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Leptin inhibits bone formation through a hypothalamic relay: a central control of bone mass.

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Leptin inhibits bone formation through a hypothalamic relay: a central control of bone mass. / Ducy, P; Amling, M; Takeda, S; Priemel, M; Schilling, A F; Beil, F T; Shen, J; Vinson, C; Rueger, J M; Karsenty, G.

In: CELL, Vol. 100, No. 2, 2, 21.01.2000, p. 197-207.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Ducy, P, Amling, M, Takeda, S, Priemel, M, Schilling, AF, Beil, FT, Shen, J, Vinson, C, Rueger, JM & Karsenty, G 2000, 'Leptin inhibits bone formation through a hypothalamic relay: a central control of bone mass.', CELL, vol. 100, no. 2, 2, pp. 197-207. https://doi.org/10.1016/s0092-8674(00)81558-5

APA

Ducy, P., Amling, M., Takeda, S., Priemel, M., Schilling, A. F., Beil, F. T., Shen, J., Vinson, C., Rueger, J. M., & Karsenty, G. (2000). Leptin inhibits bone formation through a hypothalamic relay: a central control of bone mass. CELL, 100(2), 197-207. [2]. https://doi.org/10.1016/s0092-8674(00)81558-5

Vancouver

Ducy P, Amling M, Takeda S, Priemel M, Schilling AF, Beil FT et al. Leptin inhibits bone formation through a hypothalamic relay: a central control of bone mass. CELL. 2000 Jan 21;100(2):197-207. 2. https://doi.org/10.1016/s0092-8674(00)81558-5

Bibtex

@article{12fc76abd17543a097c08ee47541c890,
title = "Leptin inhibits bone formation through a hypothalamic relay: a central control of bone mass.",
abstract = "Gonadal failure induces bone loss while obesity prevents it. This raises the possibility that bone mass, body weight, and gonadal function are regulated by common pathways. To test this hypothesis, we studied leptin-deficient and leptin receptor-deficient mice that are obese and hypogonadic. Both mutant mice have an increased bone formation leading to high bone mass despite hypogonadism and hypercortisolism. This phenotype is dominant, independent of the presence of fat, and specific for the absence of leptin signaling. There is no leptin signaling in osteoblasts but intracerebroventricular infusion of leptin causes bone loss in leptin-deficient and wild-type mice. This study identifies leptin as a potent inhibitor of bone formation acting through the central nervous system and therefore describes the central nature of bone mass control and its disorders.",
keywords = "Animals, Bone Density, Bone Remodeling, Carrier Proteins, Cells, Cultured, Hypothalamus, Injections, Intraventricular, Leptin, Mice, Mice, Inbred C57BL, Mice, Obese, Mice, Transgenic, Neuropeptide Y, Obesity, Osteoblasts, Osteoclasts, Osteoporosis, Phenotype, Receptors, Cell Surface, Receptors, Leptin, Signal Transduction",
author = "P Ducy and M Amling and S Takeda and M Priemel and Schilling, {A F} and Beil, {F T} and J Shen and C Vinson and Rueger, {J M} and G Karsenty",
year = "2000",
month = jan,
day = "21",
doi = "10.1016/s0092-8674(00)81558-5",
language = "English",
volume = "100",
pages = "197--207",
journal = "CELL",
issn = "0092-8674",
publisher = "Cell Press",
number = "2",

}

RIS

TY - JOUR

T1 - Leptin inhibits bone formation through a hypothalamic relay: a central control of bone mass.

AU - Ducy, P

AU - Amling, M

AU - Takeda, S

AU - Priemel, M

AU - Schilling, A F

AU - Beil, F T

AU - Shen, J

AU - Vinson, C

AU - Rueger, J M

AU - Karsenty, G

PY - 2000/1/21

Y1 - 2000/1/21

N2 - Gonadal failure induces bone loss while obesity prevents it. This raises the possibility that bone mass, body weight, and gonadal function are regulated by common pathways. To test this hypothesis, we studied leptin-deficient and leptin receptor-deficient mice that are obese and hypogonadic. Both mutant mice have an increased bone formation leading to high bone mass despite hypogonadism and hypercortisolism. This phenotype is dominant, independent of the presence of fat, and specific for the absence of leptin signaling. There is no leptin signaling in osteoblasts but intracerebroventricular infusion of leptin causes bone loss in leptin-deficient and wild-type mice. This study identifies leptin as a potent inhibitor of bone formation acting through the central nervous system and therefore describes the central nature of bone mass control and its disorders.

AB - Gonadal failure induces bone loss while obesity prevents it. This raises the possibility that bone mass, body weight, and gonadal function are regulated by common pathways. To test this hypothesis, we studied leptin-deficient and leptin receptor-deficient mice that are obese and hypogonadic. Both mutant mice have an increased bone formation leading to high bone mass despite hypogonadism and hypercortisolism. This phenotype is dominant, independent of the presence of fat, and specific for the absence of leptin signaling. There is no leptin signaling in osteoblasts but intracerebroventricular infusion of leptin causes bone loss in leptin-deficient and wild-type mice. This study identifies leptin as a potent inhibitor of bone formation acting through the central nervous system and therefore describes the central nature of bone mass control and its disorders.

KW - Animals

KW - Bone Density

KW - Bone Remodeling

KW - Carrier Proteins

KW - Cells, Cultured

KW - Hypothalamus

KW - Injections, Intraventricular

KW - Leptin

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Obese

KW - Mice, Transgenic

KW - Neuropeptide Y

KW - Obesity

KW - Osteoblasts

KW - Osteoclasts

KW - Osteoporosis

KW - Phenotype

KW - Receptors, Cell Surface

KW - Receptors, Leptin

KW - Signal Transduction

U2 - 10.1016/s0092-8674(00)81558-5

DO - 10.1016/s0092-8674(00)81558-5

M3 - SCORING: Journal article

C2 - 10660043

VL - 100

SP - 197

EP - 207

JO - CELL

JF - CELL

SN - 0092-8674

IS - 2

M1 - 2

ER -