Growth Hormone, Insulin-Like Growth Factors, and the Skeleton
Andrea Giustina,
Gherardo Mazziotti and
Ernesto Canalis
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 andare central to the achievement of normal longitudinal bone growthand bone mass. Although GH may act directly on skeletal cells,most of its effects are mediated by IGF-I, which is presentin the systemic circulation and is synthesized by peripheraltissues. The availability of IGF-I is regulated by IGF bindingproteins. IGF-I enhances the differentiated function of theosteoblast and bone formation. Adult GH deficiency causes lowbone turnover osteoporosis with high risk of vertebral and nonvertebralfractures, and the low bone mass can be partially reversed byGH replacement. Acromegaly is characterized by high bone turnover,which can lead to bone loss and vertebral fractures, particularlyin patients with coexistent hypogonadism. GH and IGF-I secretionare decreased in aging individuals, and abnormalities in theGH/IGF-I axis play a role in the pathogenesis of the osteoporosisof anorexia nervosa and after glucocorticoid exposure.
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