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Vivekanand Jha - One of the best experts on this subject based on the ideXlab platform.
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the effect of vitamin d supplementation on bone metabolic markers in chronic kidney disease
Journal of Bone and Mineral Research, 2018Co-Authors: Ashok Kumar Yadav, Vivek Kumar, Vinod Kumar, Debasish Banerjee, Krishan Lal Gupta, Vivekanand JhaAbstract:Use of active forms of vitamin D is advocated in patients with chronic kidney disease (CKD) for treatment of mineral bone disease because of the presumption that native forms of vitamin D would not undergo significant activation to calcitriol, the most active biological form of vitamin D. We present secondary analysis looking at bone turnover in subjects who completed the randomized, double blind, placebo-controlled trial investigating the effect of Cholecalciferol supplementation on vascular function in nondiabetic CKD stage G3-G4 and vitamin D ≤20 ng/mL (Clinical Trials Registry of India: CTRI/2013/05/003648). Patients were randomized (1:1) to receive either two directly observed oral doses of 300,000 IU of Cholecalciferol or matching placebo at baseline and 8 weeks. Of the 120 subjects enrolled, 58 in the Cholecalciferol group and 59 in the placebo group completed the study. At 16 weeks, the serum 25(OH)D and 1,25(OH)2 D levels increased in the Cholecalciferol group but not in the placebo group (between-group difference in mean change: 23.40 ng/mL; 95% CI, 19.76 to 27.06; p < 0.001, and 14.98 pg/mL; 95% CI, 4.48 to 27.18; p = 0.007, respectively). Intact parathyroid hormone (iPTH) decreased in the Cholecalciferol group (between-group difference in mean change -100.73 pg/mL (95% CI, -150.50 to -50.95; p < 0.001). Serum total and bone-specific alkaline phosphatase (SAP, BAP) and serum C-terminal cross-linked collagen type I telopeptides (CTX-1) were significantly reduced in Cholecalciferol group (between group difference for change in mean: -20.25 U/L; 95% CI, -35.14 to -5.38 U/L; p = 0.008 for SAP; -12.54 U/L; 95% CI, -22.09 to -2.98 U/L; p = 0.013 for BAP; and -0.21 ng/mL; 95% CI, -0.38 to -0.05 ng/mL; p = 0.05 for CTX-1). Correlation analysis showed significant correlation of Δ25(OH)D with ΔiPTH (r = -0.409, p < 0.0001), Δ1,25(OH)2 D (r = 0.305, p = 0.001), ΔSAP (r = -0.301, p = 0.002), ΔBAP (r = -0.264, p = 0.004), and ΔCTX-1 (r = -0.210, p = 0.0230). Cholecalciferol supplementation corrects vitamin D deficiency and is effective in lowering serum intact parathyroid hormone and bone turnover markers in early stages of CKD. © 2017 American Society for Bone and Mineral Research.
Gary W. Witmer - One of the best experts on this subject based on the ideXlab platform.
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novel and current rodenticides for pocket gopher thomomys spp management in vineyards what works
Pest Management Science, 2017Co-Authors: Roger A. Baldwin, Ryan Meinerz, Gary W. WitmerAbstract:Background Rodenticides are often included as part of an integrated pest management approach for managing pocket gophers (Thomomys spp.) given that they are relatively quick and inexpensive to apply. Strychnine has historically been the most effective toxicant for pocket gophers, but its use is currently limited in the United States; alternative registered toxicants have not proven effective. Recent research with baits containing Cholecalciferol plus anticoagulant toxicants proved effective against pocket gophers in a lab setting. Therefore, we established a field study to compare Cholecalciferol plus anticoagulant combinations [0.03% Cholecalciferol plus 0.005% diphacinone (C + D), 0.015% Cholecalciferol plus 0.0025% brodifacoum (C + B1), 0.03% Cholecalciferol plus 0.0025% brodifacoum (C + B2)] with strychnine (0.5%) for pocket gopher management. Results Strychnine treatments resulted in 100% efficacy after two treatment periods. Both C + D and C + B2 resulted in efficacy significantly greater than 70% after two treatment periods (83 and 75% respectively). Efficacy from C + B1 (85%) was not significantly greater than 70%, but did yield high overall efficacy as well. Conclusion Although strychnine remains the most effective rodenticide for pocket gopher control, the Cholecalciferol plus anticoagulant baits tested would be a good alternative when strychnine is unavailable. C + D may be the best option given that it uses a first-generation anticoagulant as the synergist. © 2016 Society of Chemical Industry.
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Cholecalciferol plus diphacinone baits for vole control: a novel approach to a historic problem
Journal of Pest Science, 2016Co-Authors: Roger A. Baldwin, Ryan Meinerz, Gary W. WitmerAbstract:Combination baits containing Cholecalciferol plus an anticoagulant are effective against commensal rodents resistant to anticoagulants, and they likely pose less risk than anticoagulant-only rodenticides due to lower concentrations of active ingredients and shorter time to death. However, these combination baits have not been tested for agricultural rodent pests. Therefore, we established a study to test the efficacy of Cholecalciferol plus diphacinone artichoke bract and pellet baits to determine their ability to manage California voles Microtus californicus in artichokes, where resistance to anticoagulants is known to occur. Field tests using radiocollared voles indicated that bract baits were highly efficacious (85 %), although pellet baits were less effective (60 %). Low observed efficacy of pellet baits may have resulted from poor weather following application during the second sampling period; further testing may yield more positive results. We observed a bimodal distribution in timing of death, with one group of voles dying between 4.3 and 5.8 days post-consumption; the other group died between 9.0 and 14.5 days post-consumption. Deaths in the first group were attributed to Cholecalciferol, while deaths in the second group were likely due to chronic anticoagulant exposure. Almost double the proportion of voles that died from bract consumption did so during the early period when compared to their pellet plot counterparts. This suggests that voles were consuming greater quantities of bract baits over a shorter period of time when compared to the pellet bait. Collectively, these findings indicate that baiting with Cholecalciferol plus diphacinone coated bracts is an effective method for controlling vole populations in artichokes.
Vin Tangpricha - One of the best experts on this subject based on the ideXlab platform.
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high dose Cholecalciferol reduces parathyroid hormone in patients with early chronic kidney disease a pilot randomized double blind placebo controlled trial
The American Journal of Clinical Nutrition, 2012Co-Authors: Jessica A Alvarez, Jennie Law, Kathryn E Coakley, Susu M Zughaier, Li Hao, Khadijeh Shahid Salles, Haimanot Wasse, Orlando M Gutierrez, Thomas R Ziegler, Vin TangprichaAbstract:Background: Vitamin D deficiency contributes to secondary hyperparathyroidism, which occurs early in chronic kidney disease (CKD). Objectives: We aimed to determine whether high-dose Cholecalciferol supplementation for 1 y in early CKD is sufficient to maintain optimal vitamin D status (serum 25-hydroxyvitamin D [25(OH)D] concentration ≥30 ng/mL) and decrease serum parathyroid hormone (PTH). A secondary aim was to determine the effect of Cholecalciferol on blood pressure and serum fibroblast growth factor-23 (FGF23). Design: This was a double-blind, randomized, placebo-controlled trial. Forty-six subjects with early CKD (stages 2–3) were supplemented with oral Cholecalciferol (vitamin D group; 50,000 IU/wk for 12 wk followed by 50,000 IU every other week for 40 wk) or a matching placebo for 1 y. Results: By 12 wk, serum 25(OH)D increased in the vitamin D group only [baseline (mean ± SD): 26.7 ± 6.8 to 42.8 ± 16.9 ng/mL; P < 0.05] and remained elevated at 1 y (group-by-time interaction: P < 0.001). PTH decreased from baseline only in the vitamin D group (baseline: 89.1 ± 49.3 to 70.1 ± 24.8 pg/mL; P = 0.01) at 12 wk, but values were not significantly different from baseline at 1 y (75.4 ± 29.5 pg/mL; P = 0.16; group-by-time interaction: P = 0.09). Group differences were more pronounced in participants with secondary hyperparathyroidism (group-by-time interaction: P = 0.004). Blood pressure and FGF23 did not change in either group. Conclusions: After 1 y, this oral Cholecalciferol regimen was safe and sufficient to maintain serum 25(OH)D concentrations and prevent vitamin D insufficiency in early CKD. Furthermore, serum PTH improved after Cholecalciferol treatment, particularly in patients who had secondary hyperparathyroidism. This trial was registered at clinicaltrials.gov as {"type":"clinical-trial","attrs":{"text":"NCT00427037","term_id":"NCT00427037"}}NCT00427037.
Lars Rejnmark - One of the best experts on this subject based on the ideXlab platform.
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the effect of high dose vitamin d supplementation on calciotropic hormones and bone mineral density in obese subjects with low levels of circulating 25 hydroxyvitamin d results from a randomized controlled study
Calcified Tissue International, 2013Co-Authors: Louise Wamberg, Steen B Pedersen, Bjorn Richelsen, Lars RejnmarkAbstract:Low levels of 25-hydroxyvitamin D (25OHD) are associated with increased bone turnover and risk of fractures. Plasma 25OHD is inversely related to body mass index, and vitamin D deficiency is common in obesity. We aimed to determine whether vitamin D supplementation affects bone turnover and bone mineral density (BMD) in obese subjects. Fifty-two healthy obese men and women aged 18–50 years with plasma 25OHD levels below 50 nmol/L were randomized to 7,000 IU of Cholecalciferol daily or placebo for 26 weeks. We measured plasma levels of 25OHD, parathyroid hormone (PTH), and markers of bone turnover, as well as BMD at the hip, spine, forearm, and whole body. Compared with placebo, treatment with Cholecalciferol increased mean plasma 25OHD from 35 to 110 nmol/L (p < 0.00001) and significantly decreased PTH (p < 0.05). BMD increased significantly at the forearm by 1.6 ± 0.7 % (p = 0.03). The bone resorption marker C-terminal telopetide of type 1 collagen (CTX) decreased borderline significantly in the Cholecalciferol group compared with the placebo group (p = 0.07). Changes in plasma 25OHD correlated inversely with changes in plasma levels of bone-specific alkaline phosphatase (r = −0.38, p = 0.01) and CTX (r = −0.33, p = 0.03). Changes in CTX correlated inversely with changes in spine BMD (r = −0.45, p = 0.04). Increasing circulating 25OHD levels by Cholecalciferol treatment is of importance to bone health in young obese subjects as increased levels of 25OHD are associated with a decrease in both PTH and bone turnover and with an increase in BMD at the forearm.
Mukta M Webber - One of the best experts on this subject based on the ideXlab platform.
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Cholecalciferol vitamin d3 inhibits growth and invasion by up regulating nuclear receptors and 25 hydroxylase cyp27a1 in human prostate cancer cells
Clinical & Experimental Metastasis, 2005Co-Authors: Erik J Tokar, Mukta M WebberAbstract:Epidemiological evidence suggests an inverse relationship between prostate cancer and serum vitamin D levels. We examined the ability of Cholecalciferol (vitamin D(3)), a calcitriol precursor, to inhibit or reverse cellular changes associated with malignant transformation and invasion and explored its mechanisms of action. The RWPE2-W99 human prostate epithelial cell line, which forms slow-growing tumors in nude mice, was used because it mimics the behavior of the majority of primary human prostate cancers. Cholecalciferol, at physiological levels: (i) inhibited anchorage-dependent and -independent growth; (ii) induced differentiation by decreasing vimentin expression with a concomitant decrease in motility/chemotaxis; (iii) decreased MMP-9 and MMP-2 activity with concomitant decrease in invasion; and (iv) exerted its effects by up-regulating vitamin D receptor (VDR), retinoid-X receptor-alpha (RXR-alpha), and androgen receptor (AR) in a dose-dependent manner. Furthermore, we found that RWPE2-W99 prostate cancer cells, similar to RWPE-1 cells (Tokar and Webber. Clin Exp Metast 2005; 22: 265-73), constitutively express the enzyme 25-hydroxylase CYP27A1 which is markedly up-regulated by Cholecalciferol. Cholecalciferol has effects similar to those of calcitriol on growth, MMP activity, and VDR. The ability of CYP27A1 to catalyze the conversion of Cholecalciferol to 25(OH)D(3) and of 25(OH)D(3) to calcitriol has been reported. RWPE2-W99 cells, similar to RWPE-1 cells, appear to have the rare ability to locally convert Cholecalciferol to the active hormone calcitriol. Because it can inhibit cellular changes associated with malignant transformation and invasion, we propose that Cholecalciferol may be an effective agent for the treatment of prostate cancer.
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chemoprevention of prostate cancer by Cholecalciferol vitamin d3 25 hydroxylase cyp27a1 in human prostate epithelial cells
Clinical & Experimental Metastasis, 2005Co-Authors: Erik J Tokar, Mukta M WebberAbstract:The 20-30 year latency period for prostate cancer provides an important opportunity to prevent the development of invasive cancer. A logical approach for chemoprevention to reduce incidence is to identify agents, such as, vitamin D, which can inhibit cell proliferation and induce differentiation, are safe, and readily available to the public at low cost. Epidemiological evidence suggests that vitamin D deficiency is associated with increased risk for prostate cancer. We examined the ability and mechanisms of action of Cholecalciferol (vitamin D(3)), a precursor of the most biologically active hormone calcitriol, to block or reverse premalignant changes. The immortalized, non-tumorigenic, RWPE-1 human prostate epithelial cell line, was used. Results show that Cholecalciferol, at physiological levels: (i) inhibits anchorage-dependent growth (ii) induces differentiation by increasing PSA expression and (iii) exerts its effects by up-regulating vitamin D receptor (VDR), retinoid-X receptors (RXRs), and androgen receptor (AR). Furthermore, we discovered that human prostate epithelial cells constitutively express appreciable levels of 25-hydroxylase CYP27A1 protein, the enzyme which catalyzes the conversion of Cholecalciferol to 25(OH)D(3), and that CYP27A1 is up-regulated by Cholecalciferol. Recent studies show that human mitochondrial CYP27A1 can also catalyze 1alpha-hydroxylation of 25(OH)D(3) to calcitriol. The presence of 25-hydroxylase in human prostate epithelial cells has not previously been shown. Since human prostate epithelial cells have the necessary enzymes and the rare ability to locally convert Cholecalciferol to the active hormone calcitriol, we propose that they are a prime target for chemoprevention of prostate cancer with Cholecalciferol whose safety is well established as a supplement in vitamins and fortified foods.