Wenzhen Fu

Shanghai University, Shanghai, Shanghai Shi, China

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Publications (4)25.06 Total impact

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    ABSTRACT: Objective: The aims of this study were to (1) evaluate the association of serum sclerostin with bone mineral density (BMD) and markers of bone metabolism in postmenopausal Chinese women and (2) observe the relationships of single nucleotide polymorphisms (SNPs) within the sclerostin (SOST) gene with serum sclerostin, BMD, and markers of bone metabolism. Design: A cross-sectional study was conducted with 703 postmenopausal Chinese women. Ten tagging SNPs (rs1234612, rs1513670, rs1634330, rs1708635, rs2023794, rs7220711, rs74252774, rs851057, rs851058, and rs865429) of the SOST gene were genotyped. Serum sclerostin and markers of bone metabolismwere measured, including serum intact parathyroid hormone, 25-hydroxyvitamin D [25(OH)D], procollagen type 1 N-terminal propeptide (P1NP), and β-CrossLaps of type I collagen containing cross-linked C-telopeptide (β-CTX). The BMD of the lumbar spine and proximal femur were measured by dual-energy X-ray absorptiometry. Results: Serum sclerostin was positively correlated with BMD at lumbar spine, femoral neck, total hip and with serum 25(OH)D (all P<0.01), but negatively correlated with β-CTX (P<0.01). The significant relationships between serum sclerostin and BMD and with serum β-CTX persisted even after adjustments for age, BMI and serum 25(OH)D (all P<0.01). However, there was no correlation between serum sclerostin and age or serum P1NP. We failed to identify a significant association between the SNP, haplotypes of SOST and BMD, serum sclerostin, or markers of bone metabolism. Conclusion: Our results suggested that serum sclerostin was positively correlated with the BMD at lumbar spine, femoral neck, total hip and with serum 25(OH)D but was negatively correlated with serum β-CTX. Genetic polymorphisms of SOST may not be a major contributor to variations in the serum sclerostin or BMD in postmenopausal Chinese women.
    The Journal of Clinical Endocrinology and Metabolism 01/2014; · 6.31 Impact Factor
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    ABSTRACT: Lipoxygenase (LOX) is one of the major metabolic enzymes for arachidonic acid, which has been reported to be associated with many postmenopausal and many hormone-related diseases. In rats, selective inhibition of the LOX pathway led to defective ovulation. However, little is known about the association of the LOX-related genes with menstruation in women. In this study, we investigated the possible association of two key gene (ALOX12 and ALOX15) polymorphisms with age of menarche and menopause in Chinese women. Six tagging single nucleotide polymorphisms (SNPs) of ALOX12 and five SNPs of ALOX15 were genotyped. The association of single SNPs and haplotypes in two candidate genes and age at menarche (AAM) variation was tested in 401 Chinese nuclear families using the quantitative transmissing disequilibrium test. Furthermore, the association between these SNPs and haplotypes and age at natural menopause (AANM) in 710 postmenopausal Chinese women was measured. Using family- and population-based statistical procedures, significant association was found between SNPs rs312462 in ALOX12 and AAM in nuclear families (P = 0.043), and three SNPs (rs2292350, rs312470, and rs312462) in ALOX12 were significantly associated with AANM in postmenopausal women (P = 0.012, P = 0.045, and P = 0.033, respectively). Haplotype analyses corroborated our single SNP results (P = 0.030). However, we failed to find a significant association between ALOX15 gene polymorphisms and AAM as well as AANM (P > 0.05). Our present results suggest that genetic variations in ALOX12 are associated with both the onset and cessation of menstruation in Chinese women living in Shanghai.
    Menopause (New York, N.Y.) 06/2012; 19(9):1029-36. · 3.08 Impact Factor
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    ABSTRACT: By using whole-exome sequencing, we identified a homozygous guanine-to-adenine transition at the invariant -1 position of the acceptor site of intron 1 (c.97-1G>A) in solute carrier organic anion transporter family member 2A1 (SLCO2A1), which encodes a prostaglandin transporter protein, as the causative mutation in a single individual with primary hypertrophic osteoarthropathy (PHO) from a consanguineous family. In two other affected individuals with PHO from two unrelated nonconsanguineous families, we identified two different compound heterozygous mutations by using Sanger sequencing. These findings confirm that SLCO2A1 mutations inactivate prostaglandin E(2) (PGE(2)) transport, and they indicate that mutations in SLCO2A1 are the pathogenic cause of PHO. Moreover, this study might also help to explain the cause of secondary hypertrophic osteoarthropathy.
    The American Journal of Human Genetics 12/2011; 90(1):125-32. · 11.20 Impact Factor
  • Wenzhen Fu, Yaohua Ke, Zhenlin Zhang
    Bone 01/2010; 47. · 4.46 Impact Factor