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Article: FGF23, klotho and vitamin D interactions: What have we learned from in vivo mouse genetics studies?

Razzaque, M Shawkat

Advances in experimental medicine and biology

2012 Volume 728, Page(s) 84–91

Abstract: The molecular interactions of fibroblast growth factor 23 (FGF23), klotho and vitamin D coordinate to regulate the delicate phosphate levels of the body. Vitamin D can induce both FGF23 and klotho synthesis to influence renal phosphate balance. In the ... ...

Abstract	The molecular interactions of fibroblast growth factor 23 (FGF23), klotho and vitamin D coordinate to regulate the delicate phosphate levels of the body. Vitamin D can induce both FGF23 and klotho synthesis to influence renal phosphate balance. In the presence of klotho, FGF23 protein gains bioactivity to influence systemic phosphate homeostasis. Experimental studies have convincingly shown that in the absence of klotho, FGF23 is unable to regulate in vivo phosphate homeostasis. Furthermore, genetic inactivation of FGF23, klotho or both of the genes have resulted in markedly increased renal expression of 1-alpha hydroxylase [1α(OH)ase] and concomitant elevated serum levels of 1,25, dihydroxyvitamin D [1,25(OH)(2)D] in the mutant mice. Vitamin D can induce the expression of both FGF23 and klotho while, FGF23 can suppress renal expression of 1α(OH)ase to reduce 1,25(OH)(2)D activity. In this brief chapter, I will summarize the possible in vivo interactions of FGF23, klotho and vitamin D, in the light of recent mouse genetics studies.
MeSH term(s)	Animals ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Glucuronidase/genetics ; Glucuronidase/metabolism ; Humans ; Kidney Diseases/genetics ; Kidney Diseases/metabolism ; Kidney Diseases/pathology ; Mice ; Protein Binding ; Signal Transduction ; Vitamin D/metabolism
Chemical Substances	fibroblast growth factor 23 ; Vitamin D (1406-16-2) ; Fibroblast Growth Factors (62031-54-3) ; Glucuronidase (EC 3.2.1.31) ; klotho protein (EC 3.2.1.31)
Language	English
Publishing date	2012
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-1-4614-0887-1_5
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The role of Klotho in energy metabolism.

Razzaque, M Shawkat

Nature reviews. Endocrinology

2012 Volume 8, Issue 10, Page(s) 579–587

Abstract: A disproportionate expansion of white adipose tissue and abnormal recruitment of adipogenic precursor cells can not only lead to obesity but also impair glucose metabolism, which are both common causes of insulin resistance and diabetes mellitus. The ... ...

Abstract	A disproportionate expansion of white adipose tissue and abnormal recruitment of adipogenic precursor cells can not only lead to obesity but also impair glucose metabolism, which are both common causes of insulin resistance and diabetes mellitus. The development of novel and effective therapeutic strategies to slow the progression of obesity, diabetes mellitus and their associated complications will require improved understanding of adipogenesis and glucose metabolism. Klotho might have a role in adipocyte maturation and systemic glucose metabolism. Klotho increases adipocyte differentiation in vitro, and mice that lack Klotho activity are lean owing to reduced white adipose tissue accumulation; moreover, mice that lack the Kl gene (which encodes Klotho) are resistant to obesity induced by a high-fat diet. Knockout of Kl in leptin-deficient Lep(ob/ob) mice reduces obesity and increases insulin sensitivity, which lowers blood glucose levels. Energy metabolism might also be influenced by Klotho. However, further studies are needed to explore the possibility that Klotho could be a novel therapeutic target to reduce obesity and related complications, and to determine whether and how Klotho might influence the regulation and function of a related protein, β-Klotho, which is also involved in energy metabolism.
MeSH term(s)	Animals ; Energy Metabolism/genetics ; Energy Metabolism/physiology ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Glucuronidase/genetics ; Glucuronidase/metabolism ; Humans ; Insulin Resistance/genetics ; Insulin Resistance/physiology ; Leptin/genetics ; Leptin/metabolism ; Obesity/genetics ; Obesity/metabolism
Chemical Substances	Leptin ; Fibroblast Growth Factors (62031-54-3) ; fibroblast growth factor 23 (7Q7P4S7RRE) ; Glucuronidase (EC 3.2.1.31) ; klotho protein (EC 3.2.1.31)
Language	English
Publishing date	2012-05-29
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2489381-X
ISSN	1759-5037 ; 1759-5029
ISSN (online)	1759-5037
ISSN	1759-5029
DOI	10.1038/nrendo.2012.75
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Article ; Online: The dualistic role of vitamin D in vascular calcifications.

Razzaque, M Shawkat

Kidney international

2010 Volume 79, Issue 7, Page(s) 708–714

Abstract: Vitamin D is a multifunctional hormone that can affect many essential biological functions, ranging from the immune regulation to mineral ion metabolism. A close association between altered activity of vitamin D and vascular calcification has been ... ...

Abstract	Vitamin D is a multifunctional hormone that can affect many essential biological functions, ranging from the immune regulation to mineral ion metabolism. A close association between altered activity of vitamin D and vascular calcification has been reported in various human diseases, including in patients with atherosclerosis, osteoporosis, and chronic kidney disease (CKD). Vascular calcification is a progressive disorder and is a major determinant of morbidity and mortality of the affected patients. Experimental studies have shown that excessive vitamin D activities can induce vascular calcification, and such vascular pathology can be reversed by reducing vitamin D activities. The human relevance of these experimental studies is not clear, as vitamin D toxicity is relatively rare in the general population. Contrary to the relationship between vitamin D and vascular calcification, in experimental uremic models, low levels of vitamin D were shown to be associated with extensive vascular calcification, a phenomenon that is very similar to the vascular pathology seen in patients with CKD. The current treatment approach of providing vitamin D analogs to patients with CKD often poses a dilemma, as studies linked vitamin D treatment to subsequent vascular calcification. Recent genetic studies, however, have shown that vascular calcification can be prevented by reducing serum phosphate levels, even in the presence of extremely high serum 1,25-dihydroxyvitamin D and calcium levels. This article will briefly summarize the dual effects of vitamin D in vascular calcification and will provide evidence of vitamin D-dependent and -independent vascular calcification.
MeSH term(s)	Animals ; Calcinosis/etiology ; Calcinosis/metabolism ; Calcinosis/prevention & control ; Calcium/metabolism ; Humans ; Kidney/metabolism ; Phosphates/metabolism ; Receptors, Calcitriol/metabolism ; Signal Transduction ; Vascular Diseases/etiology ; Vascular Diseases/metabolism ; Vascular Diseases/prevention & control ; Vitamin D/adverse effects ; Vitamin D/metabolism ; Vitamin D/therapeutic use
Chemical Substances	Phosphates ; Receptors, Calcitriol ; Vitamin D (1406-16-2) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2010-10-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1038/ki.2010.432
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Article ; Online: Phosphate toxicity: new insights into an old problem.

Razzaque, M Shawkat

Clinical science (London, England : 1979)

2010 Volume 120, Issue 3, Page(s) 91–97

Abstract: Phosphorus is an essential nutrient required for critical biological reactions that maintain the normal homoeostatic control of the cell. This element is an important component of different cellular structures, including nucleic acids and cell membranes. ...

Abstract	Phosphorus is an essential nutrient required for critical biological reactions that maintain the normal homoeostatic control of the cell. This element is an important component of different cellular structures, including nucleic acids and cell membranes. Adequate phosphorus balance is vital for maintaining basic cellular functions, ranging from energy metabolism to cell signalling. In addition, many intracellular pathways utilize phosphate ions for important cellular reactions; therefore, homoeostatic control of phosphate is one of the most delicate biological regulations. Impaired phosphorus balance can affect the functionality of almost every human system, including musculoskeletal and cardiovascular systems, ultimately leading to an increase in morbidity and mortality of the affected patients. Human and experimental studies have found that delicate balance among circulating factors, like vitamin D, PTH (parathyroid hormone) and FGF23 (fibroblast growth factor 23), are essential for regulation of physiological phosphate balance. Dysregulation of these factors, either alone or in combination, can induce phosphorus imbalance. Recent studies have shown that suppression of the FGF23-klotho system can lead to hyperphosphataemia with extensive tissue damage caused by phosphate toxicity. The cause and consequences of phosphate toxicity will be briefly summarized in the present review.
MeSH term(s)	Animals ; Fibroblast Growth Factor-23 ; Fibroblast Growth Factors/physiology ; Glucuronidase/physiology ; Homeostasis/physiology ; Humans ; Klotho Proteins ; Phosphates/adverse effects ; Phosphates/metabolism ; Phosphates/toxicity
Chemical Substances	FGF23 protein, human ; Phosphates ; Fibroblast Growth Factors (62031-54-3) ; Fibroblast Growth Factor-23 (7Q7P4S7RRE) ; Glucuronidase (EC 3.2.1.31) ; Klotho Proteins (EC 3.2.1.31)
Language	English
Publishing date	2010-10-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	206835-7
ISSN	1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
ISSN (online)	1470-8736
ISSN	0301-0538 ; 0009-0360 ; 0143-5221
DOI	10.1042/CS20100377
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Article ; Online: The FGF23-Klotho axis: endocrine regulation of phosphate homeostasis.

Razzaque, M Shawkat

Nature reviews. Endocrinology

2009 Volume 5, Issue 11, Page(s) 611–619

Abstract: Appropriate levels of phosphate in the body are maintained by the coordinated regulation of the bone-derived growth factor FGF23 and the membrane-bound protein Klotho. The endocrine actions of FGF23, in association with parathyroid hormone and vitamin D, ...

Abstract	Appropriate levels of phosphate in the body are maintained by the coordinated regulation of the bone-derived growth factor FGF23 and the membrane-bound protein Klotho. The endocrine actions of FGF23, in association with parathyroid hormone and vitamin D, mobilize sodium-phosphate cotransporters that control renal phosphate transport in proximal tubular epithelial cells. The availability of an adequate amount of Klotho is essential for FGF23 to exert its phosphaturic effects in the kidney. In the presence of Klotho, FGF23 activates downstream signaling components that influence the homeostasis of phosphate, whereas in the absence of this membrane protein, it is unable to exert such regulatory effects, as demonstrated convincingly in animal models. Several factors, including phosphate and vitamin D, can regulate the production of both FGF23 and Klotho and influence their functions. In various acquired and genetic human diseases, dysregulation of FGF23 and Klotho is associated with vascular and skeletal anomalies owing to altered phosphate turnover. In this Review, I summarize how the endocrine effects of bone-derived FGF23, in coordination with Klotho, can regulate systemic phosphate homeostasis, and how an inadequate balance of these molecules can lead to complications that are caused by abnormal mineral ion metabolism.
MeSH term(s)	Fibroblast Growth Factors/blood ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Glucuronidase/genetics ; Glucuronidase/metabolism ; Homeostasis/genetics ; Homeostasis/physiology ; Humans ; Phosphates/metabolism ; Phosphates/physiology
Chemical Substances	Phosphates ; Fibroblast Growth Factors (62031-54-3) ; fibroblast growth factor 23 (7Q7P4S7RRE) ; Glucuronidase (EC 3.2.1.31) ; klotho protein (EC 3.2.1.31)
Language	English
Publishing date	2009-10-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2489381-X
ISSN	1759-5037 ; 1759-5029
ISSN (online)	1759-5037
ISSN	1759-5029
DOI	10.1038/nrendo.2009.196
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Article: Cisplatin nephropathy: is cytotoxicity avoidable?

Razzaque, M Shawkat

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2007 Volume 22, Issue 8, Page(s) 2112–2116

MeSH term(s)	Animals ; Antineoplastic Agents/adverse effects ; Cisplatin/adverse effects ; Humans ; Kidney Diseases/chemically induced ; Kidney Diseases/prevention & control ; MAP Kinase Kinase 4/metabolism ; Models, Biological ; Rats ; Swine
Chemical Substances	Antineoplastic Agents ; MAP Kinase Kinase 4 (EC 2.7.12.2) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2007-08
Publishing country	England
Document type	Comment ; Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gfm378
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Article: FGF23-mediated regulation of systemic phosphate homeostasis: is Klotho an essential player?

Razzaque, M Shawkat

American journal of physiology. Renal physiology

2008 Volume 296, Issue 3, Page(s) F470–6

Abstract: Understanding the physiological regulation of mineral ion metabolism is essential for determining the pathomechanisms of skeletal, vascular, and renal diseases associated with an abnormal regulation of calcium and phosphate homeostasis. Normal calcium ... ...

Abstract	Understanding the physiological regulation of mineral ion metabolism is essential for determining the pathomechanisms of skeletal, vascular, and renal diseases associated with an abnormal regulation of calcium and phosphate homeostasis. Normal calcium and phosphate balance is delicately maintained by endocrine factors that coordinate to influence the functions of the intestine, bone, parathyroid gland, and kidney. Under physiological conditions, the kidneys play an important role in maintaining normal mineral ion balance by fine-tuning the amount of urinary excretion of calcium and phosphate according to the body's needs. Fibroblast growth factor (FGF)23 regulates urinary phosphate excretion to maintain systemic phosphate homeostasis. The exact mode of action of the phosphaturic effects of FGF23 is not fully understood and is an intense area of research. Studies suggest, however, that FGF23, by interacting with FGF receptors, can initiate downstream signaling events and that Klotho, a transmembrane protein, facilitates the interaction of FGF23 with its receptor. FGF23 can inhibit the activities of 1-alpha-hydroxylase and sodium-phosphate cotransporter in the kidney to influence the overall systemic phosphate balance. This article briefly summarizes how FGF23 might coordinately regulate systemic phosphate homeostasis and how Klotho is involved in such regulation.
MeSH term(s)	Animals ; Fibroblast Growth Factors/metabolism ; Glucuronidase/metabolism ; Homeostasis ; Humans ; Kidney/metabolism ; Kidney Diseases/metabolism ; Phosphates/metabolism ; Signal Transduction ; Vitamin D/metabolism
Chemical Substances	Phosphates ; Vitamin D (1406-16-2) ; Fibroblast Growth Factors (62031-54-3) ; fibroblast growth factor 23 (7Q7P4S7RRE) ; Glucuronidase (EC 3.2.1.31) ; klotho protein (EC 3.2.1.31)
Language	English
Publishing date	2008-11-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603837-2
ISSN	1522-1466 ; 1931-857X ; 0363-6127
ISSN (online)	1522-1466
ISSN	1931-857X ; 0363-6127
DOI	10.1152/ajprenal.90538.2008
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Article ; Online: Can fibroblast growth factor 23 fine-tune therapies for diseases of abnormal mineral ion metabolism?

Razzaque, M Shawkat

Nature clinical practice. Endocrinology & metabolism

2007 Volume 3, Issue 12, Page(s) 788–789

MeSH term(s)	Animals ; Fibroblast Growth Factors/antagonists & inhibitors ; Fibroblast Growth Factors/blood ; Fibroblast Growth Factors/genetics ; Gene Silencing ; Humans ; Hyperparathyroidism/blood ; Metabolic Diseases/blood ; Metabolic Diseases/drug therapy ; Metabolic Diseases/genetics ; Phosphorus Metabolism Disorders/blood ; Phosphorus Metabolism Disorders/drug therapy ; Phosphorus Metabolism Disorders/genetics ; Vitamin D/blood
Chemical Substances	fibroblast growth factor 23 ; Vitamin D (1406-16-2) ; Fibroblast Growth Factors (62031-54-3)
Language	English
Publishing date	2007-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2228540-4
ISSN	1745-8374 ; 1745-8366
ISSN (online)	1745-8374
ISSN	1745-8366
DOI	10.1038/ncpendmet0667
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Article ; Online: Klotho and Na+,K+-ATPase activity: solving the calcium metabolism dilemma?

Razzaque, M Shawkat

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2007 Volume 23, Issue 2, Page(s) 459–461

MeSH term(s)	Animals ; Calcium/metabolism ; Glucuronidase/metabolism ; Homeostasis ; Humans ; Mice ; Parathyroid Hormone/physiology ; Sodium-Potassium-Exchanging ATPase/metabolism
Chemical Substances	Parathyroid Hormone ; Glucuronidase (EC 3.2.1.31) ; klotho protein (EC 3.2.1.31) ; Sodium-Potassium-Exchanging ATPase (EC 7.2.2.13) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2007-10-31
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gfm702
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Article: Does renal ageing affect survival?

Razzaque, M Shawkat

Ageing research reviews

2007 Volume 6, Issue 3, Page(s) 211–222

Abstract: The effects of ageing on progressive deterioration of renal function, both in human and experimental animals, are described elsewhere, but the effect of renal damage on overall survival and longevity is not yet clearly established. The wild-type animals ... ...

Abstract	The effects of ageing on progressive deterioration of renal function, both in human and experimental animals, are described elsewhere, but the effect of renal damage on overall survival and longevity is not yet clearly established. The wild-type animals of various genetic backgrounds, fed with regular diet, overtime develop severe age-associated nephropathy, that include but not limited to inflammatory cell infiltration, glomerulosclerosis, and tubulointerstitial fibrosis. Such renal damage significantly reduces their survival. Reducing renal damage, either by caloric restriction or by suppressing growth hormone (GH)/insulin-like growth factor-1 (IGF-1) activity could significantly enhance the longevity of these animals. Available survival studies using experimental animals clearly suggest that kidney pathology is one of the important non-neoplastic lesions that could affect overall survival, and that restoration of renal function by preventing kidney damage could significantly extend longevity. Careful long-term studies are needed to determine the human relevance of these experimental studies.
MeSH term(s)	Aging/pathology ; Aging/physiology ; Animals ; Food Deprivation/physiology ; Glycation End Products, Advanced/metabolism ; Growth Hormone/antagonists & inhibitors ; Growth Hormone/metabolism ; Humans ; Insulin-Like Growth Factor I/antagonists & inhibitors ; Insulin-Like Growth Factor I/metabolism ; Kidney/metabolism ; Kidney/physiopathology ; Kidney Diseases/complications ; Kidney Diseases/physiopathology ; Kidney Diseases/prevention & control ; Kidney Tubules/metabolism ; Kidney Tubules/physiopathology ; Longevity/physiology ; Oxidative Stress/physiology
Chemical Substances	Glycation End Products, Advanced ; Insulin-Like Growth Factor I (67763-96-6) ; Growth Hormone (9002-72-6)
Language	English
Publishing date	2007-10
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2075672-0
ISSN	1872-9649 ; 1568-1637
ISSN (online)	1872-9649
ISSN	1568-1637
DOI	10.1016/j.arr.2007.06.001
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