tisdag 30 november 2021

Role of Vitamins in Neurodegenerative Diseases: A Review

https://pubmed.ncbi.nlm.nih.gov/34802410/

Background: Vitamins are the micronutrients required for boosting the immune system and managing any future infection. Vitamins are involved in neurogenesis, a defense mechanism working in neurons, metabolic reactions, neuronal survival, and neuronal transmission. Their deficiency leads to abnormal functions in the brain like oxidative stress, mitochondrial dysfunction, accumulation of proteins (synuclein, Aβ plaques), neurodegeneration, and excitotoxicity.”

Conclusion: The deficiency of vitamins in the body causes various neurological disorders like Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and depression. We have discussed the role of vitamins in neurological disorders and the normal human body. Depression is linked to a deficiency of vitamin-C and vitamin B. In the case of Alzheimer’s disease, there is a lack of vitamin-B1, B12, and vitamin-A, which results in Aβ-plaques. Similarly, in Parkinson’s disease, vitamin-D deficiency leads to a decrease in the level of dopamine, and imbalance in vitamin D leads to accumulation of synuclein. In MS, Vitamin-C and Vitamin-D deficiency causes demyelination of neurons. In Huntington’s disease, vitamin- C deficiency decreases the antioxidant level, enhances oxidative stress, and disrupts the glucose cycle. Vitamin B5 deficiency in Huntington’s disease disrupts the synthesis of acetylcholine and hormones in the brain.”

Kumar RR, Singh L, Thakur A, Singh S, Kumar B. Role of Vitamins in Neurodegenerative Diseases: A Review. CNS Neurol Disord Drug Targets. 2021 Nov 19. doi: 10.2174/1871527320666211119122150. Epub ahead of print. PMID: 34802410.



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onsdag 24 november 2021

Vitamin A supplementation and serum Th1- and Th2-associated cytokine response in women

https://pubmed.ncbi.nlm.nih.gov/24024773/

Conclusions: Decline in serum concentrations of IL-1β and IL-1β/IL-4 ratio in obese women suggests that vitamin A is capable of regulating the immune system and possibly reducing the risk of autoimmune disease in this group.”

Farhangi MA, Keshavarz SA, Eshraghian M, Ostadrahimi A, Saboor-Yaraghi AA. Vitamin A supplementation and serum Th1- and Th2-associated cytokine response in women. J Am Coll Nutr. 2013;32(4):280-5. doi: 10.1080/07315724.2013.816616. PMID: 24024773.



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onsdag 10 november 2021

The Role of Vitamin A in Wound Healing

https://pubmed.ncbi.nlm.nih.gov/31389093/

Abstract

Vitamin A is an essential micronutrient that comes in multiple forms, including retinols, retinals, and retinoic acids. Dietary vitamin A is absorbed as retinol from preformed retinoids or as pro-vitamin A carotenoids that are converted into retinol in the enterocyte. These are then delivered to the liver for storage via chylomicrons and later released into the circulation and to its biologically active tissues bound to retinol-binding protein. Vitamin A is a crucial component of many important and diverse biological functions, including reproduction, embryological development, cellular differentiation, growth, immunity, and vision. Vitamin A functions mostly through nuclear retinoic acid receptors, retinoid X receptors, and peroxisome proliferator-activated receptors. Retinoids regulate the growth and differentiation of many cell types within skin, and its deficiency leads to abnormal epithelial keratinization. In wounded tissue, vitamin A stimulates epidermal turnover, increases the rate of re-epithelialization, and restores epithelial structure. Retinoids have the unique ability to reverse the inhibitory effects of anti-inflammatory steroids on wound healing. In addition to its role in the inflammatory phase of wound healing, retinoic acid has been demonstrated to enhance production of extracellular matrix components such as collagen type I and fibronectin, increase proliferation of keratinocytes and fibroblasts, and decrease levels of degrading matrix metalloproteinases.

Polcz ME, Barbul A. The Role of Vitamin A in Wound Healing. Nutr Clin Pract. 2019 Oct;34(5):695-700. doi: 10.1002/ncp.10376. Epub 2019 Aug 7. PMID: 31389093.



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