Vitamin D-treated Group Research Articles

Randomized Controlled Trial Assessing Vitamin D's Role in Reducing BPPV Recurrence in Older Adults.

To determine if the recurrence rates of BPPV in older adults were lower in the vitamin D-treated group as compared to placebo groups. Double-blinded randomized control placebo trial. A single-centre study. Double-blinded randomized controlled trial design with 12 months follow-up. Vitamin D3 deplete participants were randomized into treatment (Group A) or placebo groups (Group B). Treatment group received 13 weeks of 2000 IU vitamin D3 followed by 1000 IU for the next 13 weeks. Patients who were replete were allocated to a control group (Group C) for observation and follow up. All groups had dietary interventions for vitamin D3 and calcium. Results showed an 87% reduction in recurrence rates of BPPV in the treatment group (Group A), with 0.75 fewer clinical episodes per 1 person-year as compared to placebo (Group B). Time to first recurrence was also significantly longer in Group A. There was no statistically significant difference between Group A and C in both recurrence rates and dizziness handicap scores. This clinical trial has laid the foundation to expand the investigation of vitamin D as standard of care treatment in BPPV patients in future phase IIb and III studies. A reduction in BPPV episodes in older adults has implications on fall risk, as dizziness from BPPV may cause falls. With fewer BPPV episodes and longer time to recurrence, seniors may have better postural stability and hence reduced risk of falls.

Effects of vitamin D supplementation in extender on sperm kinematics and apoptosis following the freeze-thaw process in normozoospermic and asthenozoospermic Holstein bulls

BackgroundAsthenozoospermia is a usual male infertility factor, characterized by decreased semen quality. It has been revealed that antioxidants improve sperm function, enhance endogenous antioxidant activities, and protect spermatozoa against oxidative damage during cryopreservation. This aimed to evaluate the effects of vitamin D on sperm kinematics and apoptosis in the semen of bulls with normozoospermia and asthenozoospermia after the freeze-thaw process. For this purpose, 32 semen samples of four Holstein bulls (normozoospermic, progressive motility > 70 %) and 32 semen samples of four bull (asthenozoospermic progressive motility < 40 %) were collected and pooled separately (normozoospermic and asthenozoospermic). Samples were then diluted into four equal aliquots of extender containing different vitamin D concentrations (0, 5, 10, and 50 ng/mL) and aspirated into a 0.5 mL straw.ResultsThe percentages of sperm progressive motility and viability were significantly higher (P < 0.05) in 50 ng/mL of vitamin D in normozoospermic group. Sperm kinematics parameters including curvilinear velocity (VCL), straight-line velocity (VSL), and average path velocity (VAP) were significantly higher in the high dose (50 ng/mL) vitamin D-treated group compared to the low dose vitamin D-treated group (5ng/mL) in normozoospermic bull semen samples. The supplementation of the semen extender with different concentrations of vitamin D could not increase the rate of acrosome integrity in normozoospermic bulls compared to the control group (P < 0.05). In the asthenozoospermic group, 10 ng/mL vitamin D-treated group could increase the rate of plasma membrane integrity compared to 5 ng/mL vitamin D-treated group (P < 0.05). The percentages of early-apoptosis (P = 0.049) and late-apoptosis (P = 0.005) were significantly higher in the asthenozoospermic than the normozoospermic group.ConclusionsThe present study revealed that a high dose (50 ng/mL) of vitamin D protected normozoospermic bulls’ sperms from the freezing procedure and lead to higher quality of frozen-thawed bull sperm.

Effect of vitamin D on experimental model of polycystic ovary syndrome in female rats

AimsVitamin D plays an important role in the regulation of ovulatory dysfunction. We aimed to study the effect of vitamin D on letrozole-induced PCOS in female rats. Material & methods40 non-pregnant Wistar rats were divided into four groups: group I control (received 1 ml of 1% aqueous solution of (CMC)/d orally), group II letrozole-induced PCOS group (received letrozole 200 μg/d orally), group III vitamin D-treated group (received vitamin D 1000 IU/kg/d), group IV letrozole and vitamin D treated group (received letrozole and vitamin D as group II and group III for 90 days. BMI, ovarian weight, serum vitamin D, biochemical metabolic and oxidative stress markers were evaluated, ovarian tissues glutathione, malondialdehyde levels and caspase-3 activity were measured. Histopathological examination of the ovary and coronary artery were done. Key findingsLetrozole-induced typical PCOS with significant decrease in vitamin D and coronary vasculopathy. Group II shows insignificant change in all parameters but there is significant increase in vitamin D and decrease in triglyceride and glutathione. In group VI all parameters were significantly improved but coronary vasculopathy was partly improved. Vitamin D was significantly negatively correlated with all parameters but significantly positively correlated with estradiol, insulin sensitivity, and HDL and insignificantly correlated with glutathione. Both Insulin resistance and testosterone were significantly positively correlated with all parameters but significantly negatively correlated with estradiol, insulin sensitivity, HDL and glutathione. SignificanceThese results holding the promise of beneficial impact of vitamin D administration to PCOS and its associated cardiovascular disorders.

Short- and Long-Term Effects of Vitamin D Treatment on Bacillus Calmette-Guerin-Induced Depressive-Like Behavior in Mice.

PurposeDepression is one of the most common psychological disorders. The nutritional etiology of the depression proposes that vitamin D may play a significant role in the pathogenesis of depression. Further, vitamin D deficiency has been found to aggravate depression in animals. Therefore, vitamin D treatment might be a potential therapeutic aid in depression management. This study aimed to explore the antidepressant effects of vitamin D in a Bacillus Calmette-Guerin (BCG)-induced depression model.MethodsThirty-six mice were randomly assigned to short-term and long-term experimental groups. In each group, mice were randomly subcategorized into three subgroups: 1. control (received vehicle), 2. BCG (received BCG [107 CFU/mouse]), and 3. BCG + vitamin D (received vitamin D [60.000 IU/kg] before BCG [107 CFU/mouse] inoculation). After completion of the two experimental periods (3 days for the short-term group and 2 weeks for the long-term group), the mice underwent three behavioral tests: locomotor activity, the forced swimming test (FST), and the tail suspension test (TST).ResultsLocomotor activity did not significantly differ among the subgroups in either the long-term or short-term groups. In the short-term group, the total immobility time on the FST was decreased in the vitamin D-treated group compared to the BCG group. However, in the TST, no significant difference was found between the vitamin D-treated group and the BCG group. In the long-term group, the immobility time on the FST was decreased in the vitamin D-treated group compared to the BCG group. Similarly, the total immobility time on the TST was also significantly lower in the vitamin D-treated mice than in the BCG-treated mice.ConclusionVitamin D is useful in the management of depressive behavior. The potential role of vitamin D in the etiology of depression should be investigated in future work.

Morphological changes in the experimental model of polycystic ovary syndrome and effects of vitamin D treatment.

This research was designed to develop an animal model by inducing polycystic ovary syndrome (PCOS) with dehydroepiandrosterone (DHEA) and observe reproductive and morphological changes after treatment with vitamin D. Thirty pre-pubertal female Sprague-Dawley (SD) dams were recruited. The animals were distributed 10 each in control, PCOS and vitamin D-treated groups. In control group 0.2 ml of sesame oil was given. PCOS group was administered DHEA by the daily dose of 6 mg/kg for 30 days. In vitamin D-treated group, animals were injected 6 mg/kg/day DHEA daily and 120 ng 1, 25(OH) 2D3/100 g subcutaneously once a week. The occurrence of reproductive phenotypic PCOS was evaluated by estrous cycle, morphology and histological changes of ovary, uterus on light microscope. The results of this study showed significant weight gain, obesity, and estrous irregularity in PCOs group as compared to control and vitamin D-treated group. Administration of vitamin D (120 ng 1, 25(OH) 2D3/100) improved the cycle characteristics, reduced body weight and morphological features in PCOS induced animals. The results support the effect of vitamin D treatment for metabolic and reproductive characteristic features in PCOS females.

Effects of Oral Vitamin D Supplement Therapy on Clinical Outcomes of Intravitreal Bevacizumab in Diabetic Macular Edema.

PurposeTo assess the effects of oral vitamin D supplement therapy on clinical outcomes of intravitreal bevacizumab (IVB) injections in patients with diabetic macular edema (DME).Methods Seventy-one patients with center-involving DME received IVB injections three times monthly. Cases with serum 25-hydroxyvitamin D (25(OH)D) levels 30 ng/ml were divided into treatment and control groups. The treatment group received 50000 IU of oral vitamin D once a week for eight weeks. One month after the third IVB injection, changes in the best-corrected visual acuity (BCVA) and central macular thickness (CMT) were analyzed for each group.ResultsThirty-seven patients had sufficient levels of 25 (OH) D, while 34 patients had insufficient levels. Nineteen cases with deficient levels of 25(OH)D were treated with oral vitamin D, while 15 patients were assigned to the control group. The mean of serum 25(OH)D in patients was 27.9 ng/ml [mean 20.3 5.4 and 17.3 5.4 ng/ml in control and treatment groups, respectively (P = 0.231)]. After three IVB injections, BCVA improved significantly in each group, but the difference between the study groups was not statistically significant. CMT decreased significantly in all the groups. The mean CMT reduction was more prominent in the vitamin D-treated group, but the difference between groups did not reach statistical significance (P = 0.29).Conclusion In DME patients with vitamin D deficiency, vitamin D supplement therapy had some beneficial effects on CMT reduction following three injections of IVB; nevertheless, these effects were not statistically significant. Definite conclusion needs further prospective studies with a larger sample size.

Study of Cellular Senescence and Vitamin D Deficiency in Nonalcoholic Fatty Liver Disease and The Potential Protective Effect of Vitamin D Supplementation

Nonalcoholic fatty liver disease (NAFLD) is a pathological process characterized by excessive hepatic fatty deposition with possible involvement of vitamin D deficiency and cellular senescence. The aim of this study is to investigate the pathophysiologic role of vitamin D deficiency and cellular senescence in NAFLD development. Moreover, it aims to investigate the potential protective role of vitamin D supplementation. This is an experimental Case/Control study. Forty-five male albino rats were enrolled in this study. Animals were divided into four groups: negative and positive control groups (10 for each group), a model of NAFLD (11) and vitamin D-treated NAFLD groups (14). At the end of the experiment, all rats were subjected to the following investigation; biochemical estimation of serum 25 hydroxycholecalciferol, senescence marker protein-30 (SMP-30), lipid profile and calculation of homeostatic model of insulin resistance (HOMA-IR). NAFLD group shows a significant increase in glucose, insulin levels, and HOMA- IR compared with both normal controls. This finding indicates the intimate association between insulin resistance and NAFLD pathogenesis. Moreover, it was found that NAFLD group shows a significant decrease in SMP-30 level compared with normal controls. While vitamin D-treated NAFLD group shows significant increased SMP-30 and decrease in HOMA-IR in comparison with nontreated NAFLD group. Vitamin D deficiency and increased cellular senescence are key features of NAFLD. Vitamin D supplementation could play a protective role, which needs further investigation including clinical human study.

MO026TREATMENT WITH ACTIVE VITAMIN D DOES NOT IMPROVE LEFT VENTRICULAR HYPERTROPHY BUT FURTHER INCREASES FGF23 AND ACCELERATES CKD PROGRESSION IN CHILDREN

Abstract Background and Aims Elevated FGF23, activation of the renin-angiotensin-aldosterone system (RAAS), and vitamin D and Klotho deficiency promote left ventricular hypertrophy (LVH) and LV fibrosis in chronic kidney disease (CKD). Whether treatment with active vitamin D affects uremic cardiomyopathy and/or FGF23/Klotho system in CKD is unclear. Method 5/6 nephrectomized (5/6Nx) rats, as a well-established model of CKD, were dose-dependently treated with calcitriol for 10 weeks and the cardiac phenotype, including local RAAS activation, was investigated compared to untreated 5/6Nx and sham-operated rats. Additionally, 38 children with eGFR ≤ 30 ml/min/1.73 m2 selected from the Cardiovascular Comorbidity in Children with CKD (4C) study were enrolled in a case-control study. Nineteen children were started on active vitamin D treatment with either calcitriol or calcidiol (average dosage 0.4 μg/day), and 19 CKD children with non-active vitamin D treatment matched for age, eGFR, serum calcium, parathyroid hormone, and phosphate served as controls. LV mass index (LVMI), LVH prevalence (LVMI &amp;gt;95th percentile), intact (iFGF23) and C-terminal FGF23 (cFGF23), and soluble Klotho (sKlotho) were assessed at baseline and after nine months. Results In 5/6Nx rats, FGF23 synthesis in bone and heart was enhanced compared to sham-operated rats, and calcitriol further stimulated its expression in bone only. Renal Klotho expression was reduced in 5/6 rats and almost normalized after calcitriol treatment. 5/6Nx induced cardiomyocyte growth and LV fibrosis, and calcitriol treatment significantly ameliorated both. Cardiac RAAS genes, such as angiotensinogen, renin, angiotensin-converting-enzyme, and angiotensin II receptor type I, were significantly upregulated in 5/6Nx rats compared to sham-operated animals, and normalized by calcitriol treatment. In the 4C study cohort, median plasma cFGF23 and iFGF23 were significantly elevated in both groups, whereas sKlotho was not altered compared to healthy children. Forty-seven percent and 42% of active vitamin D-treated patients and controls, respectively, received blood pressure (BP) medications, however diastolic BP was slightly but significantly enhanced in both groups compared to healthy children. Mean LVMI and LVH prevalence of 47% in active vitamin D-treated patients and controls did not differ at baseline. After nine months, median cFGF23 and iFGF23 were significantly increased in active vitamin D-treated patients compared to controls. sKlotho levels were decreased in the active vitamin D-treated group compared to baseline but not in controls. A significant decline in median eGFR was observed in active vitamin D group but not in controls. Likewise, the median eGFR change during the observation period was higher in the active vitamin D group compared to controls. Median LVMI as well as frequency of LVH did not change significantly during vitamin D treatment, nor in controls. Consequently, final median LVMI as well as percentage of patients with LVH did not significantly differ between groups. Conclusion Calcitriol treatment in 5/6Nx rats improves cardiac hypertrophy and fibrosis, reduces uremia-induced cardiac RAAS gene expression, and improves renal Klotho expression. By contrast, treatment with active vitamin D does not decrease the prevalence of LVH in children with advanced CKD compared to matched controls. This may be due to further enhancement of FGF23 levels, faster progression of CKD associated with reduced Klotho in active vitamin D-treated patients and/or concomitant treatment with RAAS inhibitors. The latter may blunt the favorable effects of calcitriol on the activated RAAS.

Autophagy and mTOR Pathways Mediate the Potential Renoprotective Effects of Vitamin D on Diabetic Nephropathy.

Introduction Not only is diabetic nephropathy (DN) the most common cause of end-stage renal disease worldwide, but it also increases the risk of mortality up to fourteen times compared to normoalbuminuric diabetic patients. Aim The aim of the current study was the evaluation of the renoprotective effects of vitamin D in DN and the possible interplay between autophagy and mTOR pathways. Materials and Methods Fifty male Wistar albino rats were divided (10/group) into control, DN group, insulin-treated DN group, vitamin D-treated DN group, and combined insulin and vitamin D-treated DN group. Assessments of systolic blood pressure, albuminuria, creatinine clearance, serum glucose, insulin, urea, creatinine, inflammatory cytokines, oxidative stress markers, and rat kidney gene expression of mTOR were performed. Histopathological and immunohistochemical assessments of autophagy marker LC3 in rat kidneys were also performed. Results DN was associated with significant increases in SBP, urinary albumin, serum glucose, urea, creatinine, inflammatory cytokines, MDA, and mTOR gene expression (P < 0.05). However, there was significant decrease in creatinine clearance, serum insulin, GSH, and H score value of LC3 when compared with control group (P < 0.05). The combination of insulin and vitamin D treatment significantly restored DN changes when compared with the other treated groups, except in oxidative stress markers where there was an insignificant difference between the combination-treated and insulin-treated groups (P > 0.05). Conclusion It has been concluded that vitamin D is a potent adjuvant therapy in treatment of DN via downregulation of mTOR gene expression, stimulation of autophagy, and antioxidant, anti-inflammatory, and hypotensive effects.

Neuroprotective Role of Oral Vitamin D Supplementation on Consciousness and Inflammatory Biomarkers in Determining Severity Outcome in Acute Traumatic Brain Injury Patients: A Double-Blind Randomized Clinical Trial.

Background and ObjectiveEarly management of traumatic brain injury (TBI) is essential. We aimed to evaluate the efficacy of vitamin D over early clinical outcome and serum cytokine levels in patients with moderate to severe brain injury.MethodsThirty-five patients with moderate to severe traumatic brain injury who were admitted to the ICU unit were recruited into the study. Subjects were randomly allocated to a treatment regimen comprising either a one-time oral dose of 120,000 IU (two tablets of 60,000 IU each) of vitamin D (n = 20) or 8 mg of saccharide (two tablets of 4 g each) as placebo (n = 15). The main parameters evaluated included duration of mechanical ventilation and ICU stay, Glasgow Coma Scale (GCS) and cytokine levels (interleukin (IL)-6, tumour necrosis factor (TNF)-α, interferon (IFN)-γ, IL-2).ResultsThe results indicated an improvement in the level of consciousness after 7 days in the vitamin D-treated group compared with placebo. An elevation in GCS score by 3.86 units in the vitamin D-treated group with a 0.19-unit descent in the control group was recorded. Duration of mechanical ventilation was reduced in the vitamin D-treated group compared with the control group (4.7 days vs. 8.2 days, p value 0.0001). A noticeable reduction was recorded in inflammatory biomarkers (cytokines) in the vitamin D-treated group (IL-6 p = 0.08, TNF-α p = 0.02, IL-2 p = 0.36) with notable elevation in IFN-γ (p = 0.65) compared to the control group.ConclusionIn the acute phase of moderate to severe traumatic brain injury, vitamin D supplementation plays a vital role and has a favourable effect on the consciousness level of patients.Clinical trial Registry (CTRI) No. CTRI/2019/05/019259.

Vitamin D supplementation ameliorates severity of generalized anxiety disorder (GAD).

This study investigated the effects of vitamin D supplementation on Generalized Anxiety Disorder (GAD) clinical symptoms and neurochemical biomarkers including serotonin, neopterin and kynurenine. Thirty male and female patients diagnosed with GAD and had vitamin D deficiency were recruited from the psychiatric clinic at King Abdulaziz University Hospital and divided into two groups; one group of patients (n = 15) received standard of care (SOC) plus 50,000IU vitamin D (once/week) for 3months, while the other group (n = 15) received SOC alone. Biochemical parameters including serum vitamin D, serotonin, neopterin and kynurenine were measured for all patients enrolled in the trial. In addition, the Generalized Anxiety Disorder 7-item (GAD-7) scale was used to measure the severity of GAD symptoms in both vitamin D treated- and untreated-patients. Significant improvements in GAD scores were observed in the vitamin D-treated group compared to the group that did not receive vitamin D. In addition, serum serotonin concentrations were significantly increased while serum neopterin were significantly decreased in vitamin D-treated vs. untreated patients. In contrast, no significant differences were found in serum kynurenine concentrations at the end of the study period between the two groups. No changes either in GAD-7 scores or in any of the biochemical measurements were observed in the group that received only SOC after 3months. Vitamin D supplementation was effective in ameliorating the severity of GAD symptoms by increasing serotonin concentrations and decreasing the levels of the inflammatory biomarker neopterin in GAD patients.

Vitamin D Controls Tumor Growth and CD8+ T Cell Infiltration in Breast Cancer.

Women with low levels of vitamin D have a higher risk of developing breast cancer. Numerous studies associated the presence of a CD8+ T cell infiltration with a good prognosis. As vitamin D may play a key role in the modulation of the immune system, the objective of this work was to evaluate the impact of vitamin D on the breast cancer progression and mammary tumor microenvironment. We show that vitamin D decreases breast cancer tumor growth. Immunomonitoring of the different immune subsets in dissociated tumors revealed an increase in tumor infiltrating CD8+ T cells in the vitamin D-treated group. Interestingly, these CD8+ T cells exhibited a more active T cell (TEM/CM) phenotype. However, in high-fat diet conditions, we observed an opposite effect of vitamin D on breast cancer tumor growth, associated with a reduction of CD8+ T cell infiltration. Our data show that vitamin D is able to modulate breast cancer tumor growth and inflammation in the tumor microenvironment in vivo. Unexpectedly, this effect is reversed in high-fat diet conditions, revealing the importance of diet on tumor growth. We believe that supplementation with vitamin D can in certain conditions represent a new adjuvant in the treatment of breast cancers.

Vitamin D protection from rat diabetic nephropathy is partly mediated through Klotho expression and renin–angiotensin inhibition

Objective: We hypothesised that vitamin D has a beneficial renal protective effect from diabetic nephropathy (DN).Methods: Four rat groups were included: normal control (control), type 2 diabetes for eight weeks (DM), treated group with angiotensin receptor blocker losartan (DM + L), and vitamin D-treated group started from the onset of diabetes (DM + Vit D).Results: In the both treated groups, we found a significant (p < .05) reduction in the renal pro-inflammatory and profibrotic markers induced by diabetes. Vitamin D caused more reduction in monocyte chemoattractant protein-1 (MCP-1), transforming growth factor (TGFβ-1), and renin–angiotensin levels that gave better kidney function compared to the DM + L group.Conclusion: Vitamin D may have a valuable role in the renal protective effect from DN, this may occur via expression of its VDR, Klotho and blocking renin–angiotensin activation, so vitamin D should be considered as a target in renal prophylactic measures against DN.

Vitamin D supplementation to palliative cancer patients shows positive effects on pain and infections-Results from a matched case-control study.

BackgroundWe previously showed an association between low vitamin D levels and high opioid doses to alleviate pain in palliative cancer patients. The aim of this case-controlled study was to investigate if vitamin D supplementation could improve pain management, quality of life (QoL) and decrease infections in palliative cancer patients.MethodsThirty-nine palliative cancer patients with levels of 25-hydroxyvitamin D < 75 nmol/L were supplemented with vitamin D 4000 IE/day, and were compared to 39 untreated, matched “control”-patients from a previous study at the same ward. Opioid doses, antibiotic consumption and QoL-scores measured with the Edmonton Symptom Assessment Scale (ESAS) were monitored. The primary endpoint was the change from baseline after 1 and 3 months compared between the groups using linear regression with adjustment for a potential cofounding factor.ResultsAfter 1 month the vitamin D treated group had a significantly decreased fentanyl dose compared to the untreated group with a difference of 46 μg/h; 95% CI 24–78, which increased further at 3 months to 91 μg/h; 95% CI 56–140 μg/h. The ESAS QoL-score improved in the Vitamin D group the first month; -1.4; 95% CI -2.6 - (-0.21). The vitamin D-treated group had significantly lower consumption of antibiotics after 3 months compared to the untreated group, the difference was -26%; 95%CI -0.41%–(-0.12%). Vitamin D was well tolerated by all patients and no adverse events were reported.ConclusionVitamin D supplementation to palliative cancer patients is safe and improvement in pain management is noted as early as 1 month after treatment. Decreased infections are noted 3 months after vitamin D treatment. The results from this pilot-study have been used for the power-calculation of a future randomized, placebo-controlled, double-blind study called “Palliative-D” that will start in Nov 2017 and will include 254 palliative cancer patients.

Effect of Vitamin D3 Supplementation to 25(OH)D, IL-17, and HbA1c Level in Pediatric Type 1 Diabetes Mellitus

Type 1 Diabetes Mellitus (T1DM) is the consequence of autoimmune destruction process of β cells which associated with Th17 activity and low 25(OH)D level. This study was aimed to investigate the effect of vitamin D3 supplementation toward 25(OH)D level, Th17 activity (IL-17) and glycemic control (HbA1c) in pediatric T1DM. This study was designed as randomized clinical trials (RCT), double-blind, pre and post-test controlled study. Subject was children with T1DM who were divided into two groups: K1: subjects were treated with insulin 0.5–2 IU/day + vitamin D3 2000 IU/day for 3 months, K2: subjects were treated with insulin 0.5–2 IU/day + placebo for 3 months. Levels of 25(OH)D, IL-17 and HbA1c were evaluated after 3 months treatment using ELISA. After 3 months treatment, results showed that 25(OH)D level was significantly higher in K1 compared with K2 (p = 0.00), IL-17 level was significantly lower K1 compared with K2 (p= 0.022). Surprisingly, HbA1c level in K1 was not significantly different with K2 (p = 0.93). Furthermore, in vitamin D-treated group, 25(OH)D level was elevated significantly after 3 months treatment with vitamin D (p = 0.00), IL-17 level was reduced significantly after 3 months treatment with vitamin D (p= 0.001) and HbA1c level was reduced insignificantly after 3 months treatment with vitamin D (p= 0.76). Correlation study showed that there was no correlation between 25(OH)D level with IL-17 level (p= 0.160, r= -0.284) and 25(OH)D with HbA1c (p= 0.62, r= -0.10). This study can be conclude that vitamin D3 supplementation may elevate the 25(OH)D and reduce IL-17 level but did not change HbA1c level in pediatric T1DM.

Effect of Vitamin D deficiency treatment on thyroid function and autoimmunity markers in Hashimoto's thyroiditis: A double-blind randomized placebo-controlled clinical trial.

Background:The link between autoimmune thyroid diseases and Vitamin D deficiency has been reported. However, there are controversies in this regard. We conducted a double-blind randomized placebo-controlled clinical trial to investigate the effect of Vitamin D deficiency treatment on thyroid function and autoimmunity marker (thyroid peroxidase antibody [TPO-Ab]) in patients with Hashimoto's thyroiditis.Materials and Methods:Fifty-six patients with Hashimoto's thyroiditis and Vitamin D deficiency (25-hydroxyvitamin D level ≤20 ng/mL) were randomly allocated into two groups to receive Vitamin D (50000 IU/week, orally) or placebo for 12 weeks, as Vitamin D-treated (n = 30) and control (n = 26) groups, respectively. TPO-Ab, thyroid-stimulating hormone (TSH), parathormone, calcium, albumin, and creatinine concentrations were compared before and after trial between and within groups. The data were presented as mean (standard error [SE]) and analyzed by appropriate tests.Results:Mean (SE) of Vitamin D was increased in Vitamin D-treated group (45.5 [1.8] ng/mL vs. 12.7 [0.7] ng/mL, P = 0.01). Mean (SE) of TPO-Ab did not significantly change in both groups (734 [102.93] IU/mL vs. 820.25 [98.92] IU/mL, P = 0.14 in Vitamin D-treated and 750.03 [108.7] [IU/mL] vs. 838.07 [99.4] [IU/mL] in placebo-treated group, P = 0.15). Mean (SE) of TSH was not changed in both groups after trial, P = 0.4 and P = 0.15 for Vitamin D-treated and control groups, respectively. No significant difference was observed between two study groups in none studied variables (P > 0.05).Conclusion:Vitamin D treatment in Vitamin D deficient patients with Hashimoto's thyroiditis could not have significant effect on thyroid function and autoimmunity.

Effects of Vitamin D deficiency treatment on metabolic markers in Hashimoto thyroiditis patients.

Background:The aim of the current trial was to investigate the effect of Vitamin D treatment on metabolic markers in people with Vitamin D deficiency and thyroid autoimmunity.Materials and Methods:In this double-blind, randomized, placebo-controlled clinical trial, 65 Vitamin D deficient euthyroid or hypothyroid patients with positive TPO-Ab were enrolled. They randomly allocated into two groups to receive oral Vitamin D3 (50000 IU weekly) and placebo for 12 weeks. Serum concentration of calcium, phosphorus, albumin, C-reactive protein, blood urea nitrogen, creatinine, glycated hemoglobin (HbA1c), insulin, fasting plasma glucose (FPG), triglyceride (TG), total cholesterol, and high-density lipoprotein were measured in both groups before and after the trial. Homeostasis model assessment estimates of beta cell function (HOMA-B) and HOMA-insulin resistance (HOMA-IR) were calculated before and after trial in both groups.Results:Thirty-three and thirty-two participants were allocated to Vitamin D-treated and placebo-treated groups, respectively. Mean (standard error) level of Vitamin D increased significantly in Vitamin D-treated group (45.53 [1.84] ng/mL vs. 12.76 [0.74] ng/mL, P = 0.001). The mean of HbA1c and insulin was increased significantly both in Vitamin D-treated and placebo-treated groups (P < 0.05). Other variables did not meet a significant change after trial (P = NS). In between-group comparison, there was not any significant difference between Vitamin D-treated and placebo-treated groups regarding measures of HOMA-B, HOMA-IR, FPG, HbA1c, and TG (P = NS).Conclusion:Our findings showed that weekly 50000 IU oral Vitamin D3 for 12 weeks did not improve metabolic markers, IR, or insulin secretion in Vitamin D deficient patients with Hashimoto thyroiditis.

Therapeutic effects of 1,25-dihydroxyvitamin D3 on diabetes-induced liver complications in a rat model.

It has been suggested that 1,25-dihydroxyvitamin D3 (vitamin D) plays a protective role against inflammation and insulin resistance (IR) in type 2 diabetes mellitus (T2DM). The present study investigate the hypothesis that vitamin D may exert beneficial effects on the liver in a rat model of T2DM by regulating the expression of inflammation-related cytokines and ameliorating IR induced by inflammation. Normal control group rats were fed a basic diet (NC). Experimental rats received a high-fat diet for 8 weeks and were then injected with streptozotocin (STZ) to induce T2DM. Half of the T2DM model rats received vitamin D (0.03 µg/kg/day) for 8 weeks (vitamin D-treated group; VD; n=11), while the other (T2DM group; DM; n=10) and NC group received an equivalent quantity of peanut oil. Following sacrifice, fasting plasma glucose (FPG) and fasting insulin (FINS) were recorded and homeostasis model assessment of IR (HOMA-IR) was calculated. Liver histopathology was examined using hematoxylin and eosin staining. The levels of the inflammatory cytokines C-Jun N-terminal kinase, C-Jun, tumor necrosis factor-α and interleukin-1β were measured using immunohistology, quantitative polymerase chain reaction and western blot analyses. The results revealed that treatment with vitamin D markedly alleviated the pathological alterations of liver and reduced the expression of inflammatory cytokines at the protein and mRNA levels. Furthermore, decreased levels of FPG, HOMA-IR and increased FINS were detected. In conclusion, the results of the present study indicate that vitamin D has therapeutic effects on diabetes-induced liver complications in T2DM model rats, which may involve the modulation of the inflammatory response, attenuating the crosstalk’ between inflammation and IR and ameliorating hyperglycemic state.

Vitamin D3 Reduces Tissue Damage and Oxidative Stress Caused by Exhaustive Exercise

Exhaustive exercise results in inflammation and oxidative stress, which can damage tissue. Previous studies have shown that vitamin D has both anti-inflammatory and antiperoxidative activity. Therefore, we aimed to test if vitamin D could reduce the damage caused by exhaustive exercise. Rats were randomized to one of four groups: control, vitamin D, exercise, and vitamin D+exercise. Exercised rats received an intravenous injection of vitamin D (1 ng/mL) or normal saline after exhaustive exercise. Blood pressure, heart rate, and blood samples were collected for biochemical testing. Histological examination and immunohistochemical (IHC) analyses were performed on lungs and kidneys after the animals were sacrificed. In comparison to the exercise group, blood markers of skeletal muscle damage, creatine kinase and lactate dehydrogenase, were significantly (P < 0.05) lower in the vitamin D+exercise group. The exercise group also had more severe tissue injury scores in the lungs (average of 2.4 ± 0.71) and kidneys (average of 3.3 ± 0.6) than the vitamin D-treated exercise group did (1.08 ± 0.57 and 1.16 ± 0.55). IHC staining showed that vitamin D reduced the oxidative product 4-Hydroxynonenal in exercised animals from 20.6% to 13.8% in the lungs and from 29.4% to 16.7% in the kidneys. In summary, postexercise intravenous injection of vitamin D can reduce the peroxidation induced by exhaustive exercise and ameliorate tissue damage, particularly in the kidneys and lungs.

A randomized double-blind placebo-controlled study adding high dose vitamin D to analgesic regimens in patients with musculoskeletal pain.

The current mode of therapy for many patients with musculoskeletal pain is unsatisfactory. We aimed to assess the impact of adding 4000 IU of vitamin D on pain and serological parameters in patients with musculoskeletal pain. This was a randomized, double-blinded and placebo-controlled study assessing the effect of 4000 IU of orally given vitamin D3 (cholecalciferol) (four gel capsules of 1000 IU, (SupHerb, Israel) vs. placebo on different parameters of pain. Eighty patients were enrolled and therapy was given for 3 months. Parameters were scored at three time points: prior to intervention, at week 6 and week 12. Visual analogue scale (VAS) scores of pain perception were recorded following 6 and 12 weeks. We also measured serum levels of leukotriene B4 (LTB4), interleukin 6 (IL-6), tumor necrosis factor alpha (TNFα) and prostaglandin E2 (PGE2) by ELISA. The group receiving vitamin D achieved a statistically significant larger decline of their VAS measurement throughout the study compared with the placebo group. The need for analgesic 'rescue therapy' was significantly lower among the vitamin D-treated group. TNFα levels decreased by 54.3% in the group treated with vitamin D and increased by 16.1% in the placebo group. PGE2 decreased by39.2% in the group treated with vitamin D and increased by 16% in the placebo group. LTB4 levels decreased in both groups by 24% (p < 0.05). Adding 4000 IU of vitamin D for patients with musculoskeletal pain may lead to a faster decline of consecutive VAS scores and to a decrease in the levels of inflammatory and pain-related cytokines.