia and dyslipidemia in CKD patients to prevent CVD.

DOI： 10.3177/jnsv.61.S173

Web of Science

PubMed

[Genetic diseases of renal phosphate handling]. 査読

Kaneko I, Segawa H, Tatsumi S, Miyamoto K

Nihon Jinzo Gakkai shi 57 ( 4 ) 758 - 765 2015年

Molecular mechanisms of cadmium-induced fibroblast growth factor 23 upregulation in osteoblast-like cells. 国際誌

Kido S, Fujihara M, Nomura K, Sasaki S, Mukai R, Ohnishi R, Kaneko I, Segawa H, Tatsumi S, Izumi H, Kohno K, Miyamoto K.

Toxicol Sci. 139 ( 2 ) 301 - 316 2014年6月

Molecular Mechanisms of Cadmium-Induced Fibroblast Growth Factor 23 Upregulation in Osteoblast-Like Cells 査読

Shinsuke Kido, Marina Fujihara, Kengo Nomura, Shohei Sasaki, Rie Mukai, Ritsuko Ohnishi, Ichiro Kaneko, Hiroko Segawa, Sawako Tatsumi, Hiroto Izumi, Kimitoshi Kohno, Ken-ichi Miyamoto

TOXICOLOGICAL SCIENCES 139 ( 2 ) 301 - 316 2014年6月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：OXFORD UNIV PRESS

Itai-itai disease is thought to be the result of chronic cadmium (Cd) intoxication. Renal proximal tubules are a major target of Cd toxicity. The whole mechanism of the adverse effects of Cd remains unresolved, especially how renal damage is related to the development of bone lesions. Fibroblast growth factor 23 (FGF23) is a bone-derived phosphaturic factor that regulates vitamin D and inorganic phosphate metabolism in the kidney. To clarify the role of FGF23 on Cd toxicity, we investigated the mechanisms of Cd-induced FGF23 production in the bone. Cd injection into mice significantly increased plasma FGF23 concentrations, but did not change FGF23 mRNA expression in bone. GalNAc-T3 is involved in secreting intact FGF23. To determine potential roles of GalNAc-T3 in Cd-induced FGF23 production, we examined the effect of Cd on GalNAc-T3 mRNA expression in vivo and in vitro. GalNAc-T3 gene expression was significantly increased in the bones of Cd-injected mice. Cd also enhanced the expression of GalNAc-T3 in cultured osteosarcoma UMR106 cells and primary osteocytes. Cd activated aryl hydrocarbon receptors (AhR) and AhR were required for GalNAc-T3 gene expression induced by Cd. In addition, Cd-dependent FGF23 production was completely inhibited by an AhR antagonist. AhR siRNA markedly suppressed the stimulation of transcriptional activity by Cd. Furthermore, Cd induced AhR activation via phosphorylation of Ser-68 by p38 kinase in the nuclear export signal of AhR. Thus, Cd stimulated GalNAc-T3 gene transcription via enhanced AhR binding to the GalNAc-T3 promoter. These findings suggest that the Cd-induced increase in GalNAc-T3 suppresses proteolytic processing of FGF23 and increases serum FGF23 concentrations.

DOI： 10.1093/toxsci/kfu043

Web of Science

PubMed

Hepatectomy-related hypophosphatemia: a novel phosphaturic factor in the liver-kidney axis. 国際誌

Nomura K, Tatsumi S#, Miyagawa A, Shiozaki Y, Sasaki S, Kaneko I, Ito M, Kido S, Segawa H, Sano M, Fukuwatari T, Shibata K, Miyamoto K.

J Am Soc Nephrol. 25 ( 4 ) 761 - 772 2014年4月

Hepatectomy-Related Hypophosphatemia: A Novel Phosphaturic Factor in the Liver-Kidney Axis 査読

Kengo Nomura, Sawako Tatsumi, Atsumi Miyagawa, Yuji Shiozaki, Shohei Sasaki, Ichiro Kaneko, Mikiko Ito, Shinsuke Kido, Hiroko Segawa, Mitsue Sano, Tsutomu Fukuwatari, Katsumi Shibata, Ken-ichi Miyamoto

JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY 25 ( 4 ) 761 - 772 2014年4月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：AMER SOC NEPHROLOGY

Marked hypophosphatemia is common after major hepatic resection, but the pathophysiologic mechanism remains unknown. We used a partial hepatectomy (PH) rat model to investigate the molecular basis of hypophosphatemia. PH rats exhibited hypophosphatemia and hyperphosphaturia. In renal and intestinal brush-border membrane vesicles isolated from PH rats, Na+-dependent phosphate (Pi) uptake decreased by 50%-60%. PH rats also exhibited significantly decreased levels of renal and intestinal Na+-dependent Pi transporter proteins (NaPi-IIa [NaPi-4], NaPi-IIb, and NaPi-IIc). Parathyroid hormone was elevated at 6 hours after PH. Hyperphosphaturia persisted, however, even after thyroparathyroidectomy in PH rats. Moreover, DNA microarray data revealed elevated levels of nicotinamide phosphoribosyltransferase (Nampt) mRNA in the kidney after PH, and Nampt protein levels and total NAD concentration increased significantly in the proximal tubules. PH rats also exhibited markedly increased levels of the Nampt substrate, urinary nicotinamide (NAM), and NAM catabolites. In vitro analyses using opossum kidney cells revealed that NAM alone did not affect endogenous NaPi-4 levels. However, in cells overexpressing Nampt, the addition of NAM led to a marked decrease in cell surface expression of NaPi-4 that was blocked by treatment with FK866, a specific Nampt inhibitor. Furthermore, FK866-treated mice showed elevated renal Pi reabsorption and hypophosphaturia. These findings indicate that hepatectomy-induced hypophosphatemia is due to abnormal NAM metabolism, including Nampt activation in renal proximal tubular cells.

DOI： 10.1681/ASN.2013060569

Web of Science

PubMed

Effect of dietary components on renal inorganic phosphate (Pi) excretion induced by a Pi-depleted diet. 国際誌

Ohnishi R, Segawa H, Ohmoto T, Sasaki S, Hanazaki A, Mori A, Ikuta K, Furutani J, Kawakami E, Tatsumi S, Hamada Y, Miyamoto K.

J Med Invest. 61 ( 1.2 ) 162 - 170 2014年2月

[Sodium-dependent inorganic phosphate transporters and biomineralization]. 査読

Tatsumi S, Fujii O, Miyagawa A, Miyamoto K

Clinical calcium 24 ( 2 ) 249 - 255 2014年2月

Effect of dietary components on renal inorganic phosphate (Pi) excretion induced by a Pi-depleted diet 査読

Ritsuko Ohnishi, Hiroko Segawa, Tomoyo Ohmoto, Shohei Sasaki, Ai Hanazaki, Ayaka Mori, Kayo Ikuta, Junya Furutani, Eri Kawakami, Sawako Tatsumi, Yasuhiro Hamada, Ken-Ichi Miyamoto

Journal of Medical Investigation 61 ( 1-2 ) 162 - 170 2014年

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：University of Tokushima

Dietary inorganic phosphate (Pi) is the most important factor in the regulation of renal Pi excretion. Recent studies suggest the presence of an enteric-renal signaling axis for dietary Pi as well as the existence of a mechanism by which the intestine detects changes in luminal Pi concentrations. The mechanisms of intestinal Pi sensing, however, are unknown. In the present study, we focused on Pi depletion signals and investigated the effects of dietary components on intestinal Pi sensing. After feeding rats experimental diets for 3 days, we investigated urinary Pi excretion and plasma biochemical parameters. Renal Pi excretion was suppressed in rats fed a low-Pi diet (0.02% Pi). Elimination of dietary calcium (Ca) completely blocked the suppression of Pi excretion, suggesting that the presence of Ca is essential for the Pi depletion signal. Furthermore, a minimum Ca content of more than 0.02% was necessary for the Pi depletion signal. Magnesium, lanthanum, and strontium, which are agonists of calcium sensing receptor, instead of Ca, reduced Pi excretion. Therefore, dietary Ca appears to be important for the Pi depletion-sensing mechanism in the gastrointestinal tract. In addition, the calcium sensing receptor may be involved in the Pi depletion signal.

DOI： 10.2152/jmi.61.162

Scopus

PubMed

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