Vitamin D Deficiency Exacerbates Experimental Stroke Injury and Dysregulates Ischemia-Induced Inflammation in Adult Rats

Balden, Robyn; Selvamani, Amutha; Sohrabji, Farida

doi:10.1210/en.2011-1783

Cited by 123 publications

(108 citation statements)

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“…For example, pre-treatment with vitamin D attenuates the effects of various stressors, including 6-hydroxydopamine-induced neurotoxicity [5,6]. Moreover, vitamin D deficiency in adult rats has been shown to exacerbate stroke injuries and lead to more severe post-stroke behavioural impairments and this was accompanied by lower levels of the neuroprotective hormone, insulin-like growth factor 1 [7].…”

Section: Introductionmentioning

confidence: 99%

Adult vitamin D deficiency leads to behavioural and brain neurochemical alterations in C57BL/6J and BALB/c mice

Groves

Kesby

Eyles

et al. 2013

Behavioural Brain Research

119

110

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Epidemiological evidence suggests that low levels of vitamin D may predispose people to develop depression and cognitive impairment. While rodent studies have demonstrated that prenatal vitamin D deficiency is associated with altered brain development, there is a lack of research examining adult vitamin D (AVD) deficiency.The aim of this study was to examine the impact of AVD deficiency on behaviour and brain function in the mouse. Ten-week old male C57BL/6J and BALB/c mice were fed a control or vitamin D deficient diet for 10 weeks prior to, and during behavioural testing. We assessed a broad range of behavioural domains, excitatory and inhibitory neurotransmission in brain tissue, and, in separate groups of mice, locomotor response to D-amphetamine and MK-801. Overall, AVD deficiency resulted in hyperlocomotion in a novel open field and reduced GAD65/67 levels in brain tissue. AVD-deficient BALB/c mice had altered behaviour on the elevated plus maze, altered responses to heat, sound and shock, and decreased levels of glutamate and glutamine, and increased levels of GABA and glycine. By contrast C57BL/6 mice had a more subtle phenotype with no further behavioural changes but significant elevations in serine, homovanillic acid and 5-hydroxyindoleacetic acid.Although the behavioural phenotype of AVD did not seem to model a specific disorder, the overall reduction in GAD65/67 levels associated with AVD deficiency may be relevant to a number of neuropsychiatric conditions. This is the first study to show an association between AVD deficiency and prominent changes in behaviour and brain neurochemistry in the mouse.3

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Section: Introductionmentioning

confidence: 99%

Adult vitamin D deficiency leads to behavioural and brain neurochemical alterations in C57BL/6J and BALB/c mice

Groves

Kesby

Eyles

et al. 2013

Behavioural Brain Research

119

110

View full text Add to dashboard Cite

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“…Vitamin D deficiency should be considered as a very important factor for one's well-being, not only for prevention of classic rickets among children or osteomalacia among adults and the elderly, but also due to "demonstrated increase risks of many common cancers, type 1 diabetes, rheumatoid arthritis, and multiple sclerosis, and there are indications that they may be associated with type 2 diabetes and schizophrenia" 8 Vitamin D deficiencies can occur due to less than recommended levels of dietary intake over time, limited exposure to sunlight, the kidneys not being able to convert it to the active form, or inadequate absorption of vitamin D from the gastrointestinal tract 9 According to a study on Vitamin D deficiency among University students in Abu Dhabi, deficiency was only recently found to be prevalent in the Gulf Region despite the fact of having a sunny climate and being at favorable latitude, both of which are major factors contributing to the adequate possible exposure to Vitamin D 10 Also, studies have shown Emirati women to suffer from osteoporosis as a result of mild to severe Vitamin D deficiency as well as having low Vitamin D serum concentrations due to limited sun exposure and low dietary intake, further explains the prevalence of Vitamin D deficiency in the Middle East and the risk factors affecting its development despite the abundance of sunshine, thus registering the highest rates of rickets worldwide 11 The common factors are: limited sun exposure due to cultural practices and behavior and prolonged breast-feeding without the intake of supplements.…”

Section: Discusionmentioning

confidence: 99%

Assessing the Magnitude and Effect of Various Risk Factors Associated with Vitamin D Deficiency among Females in the UAE

Alomar¹,

Khouri²

2015

JYP

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Aim:The aim of this research is to determine the incidence and risk of developing Vitamin D deficiency, specifically among females within a certain age range in the UAE. Materials and Methods: A cross-sectional, descriptive, and observational study to observe and record lifestyle and dietary risk factors and their frequency in the selected females' daily lives and routines. An online distributed questionnaire has been designed and distributed among women of Al Ain city in Abu Dhabi (UAE). Statistical Analysis: SPSS version 20 was used for data analysis and statistical testing. The significance was tested using Chi Square. Results: Among the 124 females, 35.5% were exposed to the sun between 10 am and 3 pm and 64.5% were not exposed. Yes, 70.2% No). A high degree of association with P-values of 0.007 Pearson Chi-Square for frequent use of Sun protection factor 15 and its effect on sun exposure being daily in an in doors work/education environment, and Pvalues of 0.046 and 0.028 corresponding to "usual" use of Sun protection factor 15 and "rare" use. Conclusion: Vitamin D deficiency is common among female women who live in the UAE; many factors contribute to this deficiency. More rigorous work is needed to encourage women to avoid some of these factors in order to promote health and prevent vitamin D deficiency related health problems.

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“…The activating enzyme of vitamin D, 1α-hydroxylase, is found in a wide variety of tissues throughout the body, including the brain (Zehnder et al, 2001;Eyles et al, 2005), along with 25-hydroxylase (Garcion et al, 2002) and the enzyme required for the degradation of the biologically active form of vitamin D, 24-hydroxylase (CYP24A1) (See Figure 1.1) (Balden et al, 2012).…”

Section: Vitamin D Metabolism In the Brainmentioning

confidence: 99%

“…Vitamin D-deficient aged (22-month-old) male Fischer 344 rats have elevated inflammatory proteins in the brain, including TNFα and IL-6, indicating that baseline brain inflammation may be increased even without injury (Cekic et al, 2011). Furthermore, in middleaged (9-11-month-old) female Sprague-Dawley rats, a vitamin D-deficient diet produced elevated IL-6 levels within the brain and reduced insulin-like growth factor 1 (IGF-1) levels within plasma and brain following ischemia (Balden et al, 2012).…”

Section: Neuroprotectionmentioning

confidence: 99%

“…Studies with animal models of ischemic stroke have also looked at the effects of vitamin D on stroke severity and prognosis (Yasuhara et al, 2008;Balden et al, 2012). For example, a study examined the impact of vitamin D deficiency on stroke severity in the adult rat and found that vitamin D-deficient animals had greater infarct volumes compared to controls, and this corresponded with greater impairments, post-stroke, in sensorimotor behavioural testing.…”

Section: Vitamin D Deficiency and Strokementioning

confidence: 99%

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The role of adult vitamin D deficiency in cognition and brain function in mice

Groves¹

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Vitamin D deficiency is prevalent throughout the world. Even in a temperate climate such as Australia, one-third of the adult population has insufficient levels of serum vitamin D (25-hydroxyvitamin D levels <50 nmol/L). Epidemiological studies have shown significant associations between vitamin D deficiency and an increased risk of various neuropsychiatric and neurodegenerative disorders, such as schizophrenia, depression, Alzheimer's disease and cognitive impairment. However, studies based on observational epidemiology cannot address questions of causality; they cannot determine if vitamin D deficiency is a causal factor leading to the adverse health outcome. The use of animal experiments can examine the biological plausibility of the relationship between vitamin D deficiency and adverse brain outcomes.Vitamin D is a neurosteroid that has a wide range of functions within the brain including calcium maintenance, regulation of neurotrophic factors, neurogenesis, and neuroprotection. Using a model of adult vitamin D (AVD) deficiency in BALB/c mice, we have previously shown alterations in a range of behaviours and an imbalance between excitatory and inhibitory neurotransmission, which may be relevant to a range of neuropsychiatric disorders. Therefore, we have provided experimental evidence demonstrating that vitamin D deficiency in adulthood impacts on a range of brain functions, and is therefore a biologically plausible risk factor for the development of neuropsychiatric disorders. However, there is currently insufficient evidence to account for the mechanism(s) by which this occurs.There were four main aims of the thesis; to determine whether AVD deficiency impacts on (1) cognition, (2) adult hippocampal neurogenesis, and (3) glutamate and GABA signaling in BALB/c mice; and to determine if AVD deficiency would (4) exacerbate the effects of a secondary exposure, in this case social stress, in BALB/c mice and in the more resilient C57BL/6J mice.To address these aims I assessed attentional processing in BALB/c mice using the 5 choice serial reaction time task and found sex-dependent impairments in AVD-deficient male mice only.Structural and diffusion tensor imaging was assessed using MRI in male mice, however we found no significant alterations in gross brain structure or connectivity within the brain in the group exposed to AVD deficiency. I used immunohistological techniques to assess two measures of hippocampal neurogenesis, cell proliferation and survival of newborn neurons, and found that hippocampal neurogenesis was not affected by AVD deficiency at baseline or following wheel running stimulated neurogenesis.iii Despite no cellular level change in neurogenesis, the analysis of the proteomics of the hippocampus, although preliminary, provided clues that AVD deficiency may have an effect on synapse formation and plasticity, and dendritic arborisation and that these changes may be responsible for impaired learning and memory. The proteomics also provided convergent evidence of an effect on glutamate and...

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Vitamin D Deficiency Exacerbates Experimental Stroke Injury and Dysregulates Ischemia-Induced Inflammation in Adult Rats

Cited by 123 publications

References 119 publications

Adult vitamin D deficiency leads to behavioural and brain neurochemical alterations in C57BL/6J and BALB/c mice

Adult vitamin D deficiency leads to behavioural and brain neurochemical alterations in C57BL/6J and BALB/c mice

Assessing the Magnitude and Effect of Various Risk Factors Associated with Vitamin D Deficiency among Females in the UAE

The role of adult vitamin D deficiency in cognition and brain function in mice

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