title: Mechanisms of reduced and compensatory growth.
abstract: Growth is an integrated process, resulting from the response of cells dependent on the endocrine status and nutrient availability. During feed restriction, the production and secretion of growth hormone (GH) by the pituitary gland are enhanced, but the number of GH receptors decreases. Changes of GH binding proteins induce GH resistance and are followed by reduced insulin-like growth factor-I (IGF-I) secretion. On the other hand, high circulating levels of GH enhance the mobilization of fatty acids, which are used to support energy requirements. Thus, when feed restriction in growing animals is moderate, there is mainly protein but barely fat accretion. By contrast, a severe feed restriction enhances the release of catabolic hormones and stimulates, from muscle cells, the liberation of amino acids, which are used by hepatocytes for gluconeogenesis. During refeeding and compensatory growth, the secretion of insulin is sharply enhanced and plasma GH concentrations remain high. This situation probably allows more nutrients to be used for growth processes. The role of plasma IGF-I during compensatory growth is not clear and must be explained in connection with changes of its binding proteins. Thyroxin and 3,5,3'-triiodothyronine seem to have a permissive effect on growth. The simultaneous occurrence of puberty with refeeding can exert a synergistic effect on growth. Initially, compensatory growth is characterized by the deposition of very lean tissue, similar as during feed restriction. This lasts for some weeks. Then, protein synthesis decreases and high feed intake leads to increased fat deposition.
authors.affiliation: Nutrition Unit, Faculty of Veterinary Medicine, University of Liège, B-4000 Liège, Sart-Tilman, Belgium. jlhornick@ulg.ac.be
authors.forename: J L
authors.initials: JL
authors.lastname: Hornick
authors.forename: C
authors.initials: C
authors.lastname: Van Eenaeme
authors.forename: O
authors.initials: O
authors.lastname: Gérard
authors.forename: I
authors.initials: I
authors.lastname: Dufrasne
authors.forename: L
authors.initials: L
authors.lastname: Istasse
mesh_terms: D000818:Animals; D001823:Body Composition; D002417:Cattle / Q000254:growth & development* / Q000502:physiology; D004435:Eating; D005260:Female; D006130:Growth Disorders / Q000503:physiopathology / Q000662:veterinary*; D013006:Growth Hormone / Q000502:physiology; D007328:Insulin / Q000502:physiology; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000502:physiology; D007334:Insulin-Like Growth Factor I / Q000502:physiology; D008297:Male; D011986:Receptors, Somatotropin / Q000502:physiology; D013974:Thyroxine / Q000502:physiology; D014284:Triiodothyronine / Q000502:physiology; D015431:Weight Loss
chemical_list: D007328:Insulin; D018972:Insulin-Like Growth Factor Binding Protein 3; D011986:Receptors, Somatotropin; D014284:Triiodothyronine; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D013974:Thyroxine