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      The role of liver-derived insulin-like growth factor-I.

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          Abstract

          IGF-I is expressed in virtually every tissue of the body, but with much higher expression in the liver than in any other tissue. Studies using mice with liver-specific IGF-I knockout have demonstrated that liver-derived IGF-I, constituting a major part of circulating IGF-I, is an important endocrine factor involved in a variety of physiological and pathological processes. Detailed studies comparing the impact of liver-derived IGF-I and local bone-derived IGF-I demonstrate that both sources of IGF-I can stimulate longitudinal bone growth. We propose here that liver-derived circulating IGF-I and local bone-derived IGF-I to some extent have overlapping growth-promoting effects and might have the capacity to replace each other (= redundancy) in the maintenance of normal longitudinal bone growth. Importantly, and in contrast to the regulation of longitudinal bone growth, locally derived IGF-I cannot replace (= lack of redundancy) liver-derived IGF-I for the regulation of a large number of other parameters including GH secretion, cortical bone mass, kidney size, prostate size, peripheral vascular resistance, spatial memory, sodium retention, insulin sensitivity, liver size, sexually dimorphic liver functions, and progression of some tumors. It is clear that a major role of liver-derived IGF-I is to regulate GH secretion and that some, but not all, of the phenotypes in the liver-specific IGF-I knockout mice are indirect, mediated via the elevated GH levels. All of the described multiple endocrine effects of liver-derived IGF-I should be considered in the development of possible novel treatment strategies aimed at increasing or reducing endocrine IGF-I activity.

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          Author and article information

          Journal
          Endocr Rev
          Endocrine reviews
          The Endocrine Society
          1945-7189
          0163-769X
          Aug 2009
          : 30
          : 5
          Affiliations
          [1 ] Division of Endocrinology, Institute of Medicine, Sahlgrenska University Hospital, Göteborg, Sweden. Claes.Ohlsson@medic.gu.se
          Article
          er.2009-0010
          10.1210/er.2009-0010
          2759708
          19589948
          3d09d4d2-911c-4dec-a09b-ed19b9a8f4d4
          History

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