A paradigm of integrative physiology, the crosstalk between bone and energy metabolisms

被引:169
作者
Confavreux, Cyrille B. [1 ,2 ]
Levine, Robert L. [1 ,3 ]
Karsenty, Gerard [1 ]
机构
[1] Columbia Univ, Coll Phys & Surg, Dept Genet & Dev, New York, NY 10032 USA
[2] Univ Lyon, Hosp Civils Lyon, INSERM, U831, F-69003 Lyon, France
[3] Columbia Univ, Med Ctr, Morgan Stanley Childrens Hosp New York Presbyteri, Div Pediat Endocrinol, New York, NY USA
关键词
Bone; Osteocalcin; Leptin; SNS; Energy metabolism; MITOCHONDRIAL UNCOUPLING PROTEIN; REFLEX SYMPATHETIC DYSTROPHY; BETA-ADRENERGIC RECEPTORS; ROS; 17/2.8; CELLS; LEPTIN REGULATION; MINERAL DENSITY; GLUCOSE-HOMEOSTASIS; INSULIN-RESISTANCE; CIRCADIAN-RHYTHM; GENE-EXPRESSION;
D O I
10.1016/j.mce.2009.04.004
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Thanks to integrative physiology, new relationships between organs and homeostatic functions have emerged. This approach to physiology based on a whole organism approach has allowed the bone field to make fundamental progress. In the last decade, clinical observations and scientific evidences in vivo have uncovered that fat with leptin controls bone mass through brain including a hypothalamic relay and sympathetic nervous system. The finding that energy metabolism affects bone remodelling suggested that in an endocrine perspective, a feedback loop should exist. Beside its classical functions, bone can now be considered as a true endocrine organ secreting osteocalcin, a hormone pharmacologically active on glucose and fat metabolism. Indeed osteocalcin stimulates insulin secretion and P-cell proliferation. Simultaneously, osteocalcin acts on adipocytes to induce Adiponectin which secondarily reduce insulin resistance. This cross regulation between bone and energy metabolism offers novel therapeutic targets in type 2 diabetes and osteoporosis. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:21 / 29
页数:9
相关论文
共 63 条
[1]   Body fat, leptin, and hypothalamic amenorrhea [J].
Ahima, RS .
NEW ENGLAND JOURNAL OF MEDICINE, 2004, 351 (10) :959-962
[2]   Leptin regulation of neuroendocrine systems [J].
Ahima, RS ;
Saper, CB ;
Flier, JS ;
Elmquist, JK .
FRONTIERS IN NEUROENDOCRINOLOGY, 2000, 21 (03) :263-307
[3]   Cart overexpression is the only identifiable cause of high bone mass in melanocortin 4 receptor deficiency [J].
Ahn, Jong Deok ;
Dubern, Beatrice ;
Lubrano-Berthelier, Cecile ;
Lubrano-Berthelier, Cecile ;
Clement, Karine ;
Karsenty, Gerard .
ENDOCRINOLOGY, 2006, 147 (07) :3196-3202
[4]   Leptin [J].
Auwerx, J ;
Staels, B .
LANCET, 1998, 351 (9104) :737-742
[5]  
COLEMAN DL, 1969, AM J PHYSIOL, V217, P1298
[6]   The pancreatic β cell is a key site for mediating the effects of leptin on glucose homeostasis [J].
Covey, Scott D. ;
Wideman, Rhonda D. ;
McDonald, Christine ;
Unniappan, Suraj ;
Huynh, Frank ;
Asadi, Ali ;
Speck, Madeleine ;
Webber, Travis ;
Chua, Streamson C. ;
Kieffer, Timothy J. .
CELL METABOLISM, 2006, 4 (04) :291-302
[7]   Mouse α1(I)-collagen promoter is the best known promoter to drive efficient Cre recombinase expression in osteoblast [J].
Dacquin, R ;
Starbuck, M ;
Schinke, T ;
Karsenty, G .
DEVELOPMENTAL DYNAMICS, 2002, 224 (02) :245-251
[8]   Knock-in of nuclear localised β-galactosidase reveals that the tyrosine phosphatase Ptprv is specifically expressed in cells of the bone collar [J].
Dacquin, R ;
Mee, PJ ;
Kawaguchi, J ;
Olmsted-Davis, EA ;
Gallagher, JA ;
Nichols, J ;
Lee, K ;
Karsenty, G ;
Smith, A .
DEVELOPMENTAL DYNAMICS, 2004, 229 (04) :826-834
[9]   Increased bone formation in osteocalcin-deficient mice [J].
Ducy, P ;
Desbois, C ;
Boyce, B ;
Pinero, G ;
Story, B ;
Dunstan, C ;
Smith, E ;
Bonadio, J ;
Goldstein, S ;
Gundberg, C ;
Bradley, A ;
Karsenty, G .
NATURE, 1996, 382 (6590) :448-452
[10]   Leptin inhibits bone formation through a hypothalamic relay: A central control of bone mass [J].
Ducy, P ;
Amling, M ;
Takeda, S ;
Priemel, M ;
Schilling, AF ;
Beil, FT ;
Shen, JH ;
Vinson, C ;
Rueger, JM ;
Karsenty, G .
CELL, 2000, 100 (02) :197-207