Abstract 469: Vitamin D Deficiency Potentiates Restenosis Following Coronary Angioplasty in Hypercholesterolemic Swine

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Gaurav K Gupta ◽  
Tanupriya Agrawal ◽  
Michael G Del Core ◽  
William J Hunter ◽  
Devendra K Agrawal
Keyword(s):  
Vitamin D ◽  
Coronary Artery ◽  
Vitamin D Deficiency ◽  
Balloon Angioplasty ◽  
Coronary Intervention ◽  
Vitamin D Supplementation ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Increased Risk

Introduction: Vitamin D is a sectosteroid that functions through vitamin D receptor (VDR), a transcription factor, which regulates various downstream signaling pathways and controls the transcription of many targets genes. Vitamin D deficiency is associated increased risk of incident congestive heart failure, myocardial infarction, and cardiovascular disease mortality. However, most of the studies which identified an association between lower vitamin D intake or lower 25-hydroxyvitamin D and increased risk of cardiovascular disease are observational or cross-sectional studies. There has been no careful study evaluating the effect of vitamin D supplementation on coronary artery disease outcome following coronary intervention. Objective: The purpose of this study was to examine the effect of vitamin D deficiency and vitamin D supplementation on coronary artery restenosis following balloon angioplasty in hypercholesterolemic Yucatan microswine. Methods: Twelve female microswine were fed vitamin D-deficient or vitamin D-sufficient high cholesterol diet. At six months, animals underwent coronary angioplasty. Following coronary intervention swine in the vitamin D-sufficient high cholesterol diet group received supplementation of 1,000 IU or 3,000 IU of vitamin D3. Six months later, angiogram was performed followed by optical coherence tomography to monitor the development of intimal hyperplasia and restenosis. At the end of 12 months animals were euthanized, coronary arteries were harvested and morphological and histological studies were performed. Results: Findings from the optical coherence tomography and histomorphometric studies showed a significant decrease in neointimal hyperplasia, increase in in-segment lumen diameter, and decrease in the intima-media ratio in coronary arteries following balloon angioplasty in swine with vitamin D supplementation compared to the animals with vitamin D-deficient status. In the in-vitro studies, calcitriol inhibited proliferation of coronary artery smooth muscle cells. Conclusion: These data suggest that vitamin D deficiency increases intimal hyperplasia and restenosis following coronary balloon angioplasty in hypercholesterolemic swine. Since vitamin D inhibits smooth muscle cell proliferation, supplementation of non-secosteroidal VDR ligands prior to coronary intervention could help in preventing the neointimal formation and restenosis.

Abstract 500: Vitamin D Supplementation Attenuates ADAM-12-mediated Proliferation of Carotid Artery Smooth Muscle Cells of Hypercholesterolemic Swine

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Vikash Kansal ◽  
Eric B Patterson
Keyword(s):  
Vitamin D ◽  
Smooth Muscle ◽  
Carotid Artery ◽  
Protein Expression ◽  
Vitamin D Supplementation ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Tnf Α ◽  
Adam 12

Introduction: Risk of hypertension, peripheral artery disease, myocardial infarction and development of human atherosclerosis has been linked to vitamin D deficiency. Atheromatous cytokines, including IL-6, TNF-α and epidermal growth factor receptor (EGFR) family growth factors are released at the site of atherosclerosis and boost the activity of proteolytic enzymes such as ADAMs (a disintegrin and metalloproteinases). ADAM-12 cleaves proHB-EGF (Heparin-binding EGF-like growth factor) activating EGFR, resulting in increased proliferation of smooth muscle cells (SMCs). The aim of this study was to examine the effect of vitamin D on IL-6 and TNF-α-induced ADAM-12, pEGFR expression, HB-EGF release and SMC proliferation. Methods: Micro-swine were fed with vitamin D-deficient high cholesterol diet, high cholesterol diet containing 900 IU of vitamin D, and high cholesterol diet containing 3000 IU of vitamin D for total of 12 months. After six months, serum cholesterol levels of 500-600 mg/dL were achieved in all the three groups. The protein expression of ADAM-12 & pEGFR, and HB-EGF release, in presence or absence of IL-6, TNF-α and Calcitriol, in SMCs was quantified by western Blot. HB-EGF release was measured by ELISA. The proliferation was assayed by [3H]-Thymidine incorporation and cell counting method. Results: The protein expression of ADAM-12 & pEGFR, HB-EGF release were significantly reduced in carotid artery SMCs isolated from Vitamin D-supplemented swine. IL-6 and TNF-α treatment increased the protein expression of ADAM-12 & pEGFR and HB-EGF release in carotid artery SMCs. Proliferation capacity was higher in SMCs isolated from Vitamin D-deficient swine carotid artery, potentiated by IL-6 and TNF-α. Calcitriol inhibited the ADAM-12, pEGFR expression and HB-EGF released in SMCs of hypercholesterolemic swine. Calcitriol also inhibited the proliferation of carotid artery SMCs isolated from Vit D-deficient, D-sufficient and D-supplemented swine. Conclusion: Together, these results suggest that vitamin D deficiency enhances proliferation of SMCs, which is potentiated by atheromatous cytokines. Whereas, vitamin D supplementation regulates ADAM-12-mediated cleavage of proHB-EGF and activation of EGFR inhibiting SMC proliferation.

scholarly journals Implications of Vitamin D Research in Chickens can Advance Human Nutrition and Perspectives for the Future

2021 ◽  
Author(s):  
Matthew F Warren ◽  
Kimberly A Livingston
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Vitamin D Supplementation ◽  
The Body ◽  
Human Nutrition ◽  
Vitamin D Metabolites ◽  
Vitamin D Metabolism ◽  
Related Research ◽  
Vitamin D Intake ◽  
Increased Risk

Abstract The risk of vitamin D insufficiency in humans is a global problem that requires improving ways to increase vitamin D intake. Supplements are a primary means for increasing vitamin D intake, but without a clear consensus on what constitutes vitamin D sufficiency, there is toxicity risk with taking supplements. Chickens have been used in many vitamin D-related research studies, especially studies involving vitamin D supplementation. Our state-of-the-art review evaluates vitamin D metabolism and how the different hydroxylated forms are synthesized. We provide an overview with how vitamin D is absorbed, transported, excreted, and what tissues in the body store vitamin D metabolites. We also discuss a number of studies involving vitamin D supplementation with broilers and laying hens. Vitamin D deficiency and toxicity are also described and how they can be caused. The vitamin D receptor (VDR) is important for vitamin D metabolism. However, there is much more that can be understood with VDR in chickens. Potential research aims involving vitamin D and chickens should explore VDR mechanisms which could lead to newer insights with VDR. Utilizing chickens in future research to help with elucidating vitamin D mechanisms has great potential to advance human nutrition. Finding ways to increase vitamin D intake will be necessary because the coronavirus 2019 disease (COVID-19) pandemic is leading to increased risk of vitamin D deficiency in many populations. Chickens can provide a dual purpose with addressing pandemic-caused vitamin D deficiency: 1) vitamin D supplementation gives chickens added value with possibly leading to vitamin D-enriched meat and egg products; and 2) chickens’ use in research provides data for translational research. Expanding vitamin D-related research in chickens to include more nutritional aims in vitamin D status has great implications with developing better strategies to improve human health.

Abstract 279: Vitamin D3 Attenuates ADAM-12--Mediated Shedding of EGFR in Carotid Artery Smooth Muscle Cells of Hypercholesterolemic Swine

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Vikash Kansal ◽  
Swastika Sur ◽  
Velidi H Rao ◽  
Devendra K Agrawal
Keyword(s):  
Vitamin D ◽  
Cell Proliferation ◽  
Smooth Muscle ◽  
Carotid Artery ◽  
Smooth Muscle Cells ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Mrna Transcripts ◽  
Adam 12

Deficiency of Vitamin D is linked to an increased risk of hypertension, peripheral artery disease, and myocardial infarction and is a major risk factor for the development of human atherosclerosis. Atheromatous cytokines, including TNF-α, IL-6 and IFN-γ, and EGF receptor family growth factors are released at the site of atherosclerosis and act on proteolytic enzymes, MMPs (matrix metalloproteinases), ADAMs (a disintegrin and metalloproteinases), and ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs). ADAM-12 activates EGFR resulting in increased migration and proliferation of smooth muscle cells (SMCs). The aim of this study was to examine the effect of vitamin D on IL-6-induced ADAM-12 expression and SMC migration and proliferation. Micro-swine were fed with either vitamin D-deficient high cholesterol diet or high cholesterol diet containing 900 IU of vitamin D for 6 months. After six months when serum cholesterol levels ranged from 500-600 mg/dL, vitamin D-deficient group continued on the same deficient diet, whereas the other group received supplementation of vitamin D (1,000 IU/d) for 6 months. The mRNA expression of ADAM-12 and EGFR in whole carotid artery and in IL-6-treated SMCs was quantified by qPCR. The proliferation was assayed by CyQuant NF cell proliferation assay. The mRNA transcripts of ADAM-12 and EGFR were significantly increased in carotid arteries from Vitamin D-deficient than in vitamin D- supplemented swine. Treatment of SMCs with IL-6 also increased the mRNA transcripts of ADAM-12 and EGFR in vitamin D-deficient swine SMCs compared to vitamin D-supplemented swine SMCs. The cell proliferation was higher in SMCs isolated from Vitamin D-deficient swine carotid artery compared to vitamin D- supplemented swine carotid artery. Together, these results suggest that Vitamin D regulates ADAM-12-mediated activation of EGFR and vitamin D deficiency further enhances proliferation of SMCs, which is potentiated by atheromatous cytokines.

Prevalence of 25-hydroxyvitamin D deficiency in subgroups of elderly persons with anemia: association with anemia of inflammation

Blood ◽  
2011 ◽  
Vol 117 (10) ◽  
pp. 2800-2806 ◽  
Author(s):  
Todd S. Perlstein ◽  
Reena Pande ◽  
Nancy Berliner ◽  
Gary J. Vanasse
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Serum Levels ◽  
The Elderly ◽  
Vitamin D Supplementation ◽  
World Health ◽  
Elderly Persons ◽  
Increased Risk ◽  
Health Organization ◽  
Anemia Of Inflammation

AbstractAnemia and vitamin D deficiency are conditions that both result in significant morbidity and increase with age. The potential relationship between them remains poorly understood, particularly in the elderly. We used the Third National Health and Nutrition Examination Survey to examine the association of vitamin D deficiency with anemia subtypes in persons aged ≥ 60 years. Vitamin D deficiency was defined as serum levels < 20 ng/mL, and anemia was defined according to World Health Organization criteria. Vitamin D deficiency was associated with anemia prevalence independent of age, sex, or race/ethnicity (odds ratio, 1.47; 95% confidence interval, 1.06-2.05; P = .02) and varied significantly by anemia subtype (P overall = .003). The prevalence of vitamin D deficiency was 33.3% in the nonanemic population, 56% in anemia of inflammation (AI; P = .008), and 33.0% in unexplained anemia (P = .55). Non-Hispanic blacks had a 7-fold increased risk of AI compared with whites, and this was partially attenuated after adjusting for vitamin D deficiency. These data show that vitamin D deficiency is associated with specific subtypes of anemia in the elderly, especially in those with AI. Vitamin D may suppress inflammatory pathways, and studies to determine whether vitamin D supplementation ameliorates AI are warranted.

scholarly journals Are Indian obese children and adolescents at increased risk for Vitamin D deficiency?

2021 ◽  
Vol 0 ◽  
pp. 1-5
Author(s):  
Aashima Dabas ◽  
T. Aravind ◽  
Sangeeta Yadav ◽  
Mukta Mantan ◽  
Smita Kaushik
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Vitamin D Supplementation ◽  
Obese Children ◽  
Indian Children ◽  
Hydroxyvitamin D ◽  
Increased Risk ◽  
High Risk Factor ◽  
25 Hydroxyvitamin D ◽  
Obese Subjects

Objectives: Obesity has been mentioned as a high risk factor for Vitamin D deficiency (VDD) requiring supplementation in Indian children. Material and Methods: Forty obese and age-matched non-obese subjects (age 5–18 years) were assessed for lifestyle parameters, metabolic profile, and serum 25-hydroxyvitamin D (25OHD). VDD was defined as serum 25OHD < 12 ng/mL. Results: Mean 25OHD was comparable among obese and controls (15.0 ± 9.95 and 15.1 ± 4.79 ng/mL; P = 0.97) with VDD seen in 82% of cases and 85% of controls. Pubertal cases had lower 25OHD values than prepubertal obese cases (10.78 ± 4.69 and 17.2 ± 11 ng/mL; P = 0.06). Mean duration of physical activity (<2 h/week) and screen time (>2 h/day) was similar across prepubertal and pubertal groups and between obese and controls. Obesity was not associated with risk for VDD among cases and controls (odds ratio 0.83, 95% C.I. 0.25–2.7, P = 0.76). Conclusion: Obese pubertal subjects were more at risk for VDD than prepubertal subjects. Routine Vitamin D supplementation to obese Indian children may be considered during adolescence.

scholarly journals Nutritional Supplementation of Naturally Occurring Vitamin D to Improve Hemorrhagic Stroke Outcomes

2021 ◽  
Vol 12 ◽  
Author(s):  
Rani Ashouri ◽  
Madison Fangman ◽  
Jordan Brielmaier ◽  
Zoe A. Fields ◽  
Natalie Campo ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Hemorrhagic Stroke ◽  
Delayed Cerebral Ischemia ◽  
Vitamin D Supplementation ◽  
Dietary Vitamin ◽  
Stroke Incidence ◽  
Stroke Outcomes ◽  
Increased Risk ◽  
The Impact

Vitamin D deficiency, if left untreated, is associated with bone disorders, cardiovascular damage, and an increased risk of ischemic stroke. While there are various nutritional options for the natural intake of vitamin D, we hope to elucidate the potential mechanisms dietary vitamin D may play in hemorrhagic stroke pathology. This scoping review outlines findings from studies relevant to the biochemical activity of vitamin D, the impact of vitamin D deficiency on hemorrhagic stroke outcomes, and the potential benefit of nutritional vitamin D on hemorrhagic stroke outcomes. Here, we analyze the relevant factors that can lead to vitamin D deficiency, and subsequently, a higher risk of hemorrhagic stroke incidence with worsened subsequent outcomes. The neuroprotective mechanisms through which vitamin D works to attenuate hemorrhagic stroke onset and post-stroke outcomes have not yet been thoroughly examined. However, researchers have proposed several potential protective mechanisms, including reduction of blood brain barrier disturbance by inhibiting the production of reactive oxygen species, mitigation of inflammation through a reduction of levels of proinflammatory cytokines, and prevention of cerebral vasospasm and delayed cerebral ischemia following subarachnoid hemorrhage and intracerebral hemorrhage. While more research is needed and there are limitations to vitamin D supplementation, vitamin D as a whole may play a significant role in the dynamics of hemorrhagic stroke. Further research should focus on expanding our understanding of the neuroprotective capacity and mechanisms of vitamin D, as well as how vitamin D supplementation could serve as an effective course of treatment of hemorrhagic strokes.

scholarly journals Low Vitamin D Levels Predict Mortality in Ankylosing Spondylitis Patients: A Nationwide Population-Based Cohort Study

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1400
Author(s):  
Niv Ben-Shabat ◽  
Abdulla Watad ◽  
Aviv Shabat ◽  
Nicola Luigi Bragazzi ◽  
Doron Comaneshter ◽  
...  
Keyword(s):  
Vitamin D ◽  
Cohort Study ◽  
Ankylosing Spondylitis ◽  
Vitamin D Deficiency ◽  
Vitamin D Supplementation ◽  
Health Maintenance ◽  
Increased Risk ◽  
Vitamin D Levels ◽  
All Cause Mortality

In this study, we aimed to examine the effect of vitamin D deficiency on all-cause mortality in ankylosing spondylitis (AS) patients and in the general population. This is a retrospective-cohort study based on the electronic database of the largest health-maintenance organization in Israel. AS patients who were first diagnosed between 2002–2007 were included. Controls were matched by age, gender and enrollment-time. Follow-up continued until death or end of study follow-up on 1 July 2019. Laboratory measures of serum 25-hydroxyvitamin-D levels during the entire follow-up period were obtained. A total of 919 AS patients and 4519 controls with a mean time of follow-up of 14.3 years were included. The mean age at the time of enrollment was 52 years, and 22% of them were females. AS was associated with a higher proportion of vitamin D deficiency (odds ratio 1.27 [95% confidence-interval (CI) 1.03–1.58]). In AS patients, insufficient levels of vitamin D (<30 ng/mL) were significantly associated with increased incidence of all-cause mortality (hazard ratio (HR) 1.59 [95% CI 1.02–2.50]). This association was more prominent with the decrease in vitamin D levels (< 20 ng/mL, HR 1.63 [95% CI 1.03–2.60]; <10 ng/mL, HR 1.79 [95% CI 1.01–3.20]) and among male patients (<30 ng/mL, HR 2.11 [95% CI 1.20–3.72]; <20 ng/mL, HR 2.12 [95% CI 1.19–3.80]; <10 ng/mL, HR 2.23 [95% CI 1.12–4.43]). However, inadequate levels of vitamin D among controls were not associated with an increased all-cause mortality. Our study has shown that vitamin D deficiency is more common in AS patients than controls and is linked to an increased risk for all-cause mortality. These results emphasize the need for randomized-controlled trials to evaluate the benefits of vitamin D supplementation as a secondary prevention of mortality in patients with chronic inflammatory rheumatic disease.

Abstract 559: FTY720 Protects Against Diet Induced Coronary Artery Disease and Myocardial Infarction in Diabetic SR-B1-/- ApoE-Hypomorphic Mice

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Leticia A Gonzalez-Jara ◽  
Geoff Werstuck ◽  
Bernardo Trigatti
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Cardiac Fibrosis ◽  
Diabetic Animal ◽  
High Cholesterol Diet ◽  
Aortic Atherosclerosis ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Aortic Sinus

Background: Epidemiological studies have established diabetes as a risk factor for the development of cardiovascular diseases. Increased development of aortic atherosclerosis has been shown in diabetic animal models, but the effect on coronary artery (CA) disease is less clear. Conventional mouse models of atherosclerosis do not reproducibly develop CA atherosclerosis. SR-B1-/- apoE-hypomorphic mice develop increased aortic sinus atherosclerosis and diet-induced CA atherosclerosis when compared to SR-B1+/+ apoE-hypomorphic mice. FTY720, a sphingosine-1-phosphate analog, has been shown to play a protective role in both atherosclerosis and diabetes. We assessed the hypothesis that FTY720 supplementation will decrease the development of CA and aortic atherosclerosis and myocardial infarction in diabetic SR-B1-/- apoE-hypomorphic mice fed an atherogenic diet. Methods: Diabetes was induced by multiple low-dose i.p. injections of streptozotocin (40 mg/kg body weight). Controls received vehicle. Mice were fed a high-fat/high-cholesterol diet for 4 weeks (n=14-15). FTY720 was administered on the drinking water (0.0036 g/l, n=14-15). CA and aortic atherosclerosis and cardiac fibrosis were evaluated. Results: Diabetic SR-B1-/- apoE-hypomorphic mice fed a high-fat/high-cholesterol diet presented reduced survival (p<0.01) and significantly larger plaques in the aortic sinus (p<0.05) compared to control. CA atherosclerosis burden (p<0.001) and levels of cardiac fibrosis (p<0.01) were increased as well. FTY720 supplementation significantly protected diabetic mice against aortic and CA atherosclerosis (p<0.05) and myocardial fibrosis (p<0.05). Conclusion: FTY720 significantly reduced the burden of aortic and CA atherosclerosis and cardiac fibrosis in diabetic SR-B1-/- apoE-hypomorphic mice challenged with a high-fat/high-cholesterol diet.

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