Regulation of skeletal growth and mineral acquisition by the GH/IGF-1 axis: Lessons from mouse models

• The growth hormone (GH) and its downstream mediator, the insulin-like growth factor-1 (IGF-1), construct a pleotropic axis affecting growth, metabolism, and organ function. Serum levels of GH/IGF-1 rise during pubertal growth and associate with peak bone acquisition, while during aging their levels decline and associate with bone loss. The GH/IGF-1 axis was extensively studied in numerous biological systems including rodent models and cell cultures. Both hormones act in an endocrine and autocrine/paracrine fashion and understanding their distinct and overlapping contributions to skeletal acquisition is still a matter of debate. GH and IGF-1 exert their effects on osteogenic cells via binding to their cognate receptor, leading to activation of an array of genes that mediate cellular differentiation and function. Both hormones interact with other skeletal regulators, such as sex steroids, thyroid hormone, and parathyroid hormone, to facilitate skeletal growth and metabolism. In this review we summarized several rodent models of the GH/IGF-1 axis and described key experiments that shed new light on the regulation of skeletal growth by the GH/IGF-1 axis. (C) 2015 Elsevier Ltd. All rights reserved.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Endokrinologi och diabetes (hsv//swe)

MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Endocrinology and Diabetes (hsv//eng)

Nyckelord

Growth hormone (GH)

Growth hormone receptor (GHR)

Insulin-like growth factor-1 (IGF-1)

Growth

estrogen-receptor-alpha

igf-i-receptor

unloading induces resistance

periosteal bone-formation

factor-binding protein-1

hormone transgenic

mice

osteoblast-like cells

strain gradients correlate

nitric-oxide

synthase

acid-labile subunit

Cell Biology

Endocrinology & Metabolism

chiara tm

1991

cell

v64

p849

wellbraxton l

1993

role of insulin-like growth factors in the nervous systemsconf

wellbraxton l

1993

genes & development

v7

p2609

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