Serum Osteocalcin as a Marker for Vitamin K-Status in Pregnant Women and Their Newborn Babies

Jie, Kon‐Siong G.; Hamulyák, Karly; Gijsbers, Birgit L. M. G.; Roumen, Frans J.M.E.; Vermeer, Cees

doi:10.1055/s-0038-1646282

Cited by 27 publications

(37 citation statements)

References 25 publications

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“…Our data confirms a prior report that dietary K insufficiency also elevates serum ucOC (21) . This elevation is produced by a degree of K insufficiency that did not prolong PT, verifying ucOC as a more sensitive indicator of K adequacy than PT (22) …”

Section: Discussionsupporting

confidence: 92%

Diet- or Warfarin-Induced Vitamin K Insufficiency Elevates Circulating Undercarboxylated Osteocalcin Without Altering Skeletal Status in Growing Female Rats

Haffa

Krueger

Bruner

et al. 2000

Journal of Bone and Mineral Research

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Section: Discussionsupporting

confidence: 92%

Diet- or Warfarin-Induced Vitamin K Insufficiency Elevates Circulating Undercarboxylated Osteocalcin Without Altering Skeletal Status in Growing Female Rats

Haffa

Krueger

Bruner

et al. 2000

Journal of Bone and Mineral Research

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“…Undercarboxylation of the bone matrix protein osteocalcin appears to be a sensitive measure of vitamin K status (1)(2)(3). When defined as elevated concentrations of undercarboxylated osteocalcin (ucOC), vitamin K insufficiency appears to be common in postmenopausal women (4,5).…”

Section: Introductionmentioning

confidence: 99%

Vitamin K supplementation reduces serum concentrations of under-γ-carboxylated osteocalcin in healthy young and elderly adults

Binkley

Krueger

Engelke

et al. 2000

The American Journal of Clinical Nutrition

136

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Background: Subclinical vitamin K insufficiency, manifested by under-␥-carboxylation of the bone matrix protein osteocalcin, may be common. Objective: Our objective was to delineate the prevalence of submaximal ␥-carboxylation as assessed by response to phylloquinone supplementation and to evaluate the effect of this intervention on skeletal turnover in healthy North American adults. Design: Healthy subjects (n = 219), approximately equally distributed by sex and age (18-30 y and ≥ 65 y), received daily phylloquinone (1000 g) or placebo for 2 wk. Serum undercarboxylated osteocalcin (ucOC) and total osteocalcin, N-telopeptides of type I collagen (NTx), bone-specific alkaline phosphatase (BSAP), and phylloquinone concentrations were measured at baseline and after weeks 1 and 2. Results: At baseline, the mean serum phylloquinone concentration was lower in the young than in the old group; there was no effect of sex. Concomitantly, baseline %ucOC was highest in the young and lowest in the old men (P < 0.0001) but did not differ significantly by age in women. After supplementation, serum phylloquinone concentration increased Ϸ10-fold (P < 0.0001) at week 1 (from 0.93 ± 0.08 to 8.86 ± 0.70 nmol/L, x -± SEM); this was sustained through week 2. Among all supplemented groups, mean %ucOC decreased from 7.6% to 3.4% without significant differences by age or sex; 102 of 112 subjects had a > 1% decrease.

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“…Additional evidence shows that patients with osteoporosis, femoral fractures, or prior vertebral compression fractures had reduced plasma levels of vitamin K compared with age‐matched controls (37) . Supplementation with vitamin K resulted in an increased hydroxyapatite‐binding capacity of osteocalcin in adults and newborns, as well as in a reduction in calcium excretion (38–40) …”

Section: Discussionmentioning

confidence: 99%

Apolipoprotein E Gene Polymorphism and Bone Loss: Estrogen Status Modifies the Influence of Apolipoprotein E on Bone Loss

Salamone

Cauley

Zmuda

et al. 2000

Journal of Bone and Mineral Research

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The identification of genes that contribute to bone mineral density (BMD) and bone loss has widespread implications for the understanding and prevention of osteoporosis. The objective of this study was to examine the relationship between the presence and absence of the apolipoprotein E*4 (APOE*4) allele and both BMD and annualized percentage rate of change in BMD at the lumbar spine and hip in a population of 392 healthy, pre-, peri-, and postmenopausal white women participating in the Women's Healthy Lifestyle Project. APOE genotype was analyzed by restriction enzyme analysis from genomic DNA. BMD at the lumbar spine and hip was measured at baseline and after a mean of 2.5 years using dual-energy X-ray absorptiometry (DXA). In premenopausal women, there were no significant differences in BMD or in the annualized percentage rate of change in BMD at the spine or hip when comparing women with and without the APOE*4 allele. In contrast, spine bone loss was significantly greater in peri-and postmenopausal women having an APOE*4 allele than in women without this allele (؊1.75 ؉ 1.5% per year vs. ؊0.98 ؎ 1.4% per year, respectively, p ‫؍‬ 0.018). Among peri-and postmenopausal women currently using hormone replacement therapy (HRT), there were no differences in the annualized percentage rate of change in spine BMD; whereas, among non-HRT users, there was a 2-fold higher rate of spine bone loss in women with an APOE*4 allele compared with women without this allele (؊2.31 ؎ 1.5% per year vs. ؊1.27 ؎ 1.3% per year, respectively, p ‫؍‬ 0.033; APOE*4 ؋ HRT interaction, p ‫؍‬ 0.076). In conclusion, this study shows the importance of APOE*4 allele in spine bone loss in peri-and postmenopausal women and, more importantly, it provides evidence for a genetic and lifestyle interaction in modulating spine bone loss. (J Bone Miner Res 2000;15:308-314)

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Serum Osteocalcin as a Marker for Vitamin K-Status in Pregnant Women and Their Newborn Babies

Cited by 27 publications

References 25 publications

Diet- or Warfarin-Induced Vitamin K Insufficiency Elevates Circulating Undercarboxylated Osteocalcin Without Altering Skeletal Status in Growing Female Rats

Diet- or Warfarin-Induced Vitamin K Insufficiency Elevates Circulating Undercarboxylated Osteocalcin Without Altering Skeletal Status in Growing Female Rats

Vitamin K supplementation reduces serum concentrations of under-γ-carboxylated osteocalcin in healthy young and elderly adults

Apolipoprotein E Gene Polymorphism and Bone Loss: Estrogen Status Modifies the Influence of Apolipoprotein E on Bone Loss

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