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Cadmium Exposure and Toxicity
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Soisungwan Satarug, Kenneth R. Phelps
In theory, Cd toxicity could disrupt vitamin D metabolism and compromise skeletal mineralization secondarily. The proximal tubule synthesizes the active metabolite of vitamin D, 1,25-dihydroxyvitamin D (1,25(OH)2D), from the hepatic precursor 25-hydroxyvitamin D (25OHD), which tubular cells acquire through megalin:cubilin-mediated endocytosis of vitamin D-binding protein (VDBP) (Kaseda et al., 2011). Although Cd interferes with reabsorption of VDBP (Uchida et al., 2007), [25OHD]p was nevertheless normal in a simian model of Cd nephropathy (Kurata et al., 2014). [1,25(OH)2D]p was reduced in patients with Cd intoxication (Nogawa et al., 1987), but nephron loss may produce this result, and [1,25(OH)2D]p correlated with GFR in a second study (Aoshima and Kasuya, 1991). In the third examination of this issue, [1,25(OH)2D]p was not low enough to cause osteomalacia in subjects with Cd tubulopathy (Kaewnate et al. 2012). In general, it is not clear that the metal inhibits 1α-hydroxylation of vitamin D. The pathogenesis of Cd-induced osteomalacia is multifactorial, and the principal cause may vary from patient to patient.
Nanotherapeutics: Enabling Vitamin D3 as a Multifaceted Nutraceutical
Published in Bhupinder Singh, Minna Hakkarainen, Kamalinder K. Singh, NanoNutraceuticals, 2019
Krantisagar S. More, Vinod S. Ipar, Amit S. Lokhande, Anisha A. D’souza, Padma V. Devarajan
Vitamin D3 is a lipid soluble vitamin. Dietary vitamin D is absorbed through the small intestine as chylomicron fraction and then transported to the lymph. In plasma, vitamin D3 circulates as 25-hydroxy vitamin D3 and binds to a α2-globulin protein (Vitamin D-binding Protein, DBP) and accumulates in the liver. Vitamin D3 is hydroxylated in the liver by enzyme hydroxylase in the mitochondria and forms 25-hydroxyvitamin D3 (also known as 25-hydroxycholecalciferol, calcidiol or calcifediol) (Holick, 2007; Milne and Delander, 2008).
Mechanistic links between vitamin deficiencies and diabetes mellitus: a review
Published in Egyptian Journal of Basic and Applied Sciences, 2021
Tajudeen O. Yahaya, AbdulRahman B. Yusuf, Jamilu K. Danjuma, Bello M. Usman, Yahaya M. Ishiaku
Some studies in humans and animals have investigated the relationship between vitamin D levels in the body and the onset of DM. A study was conducted on animals in which vitamin D receptors were removed and the animals failed to produce normal insulin levels [70]. In a study that measured maternal vitamin D-binding protein throughout pregnancy and the risk of T1DM in offspring, lower concentration, particularly in the third trimester, tended to be associated with T1DM [71]. Moreover, in a non-randomized clinical trial involving 80 type 1 diabetics with 25-hydroxyvitamin D levels below 50 nmol/L, 4000 IU of vitamin D3 supplementation for 12 weeks produced a positive effect [72]. A systematic review and meta-analysis also linked low vitamin D levels with T2DM and insulin resistance, which were improved following vitamin D supplementation [73]. Additionally, a randomized controlled trial found that vitamin D supplementation for six months improved insulin secretion and sensitivity in 96 pre-diabetics and type 2 diabetics [74]. These findings suggest that vitamin D may help delay or manage T2DM. However, some studies, including Bizzarri et al. [75] and Al Thani et al. [76], found no link between vitamin D supplementation and improved glycemic control. However, according to Gröber and Holick [77], diabetic subjects in studies reporting no effect of vitamin D supplementation are not deficient in the vitamin and thus may not benefit from its effects. The mechanistic links between vitamin D deficiency and DM are summarized in Figure 6.
Effects of vitamin D3 supplementation for 12 weeks on serum levels of anabolic hormones, anaerobic power, and aerobic performance in active male subjects: A randomized, double-blind, placebo-controlled trial
Published in European Journal of Sport Science, 2020
Amirhossein Ramezani Ahmadi, Majid Mohammadshahi, Aliakbar Alizadeh, Kambiz Ahmadi Angali, Alireza Jahanshahi
It has been shown that inter-individual differences and genetic variation in vitamin D binding protein influence the response to supplementation (Nimitphong, Saetung, Chanprasertyotin, Chailurkit, & Ongphiphadhanakul, 2013). Moreover, in the present study, a greater response was observed in subjects with lower baseline 25-OH-D concentration. Also, vitamin D sources, sunlight exposure and dietary intakes are two most important determinants of vitamin D status (Dahlquist et al., 2015). The present study evaluated sun exposure in participants and no difference was observed in sun exposure duration, exposure time, the area of body that exposure, and use of sunscreen in the baseline and end of the study. Since this study was carried out in the season of the lowest UV radiation during the year (Behrooz et al., 2010), a reduction in the serum levels of 25-OH-D is expected during the study. Also, it has been proposed that athletes are more susceptible to vitamin D deficiency compared to general population due to higher enzymatic activities during exercise (Dahlquist et al., 2015).
Serum miRNA-146a and vitamin D values in chronic renal ailment with and without comorbid cardiovascular disease
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Fatma K. A. Hamid, Alshaymaa M. Alhabibi, Mona A. Mohamed, Hanaa Hussein El-Sayed, Nehad Rafaat Ibrahim, Ghadir Mohamed Hassan Elsawy, Entsar M. Ahmad
Regardless of the degree of disease, patients with CKD frequently have vitamin D inadequacy. Moreover, it is believed that as renal function declines, the generation of active vitamin D in the kidneys reduces. Nearly all systemic vitamin D byproducts are coupled by albumin and vitamin D binding protein (DBP), a major transportation molecule [3].