The Experts below are selected from a list of 321 Experts worldwide ranked by ideXlab platform
Seiji Fukumoto - One of the best experts on this subject based on the ideXlab platform.
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Phosphate Metabolism and vitamin d
bonekey Reports, 2014Co-Authors: Seiji FukumotoAbstract:Phosphate plays many essential roles in our body. To accomplish these functions, serum Phosphate needs to be maintained in a certain range. Serum Phosphate level is regulated by intestinal Phosphate absorption, renal Phosphate handling and equilibrium of extracellular Phosphate with that in bone or intracellular fluid. Several hormones such as parathyroid hormone, 1,25-dihydroxyvitamin D (1,25(OH)2D) and fibroblast growth factor 23 (FGF23) regulate serum Phosphate by modulating intestinal Phosphate absorption, renal Phosphate reabsorption and/or bone Metabolism. In addition, dietary Phosphate rapidly enhances renal Phosphate excretion, although detailed mechanisms of this adaptation remain to be clarified. Physiologically, extracellular concentrations of Phosphate and these hormones are maintained by several negative feedback loops. For example, 1,25(OH)2D enhances FGF23 production and FGF23 reduces 1,25(OH)2D level. In addition, Phosphate affects 1,25(OH)2D and FGF23 levels. Dysfunction of these negative feedback loops results in several diseases with abnormal Phosphate and 1,25(OH)2D levels. Especially, excess actions of FGF23 cause several hypoPhosphatemic rickets/osteomalacia with relatively low level of 1,25(OH)2D that had been classified as vitamin D-resistant rickets/osteomalacia. In contrast, deficient actions of FGF23 cause hyperPhosphatemic familial tumoral calcinosis. However, there still remain several unanswered questions regarding Phosphate and vitamin D Metabolism.
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minireview fibroblast growth factor 23 in Phosphate homeostasis and bone Metabolism
Endocrinology, 2011Co-Authors: Michiko Hori, Yuichiro Shimizu, Seiji FukumotoAbstract:Fibroblast growth factor 23 (FGF23) was identified in 2000. Since then, FGF23 has been found to physiologically regulate Phosphate Metabolism and aberrant actions of FGF23 results in several disorders of Phosphate and bone Metabolism. In addition, FGF23 plays an important role in the development of chronic kidney disease–mineral and bone disorder. However, further investigations are necessary, especially with regard to the regulation of FGF23 expression. In this minireview, we focus on the physiological and pathophysiological significance of FGF23 in Phosphate and bone Metabolism.
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physiological regulation and disorders of Phosphate Metabolism pivotal role of fibroblast growth factor 23
Internal Medicine, 2008Co-Authors: Seiji FukumotoAbstract:Fibroblast growth factor (FGF) 23 has been identified as the last member of FGF family. FGF23 reduces serum Phosphate level by suppressing proximal tubular Phosphate reabsorption and intestinal Phosphate absorption. FGF23 is produced by bone and acts on the kidney through a specific receptor system which is composed of Klotho and certain subtypes of FGF receptors. Excess actions of FGF23 cause several hypoPhosphatemic diseases characterized by impaired renal Phosphate reabsorption and rickets/osteomalacia. In contrast, deficient actions of FGF23 result in hyperPhosphatemic tumoral calcinosis with enhanced renal Phosphate reabsorption. These results indicate that FGF23 works as a hormone to regulate the serum Phosphate level.
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fgf23 is a hormone regulating Phosphate Metabolism unique biological characteristics of fgf23
Bone, 2007Co-Authors: Seiji Fukumoto, Takeyoshi YamashitaAbstract:FGF23 was identified as the last member of FGF23 family. Recent investigations indicate that excess actions of FGF23 cause several hypoPhosphatemic diseases whereas deficient FGF23 activity results in hyperPhosphatemic tumoral calcinosis. These results indicate that FGF23 is a hormone that regulates serum Phosphate level in contrast to other FGF family members that work as local factors. Furthermore, FGF23 requires Klotho for its signaling in addition to a canonical FGF receptor. These unique characteristics of FGF23 expanded our knowledge about the diversity of FGF family members and specificity of FGF23.
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vitamin d receptor independent fgf23 actions in regulating Phosphate and vitamin d Metabolism
American Journal of Physiology-renal Physiology, 2005Co-Authors: Takashi Shimada, Yuji Yamazaki, Motoo Takahashi, Hisashi Hasegawa, Itaru Urakawa, Takeshi Oshima, Makoto Kakitani, Kazuma Tomizuka, Toshiro Fujita, Seiji FukumotoAbstract:FGF23 suppresses both serum Phosphate and 1,25-dihydroxyvitamin D [1,25D] levels in vivo. Because 1,25D itself is a potent regulator of Phosphate Metabolism, it has remained unclear whether FGF23-i...
Christina A Pacak - One of the best experts on this subject based on the ideXlab platform.
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myocardial glucose and fatty acid Metabolism is altered and associated with lower cardiac function in young adults with barth syndrome
Journal of Nuclear Cardiology, 2019Co-Authors: William Todd Cade, Richard Laforest, Kathryn L Bohnert, Dominic N Reeds, Adam J Bittel, Lisa De Las Fuentes, Adil Bashir, Pamela K Woodard, Christina A PacakAbstract:BACKGROUND Barth syndrome (BTHS) is a rare X-linked condition resulting in cardiomyopathy, however; the effects of BTHS on myocardial substrate Metabolism and its relationships with cardiac high-energy Phosphate Metabolism and left ventricular (LV) function are unknown. We sought to characterize myocardial glucose, fatty acid (FA), and leucine Metabolism in BTHS and unaffected controls and examine their relationships with cardiac high-energy Phosphate Metabolism and LV function. METHODS/RESULTS Young adults with BTHS (n = 14) and unaffected controls (n = 11, Control, total n = 25) underwent bolus injections of 15O-water and 1-11C-glucose, palmitate, and leucine and concurrent positron emission tomography imaging. LV function and cardiac high-energy Phosphate Metabolism were examined via echocardiography and 31P magnetic resonance spectroscopy, respectively. Myocardial glucose extraction fraction (21 ± 14% vs 10 ± 8%, P = .03) and glucose utilization (828.0 ± 470.0 vs 393.2 ± 361.0 μmol·g-1·min-1, P = .02) were significantly higher in BTHS vs Control. Myocardial FA extraction fraction (31 ± 7% vs 41 ± 6%, P < .002) and uptake (0.25 ± 0.04 vs 0.29 ± 0.03 mL·g-1·min-1, P < .002) were significantly lower in BTHS vs Control. Altered myocardial Metabolism was associated with lower cardiac function in BTHS. CONCLUSIONS Myocardial substrate Metabolism is altered and may contribute to LV dysfunction in BTHS. Clinical Trials #: NCT01625663.
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myocardial glucose and fatty acid Metabolism is altered and associated with lower cardiac function in young adults with barth syndrome
Journal of Nuclear Cardiology, 2019Co-Authors: William Todd Cade, Richard Laforest, Kathryn L Bohnert, Dominic N Reeds, Adam J Bittel, Lisa De Las Fuentes, Adil Bashir, Pamela K Woodard, Christina A PacakAbstract:Barth syndrome (BTHS) is a rare X-linked condition resulting in cardiomyopathy, however; the effects of BTHS on myocardial substrate Metabolism and its relationships with cardiac high-energy Phosphate Metabolism and left ventricular (LV) function are unknown. We sought to characterize myocardial glucose, fatty acid (FA), and leucine Metabolism in BTHS and unaffected controls and examine their relationships with cardiac high-energy Phosphate Metabolism and LV function. Young adults with BTHS (n = 14) and unaffected controls (n = 11, Control, total n = 25) underwent bolus injections of 15O-water and 1-11C-glucose, palmitate, and leucine and concurrent positron emission tomography imaging. LV function and cardiac high-energy Phosphate Metabolism were examined via echocardiography and 31P magnetic resonance spectroscopy, respectively. Myocardial glucose extraction fraction (21 ± 14% vs 10 ± 8%, P = .03) and glucose utilization (828.0 ± 470.0 vs 393.2 ± 361.0 μmol·g−1·min−1, P = .02) were significantly higher in BTHS vs Control. Myocardial FA extraction fraction (31 ± 7% vs 41 ± 6%, P < .002) and uptake (0.25 ± 0.04 vs 0.29 ± 0.03 mL·g−1·min−1, P < .002) were significantly lower in BTHS vs Control. Altered myocardial Metabolism was associated with lower cardiac function in BTHS. Myocardial substrate Metabolism is altered and may contribute to LV dysfunction in BTHS. Clinical Trials #: NCT01625663.
Adil Bashir - One of the best experts on this subject based on the ideXlab platform.
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myocardial glucose and fatty acid Metabolism is altered and associated with lower cardiac function in young adults with barth syndrome
Journal of Nuclear Cardiology, 2019Co-Authors: William Todd Cade, Richard Laforest, Kathryn L Bohnert, Dominic N Reeds, Adam J Bittel, Lisa De Las Fuentes, Adil Bashir, Pamela K Woodard, Christina A PacakAbstract:BACKGROUND Barth syndrome (BTHS) is a rare X-linked condition resulting in cardiomyopathy, however; the effects of BTHS on myocardial substrate Metabolism and its relationships with cardiac high-energy Phosphate Metabolism and left ventricular (LV) function are unknown. We sought to characterize myocardial glucose, fatty acid (FA), and leucine Metabolism in BTHS and unaffected controls and examine their relationships with cardiac high-energy Phosphate Metabolism and LV function. METHODS/RESULTS Young adults with BTHS (n = 14) and unaffected controls (n = 11, Control, total n = 25) underwent bolus injections of 15O-water and 1-11C-glucose, palmitate, and leucine and concurrent positron emission tomography imaging. LV function and cardiac high-energy Phosphate Metabolism were examined via echocardiography and 31P magnetic resonance spectroscopy, respectively. Myocardial glucose extraction fraction (21 ± 14% vs 10 ± 8%, P = .03) and glucose utilization (828.0 ± 470.0 vs 393.2 ± 361.0 μmol·g-1·min-1, P = .02) were significantly higher in BTHS vs Control. Myocardial FA extraction fraction (31 ± 7% vs 41 ± 6%, P < .002) and uptake (0.25 ± 0.04 vs 0.29 ± 0.03 mL·g-1·min-1, P < .002) were significantly lower in BTHS vs Control. Altered myocardial Metabolism was associated with lower cardiac function in BTHS. CONCLUSIONS Myocardial substrate Metabolism is altered and may contribute to LV dysfunction in BTHS. Clinical Trials #: NCT01625663.
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myocardial glucose and fatty acid Metabolism is altered and associated with lower cardiac function in young adults with barth syndrome
Journal of Nuclear Cardiology, 2019Co-Authors: William Todd Cade, Richard Laforest, Kathryn L Bohnert, Dominic N Reeds, Adam J Bittel, Lisa De Las Fuentes, Adil Bashir, Pamela K Woodard, Christina A PacakAbstract:Barth syndrome (BTHS) is a rare X-linked condition resulting in cardiomyopathy, however; the effects of BTHS on myocardial substrate Metabolism and its relationships with cardiac high-energy Phosphate Metabolism and left ventricular (LV) function are unknown. We sought to characterize myocardial glucose, fatty acid (FA), and leucine Metabolism in BTHS and unaffected controls and examine their relationships with cardiac high-energy Phosphate Metabolism and LV function. Young adults with BTHS (n = 14) and unaffected controls (n = 11, Control, total n = 25) underwent bolus injections of 15O-water and 1-11C-glucose, palmitate, and leucine and concurrent positron emission tomography imaging. LV function and cardiac high-energy Phosphate Metabolism were examined via echocardiography and 31P magnetic resonance spectroscopy, respectively. Myocardial glucose extraction fraction (21 ± 14% vs 10 ± 8%, P = .03) and glucose utilization (828.0 ± 470.0 vs 393.2 ± 361.0 μmol·g−1·min−1, P = .02) were significantly higher in BTHS vs Control. Myocardial FA extraction fraction (31 ± 7% vs 41 ± 6%, P < .002) and uptake (0.25 ± 0.04 vs 0.29 ± 0.03 mL·g−1·min−1, P < .002) were significantly lower in BTHS vs Control. Altered myocardial Metabolism was associated with lower cardiac function in BTHS. Myocardial substrate Metabolism is altered and may contribute to LV dysfunction in BTHS. Clinical Trials #: NCT01625663.
Mohammed S. Razzaque - One of the best experts on this subject based on the ideXlab platform.
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Osteo-renal cross-talk and Phosphate Metabolism by the FGF23-Klotho system.
Contributions to nephrology, 2013Co-Authors: Mutsuko Ohnishi, Mohammed S. RazzaqueAbstract:Phosphate is widely distributed in the body and an adequate balance is required for maintaining essential cellular and organ functions. Dysregulation of Phosphate balance, either in the form of hypoPhosphatemia or hyperPhosphatemia can induce disorders ranging from rickets/osteomalacia to cardiovascular calcification. A physiologic Phosphate balance is delicately maintained by multiorgan cross-talks among the intestine, kidney, and bone. Sodium-dependent Phosphate (Na/Pi) cotransporters present in the intestine and kidney play a major role in Phosphate absorption and reabsorption, according to the body's demand. Some of the calcium regulating factors, including parathyroid hormone and vitamin D can influence the activities of Na/Pi cotransporters, and thereby can affect Phosphate balance. In addition, molecular analysis of the unexplained hypoPhosphatemic diseases, including autosomal-dominant hypoPhosphatemic rickets and tumor-induced osteomalacia has led to the identification of fibroblast growth factor 23 (FGF23). Subsequent studies have documented that bone-derived FGF23 and kidney-derived klotho can form an endocrine network to control urinary Phosphate excretion. Studies have also documented negative effect of FGF23/klotho system on vitamin D Metabolism and Na/Pi cotransporter activities. This article will summarize how the FGF23/klotho system might influence systemic Phosphate Metabolism, and consequences of its abnormal regulation will be briefly described.
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regulation of Phosphate Metabolism by fgf23
Translational Endocrinology of Bone, 2013Co-Authors: Beate Lanske, Michael J Densmore, Mohammed S. RazzaqueAbstract:Fibroblast growth factor 23 (FGF23) is a recently discovered hormone that is a key regulator of systemic Phosphate Metabolism. It is expressed in bone and has endocrine effects on renal and parathyroid gland function. FGF23 and its co-factor Klotho interact with vitamin D and parathyroid hormone to form a delicate regulatory network that maintains the optimal balance of mineral ions in the body that is critical for health and survival. This chapter explains the biology and physiology of FGF23, how it interacts with the other calcium and Phosphate regulating hormones to maintain mineral ion homeostasis, and how its dysregulation contributes to renal and skeletal disorders.
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osteo renal regulation of systemic Phosphate Metabolism
Iubmb Life, 2011Co-Authors: Mohammed S. RazzaqueAbstract:Impaired kidney function and subsequent skeletal responses play a critical role in disrupting Phosphate balance in chronic kidney disease (CKD) patients with mineral and bone disorder (CKD-MBD). In patients with CKD-MBD, the inability of the kidney to maintain normal mineral ion balance affects bone remodeling to induce skeletal fracture and extraskeletal vascular calcification. In physiological conditions, bone-derived fibroblast growth factor 23 (FGF23) acts on the kidney to reduce serum Phosphate and 1,25-dihydroxyvitamin D levels. In humans, increased bioactivity of FGF23 leads to increased urinary Phosphate excretion, which induces hypoPhosphatemic diseases (e.g., rickets/osteomalacia). However, reduced FGF23 activity is associated with hyperPhosphatemic diseases (e.g., tumoral calcinosis). In patients with CKD, high serum levels of FGF23 fail to reduce serum Phosphate levels and lead to numerous complications, including vascular calcification, one of the important determinants of mortality of CKD-MBD patients. Of particular significance, molecular, biochemical and morphological changes in patients with CKD-MBD are mostly due to osteo-renal dysregulation of mineral ion Metabolism. Furthermore, hyperPhosphatemia can partly contribute to the development of secondary hyperparathyroidism in patients with CKD-MBD. Relatively new pharmacological agents including sevelamer hydrochloride, calcitriol analogs and cinacalcet hydrochloride are used either alone, or in combination, to minimize hyperPhosphatemia and hyperparathyroidism associated complications to improve morbidity and mortality of CKD-MBD patients. This article will briefly summarize how osteo-renal miscommunication can induce Phosphate toxicity, resulting in extensive tissue injuries.
Carole Guillevin - One of the best experts on this subject based on the ideXlab platform.
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altered phospholipid and high energy Phosphate Metabolism in the basal ganglia and thalamus of severe obsessive compulsive patients with treatment resistance a phosphorus 31 nuclear magnetic resonance spectroscopy study
Psychiatry Research-neuroimaging, 2021Co-Authors: Laura Hatchondo, Alexandre Vallee, Rodolphe Vallee, Nemat Jaafari, Sylvie Maillochaud, Mathieu Naudin, J N Vallee, Remy Guillevin, Carole GuillevinAbstract:ABSTRACT Introduction Cerebral Metabolism in obsessive-compulsive-disorder(OCD) has been the subject of numerous studies using proton magnetic resonance spectroscopy(MRS). Despite heterogeneous results, some studies have unraveled membrane turnover and energy Metabolism abnormalities in different brain regions, suggesting that alterations in these processes may contribute to the pathophysiology. So far, no authors have explored phospholipids and high-energy Phosphate Metabolism using 31P-MRS, which allows in vivo quantification of phosphorus metabolites that are considered to be related to membrane turnover and energy Metabolism. Materials and Methods The aim of our study was to describe and compare brain metabolic changes using 31P-MRS in the striatum and the thalamus, between 23 severe OCD patients and 22 healthy controls. All subject underwent a clinical examination and a same 31P-MRS protocol. Results Significantly, increased concentrations of PC, PDE,PME,GPC,PME/PCr,PDE/PCr were found in patients compared to controls in the striatum and the thalamus. PCr and tATP were decreased in the striatum. Finally, significant correlations were found in the striatum and the thalamus between illness duration and some specific measured parameters. Conclusion Our results showed significant modifications of the membrane and energy Metabolism in the basal ganglia of severe OCD patients and suggests a link between energetic buffer and serotonin Metabolism disorder.