scholarly journals Vitamin D Is Necessary for Murine Gastric Epithelial Homeostasis

Biology ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 705
Author(s):  
Ifrah Ismail Ali ◽  
Iltaf Shah ◽  
Sayed Marzouk ◽  
Sherif Karam ◽  
Asma Al Menhali
Keyword(s):  
Vitamin D ◽  
Parietal Cell ◽  
Physiological Role ◽  
Standard Diet ◽  
Deficient Diet ◽  
Cell Functions ◽  
Epithelial Homeostasis ◽  
Vitamin D Levels ◽  
Acid Secreting ◽  
Normal Light

Unlike other organs, the importance of VD in a normal stomach is unknown. This study focuses on understanding the physiological role of vitamin D in gastric epithelial homeostasis. C57BL/6J mice were divided into three groups that were either fed a standard diet and kept in normal light/dark cycles (SDL), fed a standard diet but kept in the dark (SDD) or fed a vitamin D-deficient diet and kept in the dark (VDD). After 3 months, sera were collected to measure vitamin D levels by LC-MS/MS, gastric tissues were collected for immunohistochemical and gene expression analyses and gastric contents were collected to measure acid levels. The VDD group showed a significant decrease in the acid-secreting parietal cell-specific genes Atp4a and Atp4b when compared with the controls. This reduction was associated with an increased expression of an antral gastrin hormone. VDD gastric tissues also showed a high proliferation rate compared with SDL and SDD using an anti-BrdU antibody. This study indicates the requirement for normal vitamin D levels for proper parietal cell functions.

scholarly journals Restoration of Vitamin D Levels Improves Endothelial Function and Increases TASK-Like K+ Currents in Pulmonary Arterial Hypertension Associated with Vitamin D Deficiency

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 795
Author(s):  
Maria Callejo ◽  
Daniel Morales-Cano ◽  
Gema Mondejar-Parreño ◽  
Bianca Barreira ◽  
Sergio Esquivel-Ruiz ◽  
...  
Keyword(s):  
Vitamin D ◽  
Pulmonary Arterial Hypertension ◽  
Endothelial Function ◽  
Arterial Hypertension ◽  
Vascular Remodeling ◽  
Standard Diet ◽  
Pulmonary Vascular Remodeling ◽  
Vitamin D Levels ◽  
Pulmonary Arterial ◽  
K Currents

Background: Vitamin D (vitD) deficiency is highly prevalent in patients with pulmonary arterial hypertension (PAH). Moreover, PAH-patients with lower levels of vitD have worse prognosis. We hypothesize that recovering optimal levels of vitD in an animal model of PAH previously depleted of vitD improves the hemodynamics, the endothelial dysfunction and the ionic remodeling. Methods: Male Wistar rats were fed a vitD-free diet for five weeks and then received a single dose of Su5416 (20 mg/Kg) and were exposed to vitD-free diet and chronic hypoxia (10% O2) for three weeks to induce PAH. Following this, vitD deficient rats with PAH were housed in room air and randomly divided into two groups: (a) continued on vitD-free diet or (b) received an oral dose of 100,000 IU/Kg of vitD plus standard diet for three weeks. Hemodynamics, pulmonary vascular remodeling, pulmonary arterial contractility, and K+ currents were analyzed. Results: Recovering optimal levels of vitD improved endothelial function, measured by an increase in the endothelium-dependent vasodilator response to acetylcholine. It also increased the activity of TASK-1 potassium channels. However, vitD supplementation did not reduce pulmonary pressure and did not ameliorate pulmonary vascular remodeling and right ventricle hypertrophy. Conclusions: Altogether, these data suggest that in animals with PAH and severe deficit of vitD, restoring vitD levels to an optimal range partially improves some pathophysiological features of PAH.

scholarly journals Impact of Chrysin on Vitamin D and Bone Health - Preclinical Studies

2020 ◽  
Author(s):  
Siva Swapna Kasarla ◽  
Sujatha Dodoala ◽  
Sunitha Sampathi ◽  
Narendra Kumar Talluri
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Bone Health ◽  
Low Dose ◽  
Active Vitamin ◽  
Deficient Diet ◽  
Bone Parameters ◽  
Active Vitamin D ◽  
Vitamin D Levels ◽  
The Impact

AbstractVitamin D deficiency is an endemic problem existing worldwide. Although several strategies were established to enhance vitamin D3 levels, studies specifically focussing inhibition of vitamin D metabolism which may prolong the availability of active vitamin D in pathological conditions are less explored. Studies also suggest that higher doses of vitamin D3 fail to achieve optimum vitamin D levels. In this context, we focussed on the enzyme CYP3A4 which promotes inactivation of active vitamin D. The current study was aimed to decipher the impact of chrysin, a proven CYP3A4 inhibitor as an intervention and its effects in combination with low dose vitamin D3 (40 IU) and bone health in vitamin D deficiency condition. The in-vivo activity of chrysin was evaluated on female Wistar albino rats fed with a vitamin D deficient diet to attain vitamin D deficiency for 28 days. Chrysin was given alone and in combination with calcium carbonate (CaCO3) and/or vitamin D3. All the therapeutic interventions were assessed for serum 25-OH-D3 by LC-MS, biochemical, urinary, and bone parameters. Animals treated with chrysin alone and in combination with low dose vitamin D3 and/or CaCO3 showed an eminent rise in serum 25-OH-D3 levels along with increased serum biochemical parameters. On contrary, a significant decrease in the urinary parameters followed by beneficial effects on bone parameters was noticed in contrast with the vitamin D deficient diet group. Our findings revealed that although chrysin alone showed a notable effect on 25-OH-D3 and osseous tissue, comparatively it showed intensified therapeutic effect in combination with vitamin D3 and CaCO3 which can be employed as a cost-effective option to improve bone health.Graphical Abstract

scholarly journals The Restoration of Vitamin D Levels Slows the Progression of Renal Ischemic Injury in Rats Previously Deficient in Vitamin D

2021 ◽  
Vol 8 ◽  
Author(s):  
Michele Santiago dos Santos ◽  
Daniele Canale ◽  
Desiree Rita Denelle Bernardo ◽  
Maria Heloisa Massola Shimizu ◽  
Antonio Carlos Seguro ◽  
...  
Keyword(s):  
Vitamin D ◽  
Renal Function ◽  
Renal Disease ◽  
Disease Progression ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Public Health Problem ◽  
Standard Diet ◽  
Renal Disease Progression ◽  
Vitamin D Levels

Chronic kidney disease (CKD) remains a global public health problem. The initial damage after ischemia/reperfusion (I/R) injury plays an important role in the pathogenesis of acute kidney injury (AKI) and predisposition to CKD. Several studies have been showing that nontraditional risk factors such as AKI and hypovitaminosis D could also be involved in CKD progression. Vitamin D deficiency (VDD) is associated with hemodynamic changes, activation of inflammatory pathways and renal disease progression (RDP) following I/R-AKI. Strategies for prevention and/or slowing RDP have been determined and the sufficiency of vitamin D has been emerging as a renoprotective factor in many diseases. Therefore, we investigated the effect of the restoration of vitamin D levels in the progression of I/R injury (IRI) in rats previously deficient in vitamin D. On day 30, male Wistar rats were submitted to bilateral 45 min IRI and divided into three groups: IRI, standard diet for 120 days; VDD+IRI, vitamin D-free diet for 120 days; and VDD+IRI+R, vitamin D-free diet in the first 30 days and just after I/R, we reintroduced the standard diet in the last 90 days. After the 120-day protocol, VDD+IRI+R rats presented an improvement in the renal function and renal protein handling followed by a smaller fractional interstitial area. Furthermore, those animals exhibited a reestablishment regarding the hemodynamic parameters and plasma levels of aldosterone, urea and PTH. In addition, the restoration of vitamin D levels reestablished the amount of MCP1 and the renal expressions of CD68+ and CD3+ cells in the VDD+IRI+R rats. Also, VDD+IRI+R rats showed a restoration regarding the amount of collagen type III and renal expressions of fibronectin, vimentin and α-SMA. Such changes were also accompanied by a reestablishment on the renal expression of VDR, Klotho, JG12, and TGF-β1. Our findings indicate that the restoration of vitamin D levels not only improved the renal function and hemodynamics but also reduced the inflammation and fibrosis lesions observed in I/R-AKI associated with VDD. Thus, monitoring of vitamin D status as well as its replacement in the early stages of kidney injury may be a therapeutic alternative in the mitigation of renal disease progression.

Vitamin D deficiency enhances expression of autophagy-regulating miR-142-3p in mouse and 'involved' IBD patient intestinal tissues

2021 ◽  
Author(s):  
Laurel McGillis ◽  
Dana M. Bronte-Tinkew ◽  
Frances Dang ◽  
Mariana Capurro ◽  
Akriti Prashar ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Control Diet ◽  
Adaptor Protein ◽  
Paneth Cells ◽  
Deficient Diet ◽  
Vitamin D Levels ◽  
Treatment Naïve ◽  
Potential Link ◽  
Vitamin D Signaling

Vitamin D deficiency is an environmental factor involved in the pathogenesis of inflammatory bowel disease (IBD), however, the mechanisms surrounding its role remain unclear. Previous studies conducted in an intestinal epithelial-specific vitamin D receptor (VDR) knockout model suggest that a lack of vitamin D signaling causes a reduction in intestinal autophagy. A potential link between vitamin D deficiency and dysregulated autophagy is microRNA (miR)-142-3p, which suppresses autophagy. In this study, we found that wildtype C57BL/6 mice fed a vitamin D deficient diet for 5 weeks had increased miR-142-3p expression in ileal tissues compared to mice fed a matched control diet. Interestingly, there was no difference in expression of key autophagy markers ATG16L1 and LC3II in the ileum whole tissue. However, Paneth cells of vitamin D deficient mice were morphologically abnormal and had an accumulation of the autophagy adaptor protein p62 which was not present in the total crypt epithelium. These findings suggest that Paneth cells exhibit early markers of autophagy dysregulation within the intestinal epithelium in response to vitamin D deficiency and enhanced miR-142-3p expression. Finally, we demonstrated that treatment-naïve IBD patients with low levels of vitamin D have an increase in miR-142-3p expression in colonic tissues procured from 'involved' areas of disease. Taken together, our findings demonstrate that insufficient vitamin D levels alter expression of autophagy-regulating miR-142-3p in intestinal tissues of mice and IBD patients, providing insight into the mechanisms by which vitamin D deficiency modulates IBD pathogenesis.

P0722VITAMIN D-DEFICIENT RATS RECOVER RENAL ALTERATIONS AFTER VITAMIN D REPLACEMENT FOLLOWING ISCHEMIA-REPERFUSION INJURY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Antonio Carlos Seguro ◽  
Michele S Santos ◽  
Desiree Rita Denelle Bernardo ◽  
Daniele Canale ◽  
Maria Heloisa Massola Shimizu ◽  
...  
Keyword(s):  
Vitamin D ◽  
Renal Function ◽  
Reperfusion Injury ◽  
Vitamin D Deficiency ◽  
Plasma Levels ◽  
Protective Factor ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Standard Diet ◽  
Vitamin D Levels

Abstract Background and Aims Several studies have been linking vitamin D deficiency (VDD) as a non-traditional risk factor to acute kidney injury (AKI). It has been shown that VDD associated with AKI potentiates the injury and may accelerate the progression of kidney disease. Conversely, some lines of evidence have been describing that vitamin D sufficiency can be considered as a renal protective factor. Thus, we aimed to verify the effect of vitamin D replacement (R) on the renal disease progression post ischemia-reperfusion injury (IRI) in vitamin D deficient rats. Method We performed bilateral 45 min IRI on day 30 in all animal groups. Male Wistar rats were randomized into three groups: 1- IRI (fed a standard diet for 120 days); 2- VDD+IRI (fed a vitamin D-free diet for 120 days); and 3- VDD+IRI+R (fed a vitamin D-free diet for 30 days and just after IRI, on day 31, we reintroduced the standard diet for more 90 days). We evaluated inulin clearance (Cin); mean arterial pressure (MAP); renal blood flow (RBF); plasma levels of Vitamin D2+D3 [25(OH)D] and Parathormone (PTH) by ELISA. In addition, we performed histomorphometrical studies for CD3+ cells, fibronectin and vimentin as well as the fractional interstitial area (FIA). Moreover, we run qPCR studies and immunoblotted for vitamin D receptor (VDR) and Klotho. All the results are described in table 1. Results Vitamin D replacement restored the plasma levels of 25(OH)D and PTH in VDD+IRI+R group. Also, VDD+IRI+R presented an improvement of renal function and hemodynamic parameters. In addition, we observed more evident alterations in tubulointerstitial compartment, featuring interstitial expansion (renal fibrosis and inflammatory cell infiltrates) and fibronectin and vimentin expression in VDD+IRI rats. These alterations were recovered by vitamin D replacement. Concerning VDR and Klotho data, our results revealed a decreased expression of these targets in VDD+IRI group. On the other hand, vitamin D replacement retrieved the expression of VDR and Klotho. Conclusion Our study suggests that vitamin D replacement improved the recovery of renal function, hemodynamics, inflammatory and morphological alterations. In addition, vitamin D replacement was able to reestablish the expression of VDR and Klotho in IRI-AKI associated with vitamin D deficiency. Thus, it is recommendable that vitamin D levels should be observed as well as its reposition should be taken into account in renal patients.

scholarly journals Effects of memantine and high dose vitamin D on gait in the APP/PS1 mouse model of Alzheimer's disease following vitamin D deprivation

2021 ◽  
Author(s):  
Dana N Broberg ◽  
Dickson Wong ◽  
Miranda Bellyou ◽  
Manuel Montero-Odasso ◽  
Olivier Beauchet ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Amyloid Β ◽  
Glutamate Toxicity ◽  
Control Group ◽  
High Dose ◽  
Standard Diet ◽  
Deficient Diet ◽  
Gait Performance

Background: Altered gait is a frequent feature of Alzheimer's disease (AD), as is vitamin D deficiency. Treatment with memantine and vitamin D can protect cortical axons from exposure to amyloid-β and glutamate toxicity, suggesting this combination may mitigate altered gait in AD. Objective: Investigate the effects of vitamin D deprivation and subsequent treatment with memantine and vitamin D enrichment on gait performance in APPswe/PS1dE9 mice. Methods: Male APPswe/PS1dE9 mice were split into four groups (n=14 each) at 2.5 months of age. A control group was fed a standard diet throughout while the other three groups started a vitamin D-deficient diet at month 6. The VitD- group remained on this deficient diet for the rest of the study. At month 9, the remaining two groups began treatment with either memantine alone or memantine combined with 10 IU/g of vitamin D. Gait performance was assessed at months 6, 9, 12, and 15. Results: Vitamin D deprivation led to a 13% increase in hind stride width by month 15 (p<0.001). Examination of the treatment groups at month 15 revealed that mice treated with memantine alone still showed an increase in hind stride width compared to controls (p<0.01), while mice treated with memantine and vitamin D did not (p=0.21). Conclusion: Vitamin D deprivation led to impaired postural control in the APPswe/PS1dE9 model. Treatment with memantine and vitamin D, but not memantine alone, prevented this impairment. Future work should explore the potential for treatments incorporating vitamin D supplementation to improve gait in people with AD.

Effects of Memantine and High Dose Vitamin D on Gait in Male APP/PS1 Alzheimer’s Disease Mice Following Vitamin D Deprivation

2021 ◽  
pp. 1-12
Author(s):  
Dana Broberg ◽  
Dickson Wong ◽  
Miranda Bellyou ◽  
Manuel Montero-Odasso ◽  
Olivier Beauchet ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Amyloid Β ◽  
The Other ◽  
Glutamate Toxicity ◽  
Control Group ◽  
High Dose ◽  
Standard Diet ◽  
Deficient Diet

Background: Altered gait is a frequent feature of Alzheimer’s disease (AD), as is vitamin D deficiency. Treatment with memantine and vitamin D can protect cortical axons from exposure to amyloid-β and glutamate toxicity, suggesting this combination may mitigate altered gait in AD. Objective: Investigate the effects of vitamin D deprivation and subsequent treatment with memantine and vitamin D enrichment on gait performance in APPswe/PS1dE9 mice. Methods: Male APPswe/PS1dE9 mice were split into four groups (n = 14 each) at 2.5 months of age. A control group was fed a standard diet throughout while the other three groups started a vitamin D-deficient diet at month 6. One group remained on this deficient diet for the rest of the study. At month 9, the other two groups began treatment with either memantine alone or memantine combined with 10 IU/g of vitamin D. Gait was assessed using CatWalk at months 6, 9, 12, and 15. Results: Vitamin D deprivation led to a 13% increase in hind stride width by month 15 (p <  0.001). Examination of the treatment groups at month 15 revealed that mice treated with memantine alone still showed an increase in hind stride width compared to controls (p <  0.01), while mice treated with memantine and vitamin D did not (p = 0.21). Conclusion: Vitamin D deprivation led to impaired postural control in the APPswe/PS1dE9 model. Treatment with memantine and vitamin D, but not memantine alone, prevented this impairment. Future work should explore the potential for treatments incorporating vitamin D supplementation to improve gait in people with AD.

scholarly journals Diet-induced vitamin D deficiency has no effect on acute post-stroke outcomes in young male mice

2017 ◽  
Vol 38 (11) ◽  
pp. 1968-1978 ◽  
Author(s):  
Megan A Evans ◽  
Hyun Ah Kim ◽  
T Michael De Silva ◽  
Thiruma V Arumugam ◽  
Andrew N Clarkson ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Immune Cells ◽  
Functional Outcomes ◽  
Infarct Volume ◽  
Control Group ◽  
Deficient Diet ◽  
Stroke Outcomes ◽  
Post Stroke ◽  
Vitamin D Levels

Recent observational studies have reported that patients with low circulating levels of vitamin D experience larger infarct volumes and worse functional outcomes after ischemic stroke compared to those with sufficient levels. However, it is unknown whether a causal relationship exists between low vitamin D levels and poor stroke outcome. This study aimed to assess the effect of vitamin D deficiency on acute outcomes post-stroke. Male C57Bl6 mice (six week old) were assigned to either a control or vitamin D deficient diet for four weeks prior to stroke. Stroke was induced by 1 h middle cerebral artery occlusion (MCAO) with reperfusion. At 24 h, we assessed functional outcomes, infarct volume, quantified immune cells in the brain by immunofluorescence and examined susceptibility to lung infection. ELISAs showed that the plasma level of hydroxyvitamin D3 was 85% lower in mice fed the vitamin D-deficient diet compared with the control group. Despite this, vitamin D deficiency had no impact on functional outcomes or infarct volume after stroke. Further, there were no differences in the numbers of infiltrating immune cells or bacterial load within the lungs. These data suggest that diet-induced vitamin D deficiency has no effect on acute post-stroke outcomes.

scholarly journals Correlation of Vitamin D Levels with Pigmentation in Vitiligo Patients Treated with NBUVB Therapy

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Manu Sehrawat ◽  
Tarlok Chand Arora ◽  
Amrita Chauhan ◽  
Hemanta Kumar Kar ◽  
Amitabh Poonia ◽  
...  
Keyword(s):  
Vitamin D ◽  
Human Skin ◽  
Narrow Band ◽  
Physiological Role ◽  
Severity Index ◽  
Ultraviolet B ◽  
Moderate Correlation ◽  
Vitamin D Levels ◽  
25 Hydroxy Vitamin D ◽  
Age And Sex

Cholecalciferol (vitamin D) might play a physiological role in photo-induced melanogenesis in human skin. We estimated the levels of 25-hydroxy vitamin D [25(OH)D] before, during, and after Narrow Band Ultraviolet B (NBUVB) radiation in patients of vitiligo and their correlation with NBUVB induced pigmentation. Thirty patients of vitiligo and equal number of age and sex matched controls were recruited for the study. Vitiligo patients were treated with NBUVB thrice weekly for 12 weeks. [25(OH)D] levels and Vitiligo Area and Severity Index (VASI) were calculated at 0 (baseline), 6, and 12 weeks. Baseline [25(OH)D] levels were measured in controls. Significant reduction in VASI score was observed after 12 weeks of therapy. Comparison and correlation between mean improvement in VASI and [25(OH)D] levels at 12 weeks showed moderate correlation, and the results were statistically insignificant. Mean reduction in VASI and increase in [25(OH)D] levels after 12 weeks of NBUVB showed moderate correlation. Thus, vitamin D might play a significant role in photo-induced melanogenesis. However, there might be additional effects of the phototherapy on melanogenesis. The complete mechanism of NBUVB induced pigmentation in vitiligo needs to be elucidated.

scholarly journals Developmental Vitamin D Deficiency in Pregnant Rats Does Not Induce Preeclampsia

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4254
Author(s):  
Asad Ali ◽  
Suzanne Alexander ◽  
Pauline Ko ◽  
James S. M. Cuffe ◽  
Andrew J. O. Whitehouse ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Rat Model ◽  
Epidemiological Studies ◽  
Late Gestation ◽  
Deficient Diet ◽  
Pregnant Rats ◽  
Increased Risk ◽  
Vitamin D Levels ◽  
Behavioural Phenotypes

Preeclampsia is a pregnancy disorder characterized by hypertension. Epidemiological studies have associated preeclampsia with an increased risk of neurodevelopmental disorders in offspring, such as autism and schizophrenia. Preeclampsia has also been linked with maternal vitamin D deficiency, another candidate risk factor also associated with autism. Our laboratory has established a gestational vitamin-D-deficient rat model that shows consistent and robust behavioural phenotypes associated with autism- and schizophrenia-related animal models. Therefore, we explored here whether this model also produces preeclampsia as a possible mediator of behavioural phenotypes in offspring. We showed that gestational vitamin D deficiency was not associated with maternal blood pressure or proteinuria during late gestation. Maternal and placental angiogenic and vasculogenic factors were also not affected by a vitamin-D-deficient diet. We further showed that exposure to low vitamin D levels did not expose the placenta to oxidative stress. Overall, gestational vitamin D deficiency in our rat model was not associated with preeclampsia-related features, suggesting that well-described behavioural phenotypes in offspring born to vitamin-D-deficient rat dams are unlikely to be mediated via a preeclampsia-related mechanism.

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