The Impact of Vitamin D and L-Cysteine Co-Supplementation on Upregulating Glutathione and Vitamin D-Metabolizing Genes and in the Treatment of Circulating 25-Hydroxy Vitamin D Deficiency.
Sushil K Jain,
Jeffrey Justin Margret,
Steven A Abrams,
Steven N Levine,
Kamal Bhusal
Review
Nutrients
2024
6 اقتباسات
PubMed
DOI
CC-BY
PDF
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Study Design
- نوع الدراسة
- review
- التدخل
- The Impact of Vitamin D and L-Cysteine Co-Supplementation on Upregulating Glutathione and Vitamin D-Metabolizing Genes and in the Treatment of Circulating 25-Hydroxy Vitamin D Deficiency. None
- المقارن
- Placebo
- اتجاه التأثير
- Positive
- خطر التحيز
- Low
Abstract
Vitamin D receptors are expressed in many organs and tissues, which suggests that vitamin D (VD) affects physiological functions beyond its role in maintaining bone health. Deficiency or inadequacy of 25(OH)VD is widespread globally. Population studies demonstrate that a positive association exists between a high incidence of VD deficiency and a high incidence of chronic diseases, including dementia, diabetes, and heart disease. However, many subjects have difficulty achieving the required circulating levels of 25(OH)VD even after high-dose VD supplementation, and randomized controlled clinical trials have reported limited therapeutic success post-VD supplementation. Thus, there is a discordance between the benefits of VD supplementation and the prevention of chronic diseases in those with VD deficiency. Why this dissociation exists is currently under debate and is of significant public interest. This review discusses the downregulation of VD-metabolizing genes needed to convert consumed VD into 25(OH)VD to enable its metabolic action exhibited by subjects with metabolic syndrome, obesity, and other chronic diseases. Research findings indicate a positive correlation between the levels of 25(OH)VD and glutathione (GSH) in both healthy and diabetic individuals. Cell culture and animal experiments reveal a novel mechanism through which the status of GSH can positively impact the expression of VD metabolism genes. This review highlights that for better success, VD deficiency needs to be corrected at multiple levels: (i) VD supplements and/or VD-rich foods need to be consumed to provide adequate VD, and (ii) the body needs to be able to upregulate VD-metabolizing genes to convert VD into 25(OH)VD and then to 1,25(OH)2VD to enhance its metabolic action. This review outlines the association between 25(OH)VD deficiency/inadequacy and decreased GSH levels, highlighting the positive impact of combined VD+LC supplementation on upregulating GSH, VD-metabolizing genes, and VDR. These effects have the potential to enhance 25(OH)VD levels and its therapeutic efficacy.
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Tables
Table 2
| Mice/Treatment | Sample Size ( | Purpose/Hypothesis | Outcome | Reference |
|---|---|---|---|---|
| HFD-induced obese mice and control mice | 28 | To investigate the effects of HFD-induced obesity on VD metabolizing enzyme expression. | HFD-induced obesity influences VD-metabolizing enzyme expression, leading to abnormal regulation of serum 1,25(OH)2D. | [ |
| HFD VD-deficient mice and control mice | 25 | Glutathione stimulates VD regulatory and glucose-metabolism genes, lowers oxidative stress and inflammation, and increases 25(OH)VD levels. | HFD downregulates VD metabolism genes, VD+LC supplementation upregulates the gene expression and is a novel and better strategy to increase VD levels. | [ |
| Female HFD and control mice | 14 | To investigate the alternative mechanism that reduced the capacity to convert parent VD to 25(OH)D due to decreased expression of | [ | |
| HFD and control mice | 20 | Obesity disrupts VD homeostasis in key organs of VD metabolism. | Adipose tissue plays a vital role in the modulation of VD metabolism during obesity. | [ |
| HFD and control mice | 19 | Nutritional deprivation-responsive mechanisms regulate VD metabolism. | Both fasting and diabetes suppressed hepatic cytochrome P450 | [ |
| HFD and control mice | 4 per group | GSH deficiency induces epigenetic alterations of VD metabolizing genes, thereby reducing the circulating 25(OH)VD3 levels in obesity. | [ | |
| Obese and control mice | 80 | To study the correlation of 25(OH)D3, physiological and pathological changes caused by obesity, and the motility of sperm. | [ | |
| HFD and control mice | 56 (6 groups) | Low VD status in obesity decreases the bioavailability of VD to sequestration in adipose tissue. | Excess of body adiposity contributes to lower serum 25(OH)D levels. | [ |
| High fat and high cholesterol diet mice and control mice | 30 | Diet could impair VD metabolism. | HFD and HCD reduce serum 25(OH)D3 by suppressing hepatic | [ |
| HFD and control mice | 20 | To investigate the impact of a short-term HFD on VD metabolism. | HFD-induced obesity decreases 25(OH)D and modulates gene expression in VD metabolism. | [ |
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