In a new study entitled “Dietary Vitamin D3 Restriction Exacerbates Disease Pathophysiology in the Spinal Cord of the G93A Mouse Model of Amyotrophic Lateral Sclerosis,” researchers evaluated the effects of a Vitamin D dietary restriction in the pathogenesis of Amyotrophic lateral sclerosis. The study was performed with ALS mouse models and included mice of both genders, with authors finding that Vitamin D deficiency causes gender-specific detrimental effects. The study was published in the journal PLOS One.
Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, is characterized by degeneration motor neurons, ultimately leading to patients’ death due to respiratory failure. ALS is the most common motor neuron disease in adults being diagnosed usually between 45 and 60 years of age. Previous reports with ALS mouse models suggested that diet-based strategies could mitigate ALS severity.
Vitamin D is a fat-soluble vitamin that is naturally present in some foods and is key to promote calcium absorption in the gut, but also has vital neuromuscular and immune functions. In fact, previous studies showed that Vitamin D reduces inflammation in diseases that share common pathophysiologies with ALS, such as multiple sclerosis, dementia and Alzheimer’s disease.
In this study, a team of researchers following their previous work where they showed that vitamin D3 restriction in an ALS mouse model significantly reduce mice motor performance, analyzed whether vitamin D3 restriction impacted directly in the Central Nervous System (CNS) of their ALS mouse model mice. Specifically, the team determined the effects of vitamin D deficiency (achieved by dietary restriction) in several factors measured at mice spinal cord, including inflammation, apoptosis, neurotrophic factors (a family of proteins responsible for growth and survival of developing neurons and for maintaining mature neurons and neuron count).
The models were divided into two groups, where the control group received food ad libitum, including their usual components and their standardize amounts, and the study group with a diet deficient in Vitamin D3. The mice spinal cord was then analyzed at day 113 after beginning the diet.
The team found that dietary vitamin D restriction exacerbated disease pathophysiology, as denoted by higher levels of apoptosis (cell death) and oxidative degradation of lipids (lipid per oxidation), crucial steps in the pathogenesis of several disease states, including ALS, when compared to control mice. Additionally, vitamin D restriction induced higher inflammation in mouse females and a reduced capacity to protect their cells against reactive oxygen species in male mice. As a result, dietary vitamin D restriction caused detrimental effects in both genders; however, the pathways affected are different in females and male mice, with the latter exhibiting the most deleterious effects.
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