title: Excess dietary methionine does not affect fracture healing in mice.
abstract: BACKGROUND
  An elevated serum concentration of homocysteine (hyperhomocysteinemia) has been shown to disturb fracture healing. As the essential amino acid, methionine, is a precursor of homocysteine, we aimed to investigate whether excess methionine intake affects bone repair.
  
  
  METHODS
  We analyzed bone repair in 2 groups of mice. One group was fed a methionine-rich diet (n=13), and the second group received an equicaloric control diet without methionine supplementation (n=12). Using a closed femoral fracture model, bone repair was analyzed by histomorphometry and biomechanical testing at 4 weeks after fracture. Blood was sampled to measure serum concentrations of homocysteine, the bone formation marker osteocalcin, and the bone resorption marker collagen I C-terminal crosslaps
  
  
  RESULTS
  Serum concentrations of homocysteine were significantly higher in the methionine group than in the control group, while serum markers of bone turnover did not differ significantly between the 2 groups. Histomorphometry revealed no significant differences in size and tissue composition of the callus between animals fed the methionine-enriched diet and those receiving the control diet. Accordingly, animals of the 2 groups showed a comparable bending stiffness of the healing bones.
  
  
  CONCLUSIONS
  We conclude that excess methionine intake causes hyperhomocysteinemia, but does not affect fracture healing in mice.
authors.affiliation: Department of Trauma, Hand and Reconstructive Surgery, University of Saarland, Homburg/Saar, Germany. joerg.holstein@uks.eu
authors.forename: Joerg H
authors.initials: JH
authors.lastname: Holstein
authors.forename: Julia
authors.initials: J
authors.lastname: Schmalenbach
authors.forename: Markus
authors.initials: M
authors.lastname: Herrmann
authors.forename: Ilona
authors.initials: I
authors.lastname: Ölkü
authors.forename: Patric
authors.initials: P
authors.lastname: Garcia
authors.forename: Tina
authors.initials: T
authors.lastname: Histing
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Herrmann
authors.forename: Michael D
authors.initials: MD
authors.lastname: Menger
authors.forename: Tim
authors.initials: T
authors.lastname: Pohlemann
authors.forename: Lutz
authors.initials: L
authors.lastname: Claes
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena / Q000187:drug effects; D024042:Collagen Type I / Q000097:blood; D004032:Diet; D019587:Dietary Supplements; D005269:Femur / Q000000981:diagnostic imaging / Q000187:drug effects / Q000473:pathology; D017102:Fracture Healing / Q000187:drug effects*; D006710:Homocysteine / Q000097:blood; D053858:Metabolic Networks and Pathways / Q000187:drug effects; D008715:Methionine / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D051379:Mice; D015675:Osteocalcin / Q000097:blood; D010455:Peptides / Q000097:blood; D011859:Radiography
chemical_list: D024042:Collagen Type I; D010455:Peptides; C052929:collagen type I trimeric cross-linked peptide; D006710:Homocysteine; D015675:Osteocalcin; D008715:Methionine