Vitamin C Prevents Hypogonadal Bone Loss

Epidemiologic studies correlate low vitamin C intake with bone loss. The genetic deletion of enzymes involved in de novo vitamin C synthesis in mice, likewise, causes severe osteoporosis. However, very few studies have evaluated a protective role of this dietary supplement on the skeleton. Here, we...

Full description

Saved in:
Bibliographic Details
Published in:PloS one 2012-10, Vol.7 (10), p.e47058-e47058
Main Authors: Zhu, Ling-Ling, Cao, Jay, Sun, Merry, Yuen, Tony, Zhou, Raymond, Li, Jianhua, Peng, Yuanzhen, Moonga, Surinder S, Guo, Lida, Mechanick, Jeffrey I, Iqbal, Jameel, Peng, Liu, Blair, Harry C, Bian, Zhuan, Zaidi, Mone, Smith, Brenda
Format: Article
Language:English
Subjects:
Acids
Animals
Ascorbic acid
Ascorbic Acid - therapeutic use
Biocompatibility
Biology
Biomedical materials
Bone density
Bone Density - drug effects
bone formation
Bone growth
Bone histomorphometry
Bone loss
Bone mineral density
bone resorption
Bone turnover
Bones
Collagen
Computed tomography
Correlation analysis
Diet
Dietary supplements
Enzymes
epidemiological studies
Epidemiology
Female
Fractures
Gene expression
Homeostasis
Ingestion
Medicine
Mice
Mice, Inbred C57BL
micro-computed tomography
Nutrition research
osteoblasts
Osteocalcin
Osteogenesis
Osteoporosis
Osteoporosis - diagnostic imaging
Osteoporosis - prevention & control
Ovariectomy
polymerase chain reaction
protective effect
quantitative polymerase chain reaction
Radiography
Skeleton
Vitamin C
vitamin supplements
Womens health
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Epidemiologic studies correlate low vitamin C intake with bone loss. The genetic deletion of enzymes involved in de novo vitamin C synthesis in mice, likewise, causes severe osteoporosis. However, very few studies have evaluated a protective role of this dietary supplement on the skeleton. Here, we show that the ingestion of vitamin C prevents the low-turnover bone loss following ovariectomy in mice. We show that this prevention in areal bone mineral density and micro-CT parameters results from the stimulation of bone formation, demonstrable in vivo by histomorphometry, bone marker measurements, and quantitative PCR. Notably, the reductions in the bone formation rate, plasma osteocalcin levels, and ex vivo osteoblast gene expression 8 weeks post-ovariectomy are all returned to levels of sham-operated controls. The study establishes vitamin C as a skeletal anabolic agent.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0047058