Fibroblast Growth Factor 23 Concentrations Reflect Sex Differences in Mineral Metabolism and Growth in Early Infancy

2016 ◽  
Vol 85 (4) ◽  
pp. 232-241 ◽  
Author(s):  
Elisa Holmlund-Suila ◽  
Heli Viljakainen ◽  
Östen Ljunggren ◽  
Timo Hytinantti ◽  
Sture Andersson ◽  
...  
Keyword(s):  
Sex Differences ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Mineral Metabolism ◽  
Fibroblast Growth Factor 23 ◽  
Early Infancy ◽  
Fibroblast Growth

scholarly journals Causal Effect of Fibroblast Growth Factor 23 on Osteoporosis and Cardiometabolic Disorders: A Mendelian Randomization Study

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A272-A272
Author(s):  
Maki Yokomoto-Umakoshi ◽  
Hironobu Umakoshi ◽  
Takashi Miyazawa ◽  
Masatoshi Ogata ◽  
Ryuichi Sakamoto ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Mendelian Randomization ◽  
Mineral Metabolism ◽  
Causal Effect ◽  
Association Studies ◽  
Fibroblast Growth Factor 23 ◽  
Genome Wide Association Studies ◽  
Fibroblast Growth ◽  
Cardiometabolic Disorders

Abstract Pathological excess of fibroblast growth factor 23 (FGF23) causes mineral and bone disorders. However, the causality of FGF23 in the development of osteoporosis remains unknown. Whether FGF23 has systemic effects on cardio-metabolic disorders beyond regulating mineral metabolism is also controversial. In this study, we evaluated the causal effect of FGF23 on osteoporosis and cardiometabolic disorders using Mendelian randomization (MR) analysis. Summary statistics for single-nucleotide polymorphisms with traits of interest were obtained from the relevant genome-wide association studies. As a result, FGF23 was found to be inversely associated with femoral neck-BMD (odds ratio [OR] 0.682, 95% confidence interval [CI] 0.546–0.853, p = 8e-04) and heel estimated BMD (eBMD) (OR 0.898, 95%CI 0.820–0.985, p = 0.022) in the inverse-variance-weighted analysis, but not lumbar spine-BMD and fractures. The results were supported by the weighted-median analysis, and there was no evidence of pleiotropy in the MR-Egger analysis. FGF23 was directly associated with FN-BMD and eBMD after adjustment for estimated glomerular filtration rate, height, and body mass index in multivariable MR analysis. On the other hand, there was no association between FGF23 and cardiometabolic traits including cardio artery disease, brachial-ankle pulse wave velocity, intima-media thickness of carotid arteries, systolic and diastolic blood pressure, fasting glucose, high and low-density lipoprotein cholesterol, and triglycerides. Therefore, FGF23 has been causally associated with bone loss. In contrast, FGF23 has not been causally associated with cardiometabolic disorders. The data of this study provides important insights into the role of FGF23 in the pathogenesis of osteoporosis and cardiometabolic disorders.

scholarly journals Fibroblast Growth Factor 23: Mineral Metabolism and Beyond

2017 ◽  
pp. 83-95 ◽  
Author(s):  
Alexander Grabner ◽  
Sandro Mazzaferro ◽  
Giuseppe Cianciolo ◽  
Stefanie Krick ◽  
Irene Capelli ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Mineral Metabolism ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth

scholarly journals The Role of Iron and Erythropoietin in the Association of Fibroblast Growth Factor 23 with Anemia in Chronic Kidney Disease in Humans

2020 ◽  
Vol 9 (8) ◽  
pp. 2640
Author(s):  
Bernhard Bielesz ◽  
Thomas Reiter ◽  
Fabian Peter Hammerle ◽  
Wolfgang Winnicki ◽  
Marija Bojic ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Fibroblast Growth Factor ◽  
Iron Metabolism ◽  
Mineral Metabolism ◽  
Fibroblast Growth Factor 23 ◽  
Biologically Active ◽  
Mean Corpuscular Hemoglobin ◽  
Fibroblast Growth

Anemia in chronic kidney disease (CKD) is an almost universal complication of this condition. Fibroblast growth factor 23 (FGF23), a key-player in mineral metabolism, is reportedly associated with anemia and hemoglobin levels in non-dialysis CKD patients. Here, we sought to further characterize this association while taking into account the biologically active, intact fraction of FGF23, iron metabolism, and erythropoietin (EPO). Hemoglobin, EPO, iron, and mineral metabolism parameters, including both intact and c-terminal-FGF23 (iFGF23 and cFGF23, respectively) were measured cross-sectionally in 225 non-dialysis CKD patients (stage 1–5, median eGFR: 30 mL/min./1.73m2) not on erythropoiesis stimulating agents or intravenous iron therapy. Statistical analysis was performed by multiple linear regression. After adjustment for eGFR and other important confounders, only cFGF23 but not iFGF23 was significantly associated with hemoglobin levels and this association was largely accounted for by iron metabolism parameters. cFGF23 but not iFGF23 was also associated with mean corpuscular hemoglobin (MCH) and mean corpuscular volume (MCV), again in dependence on iron metabolism parameters. Similarly, EPO concentrations were associated with cFGF23 but not iFGF23, but their contribution to the association of cFGF23 with hemoglobin levels was marginal. In pre-dialysis CKD patients, the observed association of FGF23 with hemoglobin seems to be restricted to cFGF23 and largely explained by the iron status.

Bone and Mineral Metabolism and Fibroblast Growth Factor 23 Levels After Kidney Donation

2012 ◽  
Vol 59 (6) ◽  
pp. 761-769 ◽  
Author(s):  
Ann Young ◽  
Anthony B. Hodsman ◽  
Neil Boudville ◽  
Colin Geddes ◽  
John Gill ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Mineral Metabolism ◽  
Fibroblast Growth Factor 23 ◽  
Kidney Donation ◽  
Fibroblast Growth

scholarly journals FGF23 as a calciotropic hormone

F1000Research ◽  
2015 ◽  
Vol 4 ◽  
pp. 1472 ◽  
Author(s):  
María E. Rodríguez-Ortiz ◽  
Mariano Rodríguez
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Calcium Homeostasis ◽  
Bone Cells ◽  
Mineral Metabolism ◽  
Fibroblast Growth Factor 23 ◽  
Calcium Deficiency ◽  
Fibroblast Growth

Maintaining mineral metabolism requires several organs and hormones. Fibroblast growth factor 23 (FGF23) is a phosphatonin produced by bone cells that reduces renal production of calcitriol – 1,25(OH)2D3 – and induces phosphaturia. The consequences of a reduction in 1,25(OH)2D3 involve changes in calcium homeostasis. There are several factors that regulate FGF23: phosphorus, vitamin D, and parathyroid hormone (PTH). More recently, several studies have demonstrated that calcium also modulates FGF23 production. In a situation of calcium deficiency, the presence of 1,25(OH)2D3 is necessary to optimize intestinal absorption of calcium, and FGF23 is decreased to avoid a reduction in 1,25(OH)2D3 levels.

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