Search Results
Search for other papers by Karolien Van De Maele in
Google Scholar
PubMed
Search for other papers by Jean De Schepper in
Google Scholar
PubMed
Search for other papers by Jesse Vanbesien in
Google Scholar
PubMed
Search for other papers by Monique Van Helvoirt in
Google Scholar
PubMed
Search for other papers by Ann De Guchtenaere in
Google Scholar
PubMed
Search for other papers by Inge Gies in
Google Scholar
PubMed
Background
Vitamin D deficiency is common in obese adolescents and a risk factor for insulin resistance. We investigated if prevailing serum 25-OH vitamin D might predict the body fat loss in a group of obese adolescents undergoing a residential weight loss program.
Methods
In 92 (35 male) obese adolescents (aged 10.6–19 years) undergoing a residential weight loss program in Belgium, fasting serum 25-OH vitamin D (25-OH-D), insulin, glucose and lipid levels were measured and body composition was assessed by dual-energy X-ray absorptiometry (DXA).
Results
Baseline median (range) serum 25-OH-D level was 17.7 µg/L (3.8–41.8). In total, 55 adolescents had a serum 25-OH-D below 20 µg/L. In 31 adolescents with a low baseline 25-OH-D level, median increase in serum 25-OH-D was 2.4 µg/L (−4.2 to 7.2) after 10 months. This resulted in normal 25-OH-D levels in seven adolescents, whereas median BMI decreased with 1.0 SDS and body fat percentage diminished with 9.9%. Obese adolescents with or without a 25-OH-D level below or above 20 µg/L at baseline had similar changes in body weight, BMI SDS, body fat percentage and body fat mass at the end of the program. The change in serum 25-OH-D did not correlate with change in serum insulin, BMI SDS or body fat percentage and body fat mass.
Conclusion
Vitamin D deficiency was present in 55 out of 92 obese adolescents at the start of the summer. Serum 25-OH-D concentration did not predict changes in body fat loss after a residential weight loss program.
Search for other papers by Haojie Zhang in
Google Scholar
PubMed
Search for other papers by Yuke Cui in
Google Scholar
PubMed
Search for other papers by Ruihua Dong in
Google Scholar
PubMed
Search for other papers by Wen Zhang in
Google Scholar
PubMed
Search for other papers by Shihan Chen in
Google Scholar
PubMed
Search for other papers by Heng Wan in
Google Scholar
PubMed
Search for other papers by Chi Chen in
Google Scholar
PubMed
Search for other papers by Yi Chen in
Google Scholar
PubMed
Search for other papers by Yuying Wang in
Google Scholar
PubMed
Search for other papers by Chunfang Zhu in
Google Scholar
PubMed
Search for other papers by Bo Chen in
Google Scholar
PubMed
Search for other papers by Ningjian Wang in
Google Scholar
PubMed
Search for other papers by Yingli Lu in
Google Scholar
PubMed
Background
Bone is thought to be the reservoir of the human lead burden, and vitamin D is associated with bone turnover. We aimed to explore whether exposure to lower 25-hydroxy vitamin D (25(OH)D) levels was associated with higher blood lead levels (BLLs) by increasing the bone turnover rate in individuals with type 2 diabetes.
Methods
A total of 4103 type 2 diabetic men and postmenopausal women in Shanghai, China, were enrolled in 2018. Their 25(OH)D, β-C-terminal telopeptide (β-CTX), N-MID osteocalcin and procollagen type 1 N-peptide (P1NP) levels were detected. Their BLLs were determined by atomic absorption spectrometry. Mediation analyses were performed to identify the possible role that bone turnover played in the underlying mechanisms.
Results
In both the men and postmenopausal women, all three bone turnover markers were inversely associated with 25(OH)D and positively associated with the BLL (all P < 0.01) after adjusting for age, current smoking habits, metabolic parameters, duration of diabetes, vitamin D intake, and use of anti-osteoporosis medication. In the mediation analyses, none of the direct associations between 25(OH)D and BLL was significant for the three bone turnover markers, but all three bone turnover markers were found to be significant mediators of the indirect associations between 25(OH)D and BLL.
Conclusion
The association between vitamin D and BLL was fully mediated by bone turnover markers in type 2 diabetic patients (mediation effect). This finding suggested that vitamin D may protect against blood lead exposure from the bone reservoir by decreasing bone turnover in individuals with type 2 diabetes.
Search for other papers by Vito Francic in
Google Scholar
PubMed
Search for other papers by Martin Keppel in
Google Scholar
PubMed
Search for other papers by Verena Schwetz in
Google Scholar
PubMed
Search for other papers by Christian Trummer in
Google Scholar
PubMed
Search for other papers by Marlene Pandis in
Google Scholar
PubMed
Search for other papers by Valentin Borzan in
Google Scholar
PubMed
Search for other papers by Martin R Grübler in
Google Scholar
PubMed
Search for other papers by Nicolas D Verheyen in
Google Scholar
PubMed
Search for other papers by Marcus E Kleber in
Google Scholar
PubMed
Search for other papers by Graciela Delgado in
Google Scholar
PubMed
Search for other papers by Angela P Moissl in
Google Scholar
PubMed
Search for other papers by Benjamin Dieplinger in
Google Scholar
PubMed
Synlab Academy, Synlab Holding Germany GmbH, Heidelberg, Germany
Search for other papers by Winfried März in
Google Scholar
PubMed
Search for other papers by Andreas Tomaschitz in
Google Scholar
PubMed
Search for other papers by Stefan Pilz in
Google Scholar
PubMed
Search for other papers by Barbara Obermayer-Pietsch in
Google Scholar
PubMed
Objective
Cardiovascular disease manifestation and several associated surrogate markers, such as vitamin D, have shown substantial seasonal variation. A promising cardiovascular biomarker, soluble ST2 (sST2), has not been investigated in this regard – we therefore determined if systemic levels of sST2 are affected by seasonality and/or vitamin D in order to investigate their clinical interrelation and usability.
Design
sST2 levels were measured in two cohorts involving hypertensive patients at cardiovascular risk, the Styrian Vitamin D Hypertension Trial (study A; RCT design, 8 weeks 2800 IU cholecalciferol daily) and the Ludwigshafen Risk and Cardiovascular Health Study (LURIC; study B; cross-sectional design).
Methods
The effects of a vitamin D intervention on sST2 levels were determined in study A using ANCOVA, while seasonality of sST2 levels was determined in study B using ANOVA.
Results
The concentrations of sST2 remained unchanged by a vitamin D intervention in study A, with a mean treatment effect (95% confidence interval) of 0.1 (−0.6 to 0.8) ng/mL; P = 0.761), despite a rise in 25(OH)D (11.3 (9.2–13.5) ng/mL; P < 0.001) compared to placebo. In study B, seasonal variations were present in 25(OH)D levels in men and women with or without heart failure (P < 0.001 for all subgroups), while sST2 levels remained unaffected by the seasons in all subgroups.
Conclusions
Our study provides the first evidence that systemic sST2 levels are not interrelated with vitamin D levels or influenced by the seasons in subjects at cardiovascular risk.
Search for other papers by Ying-Lien Cheng in
Google Scholar
PubMed
Division of Endocrinology and Metabolism, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
Search for other papers by Ting-I Lee in
Google Scholar
PubMed
Search for other papers by Yu-Mei Chien in
Google Scholar
PubMed
Division of Endocrinology and Metabolism, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
Search for other papers by Ting-Wei Lee in
Google Scholar
PubMed
Cardiovascular Research Center, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
Taipei Heart Institute, Taipei Medical University, Taipei, Taiwan
Search for other papers by Yi-Jen Chen in
Google Scholar
PubMed
Vitamin D deficiency is associated with hyperlipidemia, but it remains unclear whether vitamin D supplementation reduces serum lipid levels. The aims of this study were to investigate the associations between increased serum 25-hydroxyvitamin D (25(OH)D) concentrations and lipid levels and identify the characteristics of people with or without lipid reduction associated with increased 25(OH)D levels. The medical records of 118 individuals (53 men; mean age, 54.4 ± 10.6 years) whose serum 25(OH)D levels increased between 2 consecutive measurements were retrospectively reviewed. People with increased 25(OH)D levels (from 22.7 (17.6–29.2) to 32.1 (25.6–36.8) mg/dL; P < 0.01) had a significant reduction in serum levels of triglycerides (TGs) (from 111.0 (80–164) to 104.5 (73–142) mg/dL; P < 0.01) and total cholesterol (TC) (from 187.5 (155–213) to 181.0 (150–210) mg/dL; P < 0.05). The individuals who responded to vitamin D (≥10% reduction in TG or TC levels) exhibited significantly higher baseline TG and TC levels than those who did not. Only patients with hyperlipidemia (not those without hyperlipidemia) at baseline exhibited significantly reduced TG and TC levels at follow-up. However, increasing serum 25(OH)D concentrations were significantly correlated with decreasing lipid levels in individuals with baseline 25(OH)D levels less than 30 ng/mL and in individuals aged 50–65 years (not in patients younger than 50 years or older than 65 years). In conclusion, increasing serum 25(OH)D concentrations may be potentially helpful for the treatment of hyperlipidemia in people with vitamin D deficiency.
Search for other papers by Melissa Braga in
Google Scholar
PubMed
Search for other papers by Zena Simmons in
Google Scholar
PubMed
Search for other papers by Keith C Norris in
Google Scholar
PubMed
Department of Health & Life Sciences, Charles R. Drew University of Medicine and Science, Los Angeles, California, USA
Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
Search for other papers by Monica G Ferrini in
Google Scholar
PubMed
Department of Health & Life Sciences, Charles R. Drew University of Medicine and Science, Los Angeles, California, USA
Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
Search for other papers by Jorge N Artaza in
Google Scholar
PubMed
Skeletal muscle wasting is a serious disorder associated with health conditions such as aging, chronic kidney disease and AIDS. Vitamin D is most widely recognized for its regulation of calcium and phosphate homeostasis in relation to bone development and maintenance. Recently, vitamin D supplementation has been shown to improve muscle performance and reduce the risk of falls in vitamin D deficient older adults. However, little is known of the underlying molecular mechanism(s) or the role it plays in myogenic differentiation. We examined the effect of 1,25-D3 on myogenic cell differentiation in skeletal muscle derived stem cells. Primary cultures of skeletal muscle satellite cells were isolated from the tibialis anterior, soleus and gastrocnemius muscles of 8-week-old C57/BL6 male mice and then treated with 1,25-D3. The efficiency of satellite cells isolation determined by PAX7+ cells was 81%, and they expressed VDR. Incubation of satellite cells with 1,25-D3 induces increased expression of: (i) MYOD, (ii) MYOG, (iii) MYC2, (iv) skeletal muscle fast troponin I and T, (v) MYH1, (vi) IGF1 and 2, (vii) FGF1 and 2, (viii) BMP4, (ix) MMP9 and (x) FST. It also promotes myotube formation and decreases the expression of MSTN. In conclusion, 1,25-D3 promoted a robust myogenic effect on satellite cells responsible for the regeneration of muscle after injury or muscle waste. This study provides a mechanistic justification for vitamin D supplementation in conditions characterized by loss of muscle mass and also in vitamin D deficient older adults with reduced muscle mass and strength, and increased risk of falls.
Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands
Search for other papers by Laura P B Elbers in
Google Scholar
PubMed
Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands
Laboratory of Experimental Intensive Care and Anesthesiology, Academic Medical Center, University of Amsterdam, the Netherlands
Search for other papers by Marije Wijnberge in
Google Scholar
PubMed
Department of Plasma Proteins, Sanquin Research, Amsterdam, the Netherlands
Search for other papers by Joost C M Meijers in
Google Scholar
PubMed
Search for other papers by Dennis C W Poland in
Google Scholar
PubMed
Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands
Search for other papers by Dees P M Brandjes in
Google Scholar
PubMed
Search for other papers by Eric Fliers in
Google Scholar
PubMed
Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands
Search for other papers by Victor E A Gerdes in
Google Scholar
PubMed
Introduction
Abnormal coagulation tests have been observed in patients with primary hyperparathyroidism (HPT) suggesting a prothrombotic effect of parathyroid hormone (PTH). Vitamin D deficiency (VIDD) is the most frequent cause of secondary HPT. Aim of our study was to investigate the influence of HPT secondary to moderate-to-severe VIDD and vitamin D replacement on the coagulation and fibrinolysis system.
Subjects and methods
Prospective cohort study of patients with vitamin D <25 nmol/L with and without HPT, and a control group of patients on vitamin D suppletion. At baseline and after 2 months of vitamin D suppletion (900,000 IU in 2 months), endocrine and coagulation markers were measured.
Results
59 patients with VIDD of which 34 had secondary HPT and 36 controls were included. After 2 months of suppletion, vitamin D increased by 399% (VIDD with HPT), 442% (all patients with VIDD) and 6% (controls). PTH decreased by 34% (VIDD with HPT, P < 0.01 for decrease), 32% (all VIDD, P < 0.01) and increased by 8% in the controls (P-values: <0.01 for relative changes between VIDD with HPT or all VIDD patients vs controls). Relative changes in PT, aPTT, fibrinogen, Von Willebrand factor, factors VII, VIII and X, thrombin generation, TAFI, clot-lysis time and d-dimer were not different between patients with VIDD with HPT or all VIDD vs controls.
Discussion
Secondary HPT due to VIDD does not have a prothrombotic effect. In contrast with previous reports, PTH does not seem to influence coagulation or fibrinolysis, which is relevant because of the high prevalence of VIDD.
Search for other papers by Zhen-yu Song in
Google Scholar
PubMed
Search for other papers by Qiuming Yao in
Google Scholar
PubMed
Search for other papers by Zhiyuan Zhuo in
Google Scholar
PubMed
Search for other papers by Zhe Ma in
Google Scholar
PubMed
Search for other papers by Gang Chen in
Google Scholar
PubMed
Previous studies investigating the association of circulating 25-hydroxyvitamin D level with prognosis of prostate cancer yielded controversial results. We conducted a dose–response meta-analysis to elucidate the relationship. PubMed and EMBASE were searched for eligible studies up to July 15, 2018. We performed a dose–response meta-analysis using random-effect model to calculate the summary hazard ratio (HR) and 95% CI of mortality in patients with prostate cancer. Seven eligible cohort studies with 7808 participants were included. The results indicated that higher vitamin D level could reduce the risk of death among prostate cancer patients. The summary HR of prostate cancer-specific mortality correlated with an increment of every 20 nmol/L in circulating vitamin D level was 0.91, with 95% CI 0.87–0.97, P = 0.002. The HR for all-cause mortality with the increase of 20 nmol/L vitamin D was 0.91 (95% CI: 0.84–0.98, P = 0.01). Sensitivity analysis suggested the pooled HRs were stable and not obviously changed by any single study. No evidence of publications bias was observed. This meta-analysis suggested that higher 25-hydroxyvitamin D level was associated with a reduction of mortality in prostate cancer patients and vitamin D is an important protective factor in the progression and prognosis of prostate cancer.
Metabolism Laboratory, Department of Endocrinology, School of Medicine and Medical Sciences, St Vincent's University Hospital, Elm Park, Dublin 4, Ireland
Metabolism Laboratory, Department of Endocrinology, School of Medicine and Medical Sciences, St Vincent's University Hospital, Elm Park, Dublin 4, Ireland
Search for other papers by Malachi J McKenna in
Google Scholar
PubMed
Search for other papers by Barbara F Murray in
Google Scholar
PubMed
Search for other papers by Myra O'Keane in
Google Scholar
PubMed
Search for other papers by Mark T Kilbane in
Google Scholar
PubMed
Background
The Institute of Medicine 2011 Report on Dietary Reference Intakes for Calcium and Vitamin D specified higher intakes for all age groups compared to the 1997 report, but also cautioned against spurious claims about an epidemic of vitamin D deficiency and against advocates of higher intake requirements. Over 40 years, we have noted marked improvement in vitamin D status but we are concerned about hypervitaminosis D.
Objective
We sought to evaluate the 25-hydroxyvitamin D (25OHD) trend over 20 years.
Design
We retrieved all results of serum 25OHD from 1993 to 2013 (n=69 012) that was trimmed to one sample per person (n=43 782). We conducted a time series analysis of the monthly averages for 25OHD using a simple sequence chart and a running median smoothing function. We modelled the data using univariate auto-regressive integrated moving average (ARIMA) and forecast 25OHD levels up to 2016.
Results
The time series sequence chart and smoother function demonstrated a steady upward trend with seasonality. The yearly average 25OHD increased from 36.1 nmol/l in 1993 to 57.3 nmol/l in 2013. The ARIMA model was a good fit for the 25OHD time series; it forecasted monthly average 25OHD up to the end of 2016 with a positive stationary R 2 of 0.377.
Conclusions
Vitamin D status improved over the past 40 years, but there remains a dual problem: there are groups at risk of vitamin D deficiency who need public health preventative measures; on the other hand, random members of the population are taking unnecessarily high vitamin D intakes for unsubstantiated claims.
Fondazione Italiana Ricerca sulle Malattie dell’Osso (FIRMO Onlus), Florence, Italy
Search for other papers by Maria Luisa Brandi in
Google Scholar
PubMed
Search for other papers by Stefania Bandinelli in
Google Scholar
PubMed
Search for other papers by Teresa Iantomasi in
Google Scholar
PubMed
Search for other papers by Francesca Giusti in
Google Scholar
PubMed
Search for other papers by Eleonora Talluri in
Google Scholar
PubMed
Search for other papers by Giovanna Sini in
Google Scholar
PubMed
Search for other papers by Fabrizio Nannipieri in
Google Scholar
PubMed
Search for other papers by Santina Battaglia in
Google Scholar
PubMed
Search for other papers by Riccardo Giusti in
Google Scholar
PubMed
Search for other papers by Colin Gerard Egan in
Google Scholar
PubMed
Search for other papers by Luigi Ferrucci in
Google Scholar
PubMed
Objective
This study aimed to evaluate the association between the endocrine-disrupting chemical, bisphenol A (BPA) on circulating levels of 25-hydroxy vitamin D (25(OD)D) and other vitamin D metabolites in an elderly population in Italy.
Methods
This was a retrospective analysis of the InCHIANTI Biobank in Italy. The association between vitamin D metabolites namely 1,25(OH)D, 25(OH)D, parathyroid hormone (PTH) and BPA levels were evaluated. Multiple regression models were used to examine the association between predictor variables with 1,25(OH)D or 25(OH)D levels.
Results
Samples from 299 individuals aged 72.8 ± 15.7 years were examined. Mean levels of BPA, 1,25(OH)D and 25(OH)D were 351.2 ± 511.6 ng/dL, 43.7 ± 16.9 pg/mL and 20.2 ± 12.1 ng/mL, respectively. One hundred eighty individuals (60.2%) were deficient (<20 ng/mL) in 25(OH)D and this population also presented higher BPA levels (527.9 ± 1289.5 ng/dL vs 86.9 ± 116.8 ng/dL, P < 0.0001). Univariate analysis revealed that BPA levels were negatively correlated with both 1,25(OH)D (r= −0.67, P < 0.0001) and 25(OH)D (r= −0.69, P < 0.0001). Multivariate regression revealed that PTH (β: −0.23, 95% CI: −0.34, −0.13, P < 0.0001) and BPA (β: −0.25, 95% CI: −0.3, −0.19, P < 0.0001) remained significantly associated with 25(OH)D levels while BPA was also associated with 1,25(OH)D levels (β: −0.19, 95% CI: −0.22, −0.15, P < 0.0001). Receiver operating characteristic curve analysis showed that a BPA concentration of >113 ng/dL was the best cut-off to predict individuals deficient in 25(OH)D (area under the curve: 0.87, 95% CI: 0.82–0.90, P < 0.0001).
Conclusion
The strong negative association between BPA and vitamin D in this elderly population warrants further investigation, particularly since this population is already at greatest risk of hypovitaminosis and fracture.
Search for other papers by Maxime Duval in
Google Scholar
PubMed
Search for other papers by Kalyane Bach-Ngohou in
Google Scholar
PubMed
Search for other papers by Damien Masson in
Google Scholar
PubMed
Search for other papers by Camille Guimard in
Google Scholar
PubMed
Search for other papers by Philippe Le Conte in
Google Scholar
PubMed
Department of Emergency Medicine, CHU Nantes, Nantes, France
Search for other papers by David Trewick in
Google Scholar
PubMed
Objective
Severe hypocalcemia (Ca <1.9 mmol/L) is often considered an emergency because of a potential risk of cardiac arrest or seizures. However, there is little evidence to support this. The aim of our study was to assess whether severe hypocalcemia was associated with immediately life-threatening cardiac arrhythmias or neurological complications.
Methods
A retrospective observational study was carried out over a 2-year period in the Adult Emergency Department (ED) of Nantes University Hospital. All patients who had a protein-corrected calcium concentration measure were eligible for inclusion. Patients with multiple myeloma were excluded. The primary outcome was the number of life-threatening cardiac arrhythmias and/or neurological complications during the stay in the ED.
Results
A total of 41,823 patients had protein-corrected calcium (pcCa) concentrations measured, 155 had severe hypocalcemia, 22 were excluded because of myeloma leaving 133 for analysis. Median pcCa concentration was 1.73 mmol/L (1.57–1.84). Seventeen (12.8%) patients presented a life-threatening condition, 14 (10.5%) neurological and 3 (2.2%) cardiac during ED stay. However, these complications could be explained by the presence of underlying co-morbidities and or electrolyte disturbances other than hypocalcemia. Overall, 24 (18%) patients died in hospital. Vitamin D deficiency, chronic kidney disease and hypoparathyroidism were the most frequently found causes of hypocalcemia.
Conclusion
Thirteen percent of patients with severe hypocalcemia presented a life-threatening cardiac or neurological complication on the ED. However, a perfectly valid alternative cause could account for these complications. Further research is warranted to define the precise role of hypocalcemia.
