Bone as an endocrine organ

被引:237
作者
Fukumoto, Seiji [1 ]
Martin, T. John [2 ]
机构
[1] Tokyo Univ Hosp, Div Nephrol & Endocrinol, Dept Med, Bunkyo Ku, Tokyo 1138655, Japan
[2] Univ Melbourne, Dept Med, St Vincents Inst Med Res, Fitzroy, Vic 3065, Australia
关键词
FAMILIAL TUMORAL CALCINOSIS; FIBROBLAST-GROWTH-FACTOR; ONCOGENIC OSTEOMALACIA; REGULATING PHOSPHATE; PARATHYROID-HORMONE; INSULIN-SECRETION; MISSENSE MUTATION; ENERGY-METABOLISM; SERUM OSTEOCALCIN; DIETARY PHOSPHATE;
D O I
10.1016/j.tem.2009.02.001
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Although bone has long been recognized as a target for hormones influencing calcium and phosphorus homeostasis and bone structure, recent evidence shows that the skeleton itself produces at least two hormones, fibroblast growth factor 23 (FGF23) and osteocalcin. FGF23 is produced by osteocytes in bone and acts on the kidney to inhibit 1 alpha-hydroxylation of vitamin D and promote phosphorus excretion. Mouse genetics studies revealed that the osteoblast product, osteocalcin, acts on the pancreatic beta-cell to enhance insulin production and on peripheral tissues to increase glucose utilizations a result of increased insulin sensitivity and to reduce visceral fat. This review highlights the recent studies indicating bone's role as an endocrine organ.
引用
收藏
页码:230 / 236
页数:7
相关论文
共 66 条
[1]   A novel mutation in fibroblast growth factor 23 gene as a cause of tumoral calcinosis [J].
Araya, K ;
Fukumoto, S ;
Backenroth, R ;
Takeuchi, Y ;
Nakayama, K ;
Ito, N ;
Yoshii, N ;
Yamazaki, Y ;
Yamashita, T ;
Silver, J ;
Igarashi, T ;
Fujita, T .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2005, 90 (10) :5523-5527
[2]   The renal Na+/phosphate cotransporter NaPi-IIa is internalized via the receptor-mediated endocytic route in response to parathyroid hormone [J].
Bacic, D ;
LeHir, M ;
Biber, J ;
Kaissling, B ;
Murer, H ;
Wagner, CA .
KIDNEY INTERNATIONAL, 2006, 69 (03) :495-503
[3]   Pex/PEX tissue distribution and evidence for a deletion in the 3' region of the Pex gene in X-linked hypophosphatemic mice [J].
Beck, L ;
Soumounou, Y ;
Martel, J ;
Krishnamurthy, G ;
Gauthier, C ;
Goodyer, CG ;
Tenenhouse, HS .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 99 (06) :1200-1209
[4]   The parathyroid is a target organ for FGF23 in rats [J].
Ben-Dov, Iddo Z. ;
Galitzer, Hillel ;
Lavi-Moshayoff, Vardit ;
Goetz, Regina ;
Kuro-o, Makoto ;
Mohammadi, Moosa ;
Sirkis, Roy ;
Naveh-Many, Tally ;
Silver, Justin .
JOURNAL OF CLINICAL INVESTIGATION, 2007, 117 (12) :4003-4008
[5]   An FGF23 missense mutation causes familial tumoral calcinosis with hyperphosphatemia [J].
Benet-Pagès, A ;
Orlik, P ;
Strom, TM ;
Lorenz-Depiereux, B .
HUMAN MOLECULAR GENETICS, 2005, 14 (03) :385-390
[6]   FGF23 is processed by proprotein convertases but not by PHEX [J].
Beret-Pagès, A ;
Lorenz-Depiereux, B ;
Zischka, H ;
White, KE ;
Econs, MJ ;
Strom, TM .
BONE, 2004, 35 (02) :455-462
[7]   Secreted frizzled-related protein 4 is a potent tumor-derived phosphaturic agent [J].
Berndt, T ;
Craig, TA ;
Bowe, AE ;
Vassiliadis, J ;
Reczek, D ;
Finnegan, R ;
De Beur, SMJ ;
Schiavi, SC ;
Kumar, R .
JOURNAL OF CLINICAL INVESTIGATION, 2003, 112 (05) :785-794
[8]   SOST/sclerostin, an osteocyte-derived negative regulator of bone formation [J].
Bezooijen, RL ;
ten Dijke, P ;
Papapoulos, SE ;
Löwik, CWGM .
CYTOKINE & GROWTH FACTOR REVIEWS, 2005, 16 (03) :319-327
[9]   Osteocyte messages from a bony tomb [J].
Bonewald, Lynda F. .
CELL METABOLISM, 2007, 5 (06) :410-411
[10]   Fibroblast growth factor 7: An inhibitor of phosphate transport derived from oncogenic osteomalacia-causing tumors [J].
Carpenter, TO ;
Ellis, BK ;
Insogna, KL ;
Philbrick, WM ;
Sterpka, J ;
Shimkets, R .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2005, 90 (02) :1012-1020