title: Genetic background influences metabolic response to dietary phosphorus restriction.
abstract: Dietary phosphorus (P) is essential to bone growth and turnover; however, little research has focused on the genetic mechanisms controlling P utilization. Understanding the interactions between genetics and dietary P that optimize bone integrity could provide novel interventions for osteoporosis. Thirty-six pigs from two sire lines known to differ in bone structure [heavier boned (HB) and lighter boned (LB)] were assigned to one of the three diets (P adequate, P repletion or P deficient). After 14 days, bone marrow and intact radial bones were collected. Differences between these lines in growth rate, bone integrity and gene expression within bone marrow were observed. In HB, but not LB, pigs, the P-deficient diet decreased weight gain (P<.01). For both lines, P deficiency caused a reduction in radial bone strength (P<.01), but HB P-deficient animals had greater (P<.10) bone integrity than P-deficient LB pigs. In HB, but not LB, pigs, dietary treatment affected the expression of CALCR (calcitonin receptor) (P<.05), VDR (vitamin D receptor) (P<.04) and IGFBP3 (insulin-like growth factor binding protein 3) (P<.06). There was also a trend of increased IL6 (interleukin-6), TFIIB (transcription initiation factor IIB) and SOX9 (sex determining region Y-box 9) expression with P deficiency in HB, but not LB, pigs. Both genetic backgrounds responded similarly to P deficiency with an increase in the expression of OXTR (oxytocin receptor) and IGF1 (insulin-like growth factor 1). Differences in growth rate, bone integrity and gene expression within the bone marrow suggest a difference in the homeorhetic control of P utilization between these genetic lines. Understanding these differences could lead to novel treatments for osteoporosis and aid in the development of tests for identifying those at risk for this disease.
authors.affiliation: Department of Animal Science and Center for Integrated Animal Genomics, Iowa State University, Ames, IA 50011, USA.
authors.forename: Laura J
authors.initials: LJ
authors.lastname: Hittmeier
authors.forename: Laura
authors.initials: L
authors.lastname: Grapes
authors.forename: Renae L
authors.initials: RL
authors.lastname: Lensing
authors.forename: Max F
authors.initials: MF
authors.lastname: Rothschild
authors.forename: Chad H
authors.initials: CH
authors.lastname: Stahl
mesh_terms: D000818:Animals; D001842:Bone and Bones / Q000503:physiopathology; D002118:Calcium / Q000097:blood; D005260:Female; D005838:Genotype; D006609:High Mobility Group Proteins / Q000235:genetics; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000235:genetics; D007334:Insulin-Like Growth Factor I / Q000235:genetics; D010024:Osteoporosis / Q000235:genetics*; D010758:Phosphorus / Q000172:deficiency*; D016226:Phosphorus, Dietary / Q000008:administration & dosage*; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis; D018003:Receptors, Calcitonin / Q000235:genetics; D018167:Receptors, Calcitriol / Q000235:genetics; D018045:Receptors, Oxytocin / Q000235:genetics; D055758:SOX9 Transcription Factor; D013552:Swine; D013718:Tensile Strength; D035581:Transcription Factor TFIIB / Q000235:genetics; D014157:Transcription Factors / Q000235:genetics
chemical_list: D006609:High Mobility Group Proteins; D018972:Insulin-Like Growth Factor Binding Protein 3; D016226:Phosphorus, Dietary; D012333:RNA, Messenger; D018003:Receptors, Calcitonin; D018167:Receptors, Calcitriol; D018045:Receptors, Oxytocin; D055758:SOX9 Transcription Factor; D035581:Transcription Factor TFIIB; D014157:Transcription Factors; D010758:Phosphorus; D007334:Insulin-Like Growth Factor I; D002118:Calcium