PMID- 17586593
OWN - NLM
STAT- MEDLINE
DCOM- 20070904
LR  - 20190722
IS  - 0009-9147 (Print)
IS  - 0009-9147 (Linking)
VI  - 53
IP  - 8
DP  - 2007 Aug
TI  - Experimental hyperhomocysteinemia reduces bone quality in rats.
PG  - 1455-61
AB  - BACKGROUND: Recently, hyperhomocysteinemia (HHCY) has been suggested as a new 
      risk factor for osteoporosis. This study investigated if HHCY is a causal 
      osteoporotic factor in vivo. METHODS: We used 3 groups of rats: a control group 
      (n = 20), a moderate HHCY group (induced by a 2.4% methionine-enriched diet, n = 
      10), and an intermediate HHCY group (induced by a 2% homocystine-enriched diet, n 
      = 10). We measured bone fragility [maximum force of an axial compression test 
      (F(max))], bone area as percentage of total area (BAr/TAr, histomorphometry), and 
      biochemical bone turnover markers [osteocalcin (OC) and collagen I C-terminal 
      crosslaps (CTx)]. RESULTS: Compared with controls, 3 months of moderate or 
      intermediate HHCY increased mean (SD) bone fragility at the femoral neck by 18% 
      (6%) in methionine-fed (P = 0.001) and 36% (13%) in homocystine-fed rats (P 
      <0.001). Mean (SD) BAr/TAr at the distal femur in methionine and homocystine 
      groups was decreased by 45% (21%; P = 0.001) and 93% (9%; P = 0.001), 
      respectively. At the femoral neck, BAr/TAr was decreased by 19% (11%; P <0.001) 
      and 55% (19%; P <0.001). At the lumbar spine, the reduction of BAr/TAr was 17% 
      (23%; P = 0.099) and 44% (19%; P <0.001). Plasma OC (bone formation marker) was 
      decreased by 23% (20%; P = 0.006) and 34% (21%; P <0.001). Plasma CTx (bone 
      resorption marker) did not differ between groups. CONCLUSION: Bone quality is 
      consistently decreased in the presence of increased circulating homocysteine. The 
      results provide evidence that HHCY is a causal osteoporotic factor.
FAU - Herrmann, Markus
AU  - Herrmann M
AD  - Department of Clinical Chemistry and Laboratory Medicine, University Hospital of 
      Saarland, Homburg/Saar, Germany.
FAU - Wildemann, Britt
AU  - Wildemann B
FAU - Claes, Lutz
AU  - Claes L
FAU - Klohs, Stefan
AU  - Klohs S
FAU - Ohnmacht, Michael
AU  - Ohnmacht M
FAU - Taban-Shomal, Omid
AU  - Taban-Shomal O
FAU - Hubner, Ulrich
AU  - Hubner U
FAU - Pexa, Anette
AU  - Pexa A
FAU - Umanskaya, Natalia
AU  - Umanskaya N
FAU - Herrmann, Wolfgang
AU  - Herrmann W
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20070622
PL  - England
TA  - Clin Chem
JT  - Clinical chemistry
JID - 9421549
RN  - 0 (Biomarkers)
SB  - IM
MH  - Animals
MH  - Biomarkers/blood
MH  - Compressive Strength
MH  - Female
MH  - Femoral Fractures/*etiology/pathology/physiopathology
MH  - Femur/*metabolism/pathology/*physiopathology
MH  - Fractures, Compression/etiology/pathology/physiopathology
MH  - Hyperhomocysteinemia/complications/*metabolism/pathology/*physiopathology
MH  - Osteogenesis
MH  - Osteoporosis/etiology
MH  - Rats
MH  - Rats, Wistar
MH  - Risk Factors
EDAT- 2007/06/26 09:00
MHDA- 2007/09/05 09:00
CRDT- 2007/06/26 09:00
PHST- 2007/06/26 09:00 [pubmed]
PHST- 2007/09/05 09:00 [medline]
PHST- 2007/06/26 09:00 [entrez]
AID - clinchem.2007.086272 [pii]
AID - 10.1373/clinchem.2007.086272 [doi]
PST - ppublish
SO  - Clin Chem. 2007 Aug;53(8):1455-61. doi: 10.1373/clinchem.2007.086272. Epub 2007 
      Jun 22.