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Growth Hormone, Insulin-Like Growth Factors, and the Skeleton

Department of Medical and Surgical Sciences (A.G., G.M.), Chair of Internal Medicine, University of Brescia, 25125 Brescia, Italy; Department of Research, Saint Francis Hospital and Medical Center (E.C.), Hartford, Connecticut 06105; and The University of Connecticut School of Medicine (E.C.), Farmington, Connecticut 06030

Correspondence: Address all correspondence and requests for reprints to: Prof. Andrea Giustina, Department of Medical and Surgical Sciences, University of Brescia, c/o Endocrinology Service, Montichiari Hospital, Via Ciotti 154, 25018 Montichiari, Italy. E-mail: a.giustina{at}libero.it

GH and IGF-I are important regulators of bone homeostasis and are central to the achievement of normal longitudinal bone growth and bone mass. Although GH may act directly on skeletal cells, most of its effects are mediated by IGF-I, which is present in the systemic circulation and is synthesized by peripheral tissues. The availability of IGF-I is regulated by IGF binding proteins. IGF-I enhances the differentiated function of the osteoblast and bone formation. Adult GH deficiency causes low bone turnover osteoporosis with high risk of vertebral and nonvertebral fractures, and the low bone mass can be partially reversed by GH replacement. Acromegaly is characterized by high bone turnover, which can lead to bone loss and vertebral fractures, particularly in patients with coexistent hypogonadism. GH and IGF-I secretion are decreased in aging individuals, and abnormalities in the GH/IGF-I axis play a role in the pathogenesis of the osteoporosis of anorexia nervosa and after glucocorticoid exposure.

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