PMID- 19056526
OWN - NLM
STAT- MEDLINE
DCOM- 20090406
LR  - 20131121
IS  - 1873-2763 (Electronic)
IS  - 1873-2763 (Linking)
VI  - 44
IP  - 3
DP  - 2009 Mar
TI  - Hyperhomocysteinemia induces a tissue specific accumulation of homocysteine in 
      bone by collagen binding and adversely affects bone.
PG  - 467-75
LID - 10.1016/j.bone.2008.10.051 [doi]
AB  - BACKGROUND: Recently, hyperhomocysteinemia (HHCY) has been suggested to have 
      adverse effects on bone. This study investigated if an experimental HHCY in rats 
      induces an accumulation of homocysteine (HCY) in bone tissue that is accompanied 
      by bone loss and reduced bone strength. MATERIAL AND METHODS: HHCY was induced in 
      healthy rats by either a methionine (Meth)- or a homocystine (Homo)-enriched diet 
      and compared with controls. Homocystine is the product of two disulfide linked 
      HCY molecules. Tissue and plasma concentrations of HCY, S-adenosylhomocysteine 
      (SAH) and S-adenosylmethionine (SAM) were measured. Bones were assessed by 
      biomechanical testing, histomorphometry, microCT and the measurement of 
      biochemical bone turnover markers in plasma. RESULTS: Meth and Homo animals 
      developed a significant HHCY that was accompanied by a tissue specific 
      accumulation of HCY (1300 to 2000% vs. controls). 65% of HCY in bone was bound to 
      collagen of the extracellular matrix. The SAH / SAM-ratio in bone and plasma of 
      Meth and Homo animals exhibited a tissue specific increase indicating a reduced 
      methylation capacity. Accumulation of HCY in bone was characterized by a distinct 
      reduction of cancellous bone (proximal femur: -25 to -35%; distal femur -56 to 
      -58%, proximal tibia: -28 to -43%). Accordingly, bone strength was significantly 
      reduced (-9 to -12%). CONCLUSION: A tissue specific accumulation of HCY in bone 
      may be a promising mechanism explaining adverse effects of HHCY on bone. A 
      reduced methylation capacity of bone cells might be another relevant 
      pathomechanism.
FAU - Herrmann, Markus
AU  - Herrmann M
AD  - Department of Clinical Chemistry and Laboratory Medicine, University Hospital of 
      Saarland, Homburg, Germany. markusherr@aol.com
FAU - Tami, Andrea
AU  - Tami A
FAU - Wildemann, Britt
AU  - Wildemann B
FAU - Wolny, Martin
AU  - Wolny M
FAU - Wagner, Alexandra
AU  - Wagner A
FAU - Schorr, Heike
AU  - Schorr H
FAU - Taban-Shomal, Omid
AU  - Taban-Shomal O
FAU - Umanskaya, Natalia
AU  - Umanskaya N
FAU - Ross, Steffen
AU  - Ross S
FAU - Garcia, Patric
AU  - Garcia P
FAU - Hubner, Ulrich
AU  - Hubner U
FAU - Herrmann, Wolfgang
AU  - Herrmann W
LA  - eng
PT  - Journal Article
DEP - 20081112
PL  - United States
TA  - Bone
JT  - Bone
JID - 8504048
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 462-10-2 (Homocystine)
RN  - 7LP2MPO46S (S-Adenosylmethionine)
RN  - 9007-34-5 (Collagen)
RN  - 979-92-0 (S-Adenosylhomocysteine)
RN  - AE28F7PNPL (Methionine)
SB  - IM
MH  - Aged
MH  - Animals
MH  - Bone and Bones/anatomy & histology/chemistry/*metabolism/pathology
MH  - Collagen/*metabolism
MH  - Female
MH  - Homocysteine/*metabolism
MH  - Homocystine/administration & dosage
MH  - Humans
MH  - Hyperhomocysteinemia/chemically induced/*metabolism
MH  - Male
MH  - Methionine/administration & dosage
MH  - Myocardium/chemistry
MH  - Osteoporosis/metabolism
MH  - Porosity
MH  - Rats
MH  - Rats, Wistar
MH  - S-Adenosylhomocysteine/metabolism
MH  - S-Adenosylmethionine/metabolism
MH  - Stress, Mechanical
EDAT- 2008/12/06 09:00
MHDA- 2009/04/07 09:00
CRDT- 2008/12/06 09:00
PHST- 2008/07/23 00:00 [received]
PHST- 2008/10/20 00:00 [revised]
PHST- 2008/10/22 00:00 [accepted]
PHST- 2008/12/06 09:00 [entrez]
PHST- 2008/12/06 09:00 [pubmed]
PHST- 2009/04/07 09:00 [medline]
AID - S8756-3282(08)00865-X [pii]
AID - 10.1016/j.bone.2008.10.051 [doi]
PST - ppublish
SO  - Bone. 2009 Mar;44(3):467-75. doi: 10.1016/j.bone.2008.10.051. Epub 2008 Nov 12.