type: misc

label: url

en: 巻頭言∼食事に含まれるリンとその代謝∼

ja: 巻頭言∼食事に含まれるリンとその代謝∼

en: Clinical Calcium

ja: Clinical Calcium


en: Regulation of Phosphate Transporters and Novel Regulator of Phosphate Metabolism

en: Endocrines

ja: Endocrines


en: 抗老化因子を制御するミネラル栄養学-リン代謝恒常制御の重要性

ja: 抗老化因子を制御するミネラル栄養学-リン代謝恒常制御の重要性

en: 実験医学増刊∼栄養・代謝物シグナルと食品機能∼

ja: 実験医学増刊∼栄養・代謝物シグナルと食品機能∼


en: リントランスポーターと疾患.

ja: リントランスポーターと疾患.

en: 別冊・医学のあゆみ-トランスポーターのすべて―

ja: 別冊・医学のあゆみ-トランスポーターのすべて―


en: NAD metabolism and the SLC34 family: evidence for a liver-kidney axis regulating inorganic phosphate.

en: Pflügers Archiv : European Journal of Physiology


en: Vitamin D and muscle tissues

ja: ビタミンDと筋組織


en: Control of phosphate balance by the kidney and intestine.

en: 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.

en: Clinical and Experimental Nephrology

ja: Clinical and Experimental Nephrology

number: Suppl 1


en: Transcriptional regulation of sodium-phosphate cotransporter gene expression.

en: Molecular, Genetic, and Nutritional Aspects of Major and Trace Minerals


en: 病態生理と症例から学ぶ輸液ガイド (第4章)症例から学ぶ輸液療法とその管理の実際 低リン血症と高リン血症の是正法と輸液管理

en: Medical Practice

ja: Medical Practice


en: 食餌性リンによる血管障害

ja: 食餌性リンによる血管障害

en: Journal of Japanese Society for Dialysis Therapy

ja: 日本透析医学会雑誌


en: The Role of Sodium-Dependent Phosphate Transporter in Phosphate Homeostasis.

en: Inorganic phosphate (Pi) is an essential compound for several biologic functions. Pi levels outside the normal range, however, contribute to several pathological processes. Hypophosphatemia leads to bone abnormalities, such as rickets/osteomalacia. Hyperphosphatemia contributes to vascular calcification in patients with chronic kidney disease and hemodialysis patients and is independently associated with cardiac mortality.Pi homeostasis is regulated by the coordinated function of renal and intestinal sodium-dependent phosphate (NaPi) transporters with dietary Pi, parathyroid hormone, 1,25-dihydroxyvitamin D3, and fibroblast growth factor 23. The type II NaPi transporter/SLC34 family, with three members identified to date, is mainly responsible for Pi homeostasis in the body. SLC34A1 and SCL34A3 are predominantly expressed in the kidney, whereas SLC34A2 is expressed in the small intestine. The role of each SLC34 in the body was recently established by studies of gene-targeted mice. Mutation of SLC34A1 causes Fanconi syndrome and mutation of SLC34A3 causes autosomal recessive hereditary hypophosphatemic rickets with hypercalciuria. SLC34A2 is thought to be a major intestinal NaPi transporter and mutation of SLC34A2 causes pulmonary alveolar microlithiasis. A detailed understanding of Pi regulation in the body is important toward maintaining health.

en: Journal of Nutritional Science and Vitaminology

volume: 61 Suppl


en: Genetic diseases of renal phosphate handling

ja: 遺伝性リン代謝異常症

en: Japanese Journal of Nephrology

ja: 日本腎臓学会誌


en: [Updates on rickets and osteomalacia: the role of NaPi-2c/SLC34A3 and hypophosphataemic rickets].

en: Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) , an autosomal recessive disorder first identified in a large Bedouin tribe, is characterized by hypophosphatemia secondary to renal inorganic phosphate (Pi) wasting, resulting in increased serum1,25-dihydroxyvitamin D3 concentrations with associated intestinal calcium hyperabsorption, hypercalciuria, rickets, and osteomalacia. Recent studies identified several mutations in the NaPi-2c/NPT2c transporter gene (SLC34A3) as the cause of HHRH. The fact that HHRH is caused by NaPi-2c loss-of-function mutations is compatible with the HHRH phenotype and the prevailing view of renal Pi regulation. The NaPi-2c mutants in HHRH show defective processing and stability.

en: Clinical Calcium


en: Vitamin D and type II sodium-dependent phosphate cotransporters.

en: The type II sodium-dependent Pi (NaPi) cotransporters (NaPi-IIa, NaPi-IIb and NaPi-IIc) contribute to renal and intestinal Pi absorption. 1,25-Dihydroxyvitamin D [1,25(OH)2D3] is an important factor for NaPi-II transporters in the small intestine and kidney. In a previous study, low levels of 1,25(OH)2D3 appeared to suppress the expression of renal NaPi cotransporters. We identified a functional vitamin D receptor-responsive element in the human NaPi-IIa and NaPi-IIc genes in renal epithelial cells. In an analysis of vitamin D receptor (VDR)-null mice, we observed early onset of hypophosphatemia. The cause of the hypophosphatemia in VDR-null mice before weaning appeared to be increased plasma parathyroid hormone (PTH) levels during the suckling periods. A rescue diet (high calcium diet) decreased plasma PTH levels in VDR-null mice. The reduced plasma PTH levels normalized the renal Npt2a and Npt2c protein levels in weanling animals. Thus, the dietary intervention completely normalized the expression of the renal Pi transporters (Npt2a/Npt2c) in VDR-null mice, suggesting that the lack of VDR activity was not the cause of the impaired renal Pi reabsorption. In suckling animals, 1,25(OH)2D3 may be essential for the prevention of the phosphaturic action of PTH. In adult animals, 1,25(OH)2D3 is thought to be an important factor for posttranscriptional regulation of the Npt2b gene in the small intestine. Fibroblast growth factor 23 (FGF23) is a novel phosphaturic factor that influences vitamin D metabolism and renal reabsorption of Pi. We characterized the role of the VDR in the action of FGF23 using VDR-null mice. FGF23 reduced renal Pi transport and 25-hydroxyvitamin D 1a-hydroxylase levels by a mechanism that was independent of the VDR. By contrast, the induction of 25-hydroxyvitamin D 24-hydroxylase and the reduction in serum 1,25(OH)2D3 levels induced by FGF23 were dependent on the VDR. Thus, the VDR is not essential for the phosphaturic action of FGF23, but is essential for control of the plasma 1,25(OH)2D3 level. Moreover, FGF23 reduces intestinal NaPi transport activity and Npt2b protein levels by a mechanism that is dependent on the VDR. Klotho functions as a co-receptor for FGF23 and is increased by 1,25(OH)2D3. Klotho induces phosphaturia by inhibiting the renal NaPi-IIa transporter. In this review, we discuss the roles of 1,25(OH)2D3/VDR in the regulation of renal type II NaPi cotransporters in the kidney and small intestine.

en: Contributions to Nephrology

ja: Contributions to Nephrology


en: リンの体内動態(腸管,腎臓における吸収と排泄機序/リン輸送体の機能作用)

ja: リンの体内動態(腸管,腎臓における吸収と排泄機序/リン輸送体の機能作用)


en: FGF23およびKlothoによる尿細管でのリン輸送制御機序

ja: FGF23およびKlothoによる尿細管でのリン輸送制御機序

en: 腎と透析

ja: 腎と透析


en: [Fibroblast growth factor 23 mediates the phosphaturic actions of cadmium].

en: Phosphaturia has been documented following cadmium (Cd) exposure in both humans and experimental animals. Fibroblast growth factor 23 (FGF23) serves as an essential phosphate homeostasis pathway in the bone-kidney axis. In the present study, we investigated the effects of Cd on phosphate (Pi) homeostasis in mice. Following Cd injection into C57BL/6J mice, plasma FGF23 concentration significantly increased. The urinary Pi excretion level was significantly higher in the Cd-injected C57BL/6J mice than in the control group. Plasma Pi concentration decreased only slightly in the Cd-injected mice compared with the control group. No changes were observed in the concentration of the plasma parathyroid hormone and 1,25-dihydroxy vitamin D(3) in both groups of mice. We observed a decrease in phosphate transport activity and also a decrease in the expression level of renal phosphate transporter Npt2c, but not that of Npt2a. Furthermore, we examined the effect of Cd on Npt2c in Npt2a-knockout (KO) mice, which expresses Npt2c as a major NaPi cotransporter. Injecting Cd to Npt2aKO mice induced a significant increase in plasma FGF23 concentration and urinary Pi excretion level. Furthermore, we observed decreases in phosphate transport activity and renal Npt2c expression level in the Cd-injected Npt2a KO mice. The present study suggests that hypophosphatemia induced by Cd may be closely associated with FGF23.

en: Nihon Eiseigaku Zasshi

ja: 日本衛生学雑誌


en: Sodium-dependent phosphate cotransporters: lessons from gene knockout and mutation studies.

en: Inorganic phosphate (Pi) is an essential physiological compound, highlighted by the syndromes caused by hypo or hyperphosphatemic states. Hyperphosphatemia is associated with ectopic calcification, cardiovascular disease, and increased mortality in patients with chronic kidney disease (CKD). As phosphate control is not efficient with diet or dialysis, oral Pi binders are used in over 90% of patients with renal failure. However, achieving tight control of serum Pi is difficult, and lower levels of serum Pi (severe hypophosphatemia) do not lead to better outcomes. The inhibition of sodium-dependent Pi (NaPi) transporter would be a preferable method to control serum Pi levels in patients with CKD or patients undergoing dialysis. Three types of NaPi transporters (types I-III) have been identified: solute carrier series SLC17A1 (NPT1/NaPi-I/OATv1), SLC34 (NaPi-IIa, NaPi-IIb, NaPi-IIc), and SLC20 (PiT1, PiT2), respectively. Knockout mice have been created for types I-III NaPi transporters. In this review, we discuss the roles of the NaPi transporters in Pi homeostasis.

en: Journal of Pharmaceutical Sciences

ja: Journal of Pharmaceutical Sciences


en: 高リン血症と低リン血症

ja: 高リン血症と低リン血症

en: 循環器医のための知っておくべき電解質異常

ja: 循環器医のための知っておくべき電解質異常


en: リン, 亜鉛, 銅.

ja: リン, 亜鉛, 銅.

en: 循環器医のための知っておくべき電解質異常

ja: 循環器医のための知っておくべき電解質異常


en: 無機イオン動態とトランスポーター

ja: 無機イオン動態とトランスポーター

en: トランスポートソームの世界-膜輸送研究の源流から未来へ-

ja: トランスポートソームの世界-膜輸送研究の源流から未来へ-


en: Inorganic phosphate metabolism in the human body --- 無機リン酸の生体内代謝

ja: 無機リン酸の生体内代謝 --- 無機リン酸の生体内代謝

en: Seikagaku

ja: 生化学


en: Vitamin D and phosphate metabolism --- relationship with aging-regulating gene

ja: ビタミンDとリン代謝 --- 加齢遺伝子とのかかわり

en: CLINICAL CALCIUM

ja: CLINICAL CALCIUM


en: 栄養素の構造と機能

ja: 栄養素の構造と機能

en: 新ガイドライン準拠 エキスパート 管理栄養士養成シリーズ 基礎栄養学[第2版]

ja: 新ガイドライン準拠 エキスパート 管理栄養士養成シリーズ 基礎栄養学[第2版]


en: リン代謝関連分子の新展開

ja: リン代謝関連分子の新展開

en: 判断と治療

ja: 判断と治療


en: 生体のリン調節機構とFGF23

ja: 生体のリン調節機構とFGF23

en: 腎と骨代謝

ja: 腎と骨代謝


en: カルシトニンの腎への作用

ja: カルシトニンの腎への作用

en: Clinical Calcium

ja: Clinical Calcium


en: リン酸代謝関連遺伝子群と骨粗鬆症

ja: リン酸代謝関連遺伝子群と骨粗鬆症


en: 薬理作用と生理作用ー腸管への作用ー

ja: 薬理作用と生理作用ー腸管への作用ー

en: Nihon Rinsho. Japanese Journal of Clinical Medicine

ja: 日本臨牀


en: Roles of Parathyroid Hormone (PTH) on renal calcium, Phosphate and Vitamin D metabolism

ja: 副甲状腺ホルモン(PTH)による腎カルシウム，リン，ビタミンD代謝調節について

en: THE BONE

ja: THE BONE


en: 腸管のリントランスポーター

ja: 腸管のリントランスポーター

en: 腎と透析


en: 新しいリン調節薬の開発と実用化の可能性

ja: 新しいリン調節薬の開発と実用化の可能性


en: PHEXの真の基質`phosphatonin' とは何か?

ja: PHEXの真の基質`phosphatonin' とは何か?


en: 遺伝性くる病

ja: 遺伝性くる病

en: Internal Medicine

ja: 臨床雑誌 内科


en: Molecular targets of hyper-phosphatamia in chronic renal failure

en: Dietary phosphate restriction can prevent or retard the progress of chronic renal failure (CRF) and secondary hyperparathyroidism. The klotho gene is involved in the development of a syndrome resembling human ageing, and klotho mutant mice show abnormal calcium/vitamin D metabolism, developing hyperphosphataemia and vascular calcification. Phosphate retention rescues the phenotype of klotho mice. The level of expression of klotho RNA was greatly reduced in the kidneys of all CRF patients. Dietary P(i) restriction induced klotho expression, which enhances the beneficial effect of P(i) restriction in patients with CRF and/or on haemodialysis.

en: Nephrology, Dialysis, Transplantation

ja: Nephrology, Dialysis, Transplantation

number: Suppl 3


en: リンの消化吸収機構とリン低下薬

ja: リンの消化吸収機構とリン低下薬

en: 臨床透析

ja: 臨床透析


en: リン輸送とその異常

ja: リン輸送とその異常

en: Journal of Clinical and Experimental Medicine

ja: 医学のあゆみ


en: Sensing mechanisms of inorganic phosphate in mammalian cells

en: Current Topics in Medical Chemistry

ja: Current Topics in Medical Chemistry


en: リン代謝における上皮小体ホルモン(PTH)の役割

ja: リン代謝における上皮小体ホルモン(PTH)の役割

en: CLINICAL CALCIUM


en: アミノ酸トランスポーターの構造機能と栄養学的重要性

ja: アミノ酸トランスポーターの構造機能と栄養学的重要性

en: Reports of Research Committee of Essential Amino Acids

ja: 必須アミノ酸研究


en: 魚油(n-3系脂肪酸)の摂取と疾患予防

ja: 魚油(n-3系脂肪酸)の摂取と疾患予防

en: Shikoku Acta Medica

ja: 四国医学雑誌


en: Renal handling of phosphate

ja: Renal handling of phosphate

en: Calcium In Internal Medicine

ja: Calcium In Internal Medicine


en: 生体内の無機リン酸感受機構

ja: 生体内の無機リン酸感受機構

en: 腎と骨代謝


en: リン代謝の最近の理解とリン調節薬の将来

ja: リン代謝の最近の理解とリン調節薬の将来

en: 透析療法ネクストII 透析骨症は防げる

ja: 透析療法ネクストII 透析骨症は防げる


en: Nutritional assessment in liver disease

ja: 肝疾患における栄養アセスメント

en: 日本病態栄養学会誌

ja: 日本病態栄養学会誌


en: リンの代謝調節 --- リントランスポーターの役割

ja: リンの代謝調節 --- リントランスポーターの役割

ja: CLINICAL CALCIUM


en: Transcriptional regulation of the NPT2 gene by dietary phosphate

en: Dietary phosphate (Pi) is an important regulator for renal Pi reabsorption. The type II sodium-dependent phosphate (Na/Pi) cotransporters (NPT2) are located at the apical membranes of renal proximal tubular cells and major functional transporters associated with renal Pi reabsorption. The yeast one-hybrid system was used to clone a transcription factor that binds to a specific sequence (Pi response element) in the promoter of the NPT2 gene. Two cDNA clones that encoded protein of the mouse transcription factor mu E3 (TFE3) were isolated. TFE3 may participate in the transcriptional regulation of the NPT2 gene by dietary Pi.

en: Kidney International

ja: Kidney International


en: 腎不全骨におけるPTH抵抗性の分子機構

ja: 腎不全骨におけるPTH抵抗性の分子機構


en: Understanding and Managing Hyperphostemia in Dialysis Patients

ja: 長期透析患者における栄養管理と食生活の問題点;リンの重要性について


en: 二次性副甲状腺機能亢進症とリン代謝

ja: 二次性副甲状腺機能亢進症とリン代謝

en: 腎と透析

ja: 腎と透析


en: 大豆たん白質摂取による心肥大抑制効果の検討.

ja: 大豆たん白質摂取による心肥大抑制効果の検討.

en: SOY PROTEIN RESEACH,

ja: 大豆たん白質研究.

misc_type: others