PMID- 21339911
OWN - NLM
STAT- MEDLINE
DCOM- 20110613
LR  - 20220408
IS  - 1178-2048 (Electronic)
IS  - 1176-6344 (Print)
IS  - 1176-6344 (Linking)
VI  - 7
DP  - 2011 Jan 25
TI  - Hyperhomocysteinemia decreases bone blood flow.
PG  - 31-5
LID - 10.2147/VHRM.S15844 [doi]
AB  - Elevated plasma levels of homocysteine (Hcy), known as hyperhomocysteinemia 
      (HHcy), are associated with osteoporosis. A decrease in bone blood flow is a 
      potential cause of compromised bone mechanical properties. Therefore, we 
      hypothesized that HHcy decreases bone blood flow and biomechanical properties. To 
      test this hypothesis, male Sprague-Dawley rats were treated with Hcy (0.67 g/L) 
      in drinking water for 8 weeks. Age-matched rats served as controls. At the end of 
      the treatment period, the rats were anesthetized. Blood samples were collected 
      from experimental or control rats. Biochemical turnover markers (body weight, 
      Hcy, vitamin B(12), and folate) were measured. Systolic blood pressure was 
      measured from the right carotid artery. Tibia blood flow was measured by laser 
      Doppler flow probe. The results indicated that Hcy levels were significantly 
      higher in the Hcy-treated group than in control rats, whereas vitamin B(12) 
      levels were lower in the Hcy-treated group compared with control rats. There was 
      no significant difference in folate concentration and blood pressure in 
      Hcy-treated versus control rats. The tibial blood flow index of the control group 
      was significantly higher (0.78 +/- 0.09 flow unit) compared with the Hcy-treated 
      group (0.51 +/- 0.09). The tibial mass was 1.1 +/- 0.1 g in the control group and 0.9 
      +/- 0.1 in the Hcy-treated group. The tibia bone density was unchanged in 
      Hcy-treated rats. These results suggest that Hcy causes a reduction in bone blood 
      flow, which contributes to compromised bone biomechanical properties.
FAU - Tyagi, Neetu
AU  - Tyagi N
AD  - Department of Physiology and Biophysics, School of Medicine, University of 
      Louisville, KY, USA. n0tyag01@louisville.edu
FAU - Vacek, Thomas P
AU  - Vacek TP
FAU - Fleming, John T
AU  - Fleming JT
FAU - Vacek, Jonathan C
AU  - Vacek JC
FAU - Tyagi, Suresh C
AU  - Tyagi SC
LA  - eng
GR  - R01 HL071010/HL/NHLBI NIH HHS/United States
GR  - R01 NS051568/NS/NINDS NIH HHS/United States
GR  - HL-71010/HL/NHLBI NIH HHS/United States
GR  - NS-51568/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20110125
PL  - New Zealand
TA  - Vasc Health Risk Manag
JT  - Vascular health and risk management
JID - 101273479
RN  - 0 (Biomarkers)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 935E97BOY8 (Folic Acid)
RN  - P6YC3EG204 (Vitamin B 12)
SB  - IM
MH  - Animals
MH  - Biomarkers/blood
MH  - Biomechanical Phenomena
MH  - Blood Pressure
MH  - Bone Density
MH  - Bone Remodeling
MH  - Disease Models, Animal
MH  - Folic Acid/blood
MH  - Homocysteine/*blood
MH  - Hyperhomocysteinemia/blood/*complications/physiopathology
MH  - Laser-Doppler Flowmetry
MH  - Male
MH  - Osteoporosis/blood/*etiology/physiopathology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Regional Blood Flow
MH  - Tibia/*blood supply/physiopathology
MH  - Time Factors
MH  - Up-Regulation
MH  - Vitamin B 12/blood
PMC - PMC3037087
OTO - NOTNLM
OT  - bone density
OT  - homocysteine
OT  - tibia
EDAT- 2011/02/23 06:00
MHDA- 2011/06/15 06:00
PMCR- 2011/01/25
CRDT- 2011/02/23 06:00
PHST- 2011/02/23 06:00 [entrez]
PHST- 2011/02/23 06:00 [pubmed]
PHST- 2011/06/15 06:00 [medline]
PHST- 2011/01/25 00:00 [pmc-release]
AID - vhrm-7-031 [pii]
AID - 10.2147/VHRM.S15844 [doi]
PST - epublish
SO  - Vasc Health Risk Manag. 2011 Jan 25;7:31-5. doi: 10.2147/VHRM.S15844.