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Fermentative Production of Vitamin B6
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
Jonathan Rosenberg, Björn Richts, Fabian M. Commichau
Animals and humans have to ingest vitamin B6 with their diet because these organisms are unable to synthesize the micronutrient (Fitzpatrick et al., 2007, 2010; Kraemer et al., 2012). Vitamin B6 limitation has been associated with neurological disorders such as epileptic encephalopathy due to inherited errors in the enzymes interconverting B6 vitamers in the socalled “salvage pathway” (Mills et al., 2005; Bagci et al., 2008; di Salvo et al., 2012). Vitamin B6 deficiency can also be caused by interactions between drugs, such as contraceptives, and enzymes of the salvage pathway (Lumeng et al., 1974; Lussana et al., 2003; di Salvo et al., 2011). Therefore, vitamin B6 is of commercial interest for improving the quality of the food and for applications in the pharmaceutical industry (Rosenberg et al., 2017; Acevedo-Rocha et al., 2019). In the food industry, the hydrochloride salt of the B6 vitamer PN is usually used in combination with other vitamins in a variety of food products (Domke et al., 2005; Eggersdorfer et al., 2012). Vitamin B6 is also added to the food that is used for intensive animal farming to improve animal health and to enhance the yield (Johnson et al., 1950; Verbeek, 1975; Eggersdorfer et al., 2012). Many studies report positive effects of vitamin B6 although a large number of commercial products contain this compound. Only a few studies revealed that vitamin B6 can be toxic. A recent case described photosensitive skin darkening, hyperemesis and diarrhea as toxic effects, which disappeared soon after intoxication stopped (Cupa et al., 2015). Moreover, long-time supplementation of PN in higher doses is known to cause sensory neuropathy (Schaumburg et al., 1983; Albin et al., 1987). This effect is also used as a model for neuropathy (Hong et al., 2009; Potter et al., 2014).
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
Vitamin B6, also called pyridoxine, is present in several foods, such as poultry, pork, fish, soya beans, peanuts, bananas, wheat germ, oats, and milk [41]. The vitamin assists the cells to utilize energy from food and store excess energy for later use [41]. Vitamin B6 is also involved in the formation of hemoglobin and its active form, known as Pyridoxal 5′-phosphate (PLP), helps catalyze 150 reactions that are involved in glucose and lipid metabolisms [42]. Vitamin B6 is important in cellular metabolism and acts as an antioxidant and blocks reactive oxygen species (ROS) and advanced glycation end-products (AGEs) [42]. Moreover, vitamins B6 and B12 promote nerve function and prevent diabetic complications like diabetic neuropathy [43]. Several studies have investigated the correlation between vitamin B6 and DM and its complications. In particular, insufficient PLP disrupts insulin production in rats, while PLP administrations lessen diabetic complications and maintain chromosome integrity and glucose homeostasis [44]. The most notable study that established a link between vitamin B6 deficiency and DM was demonstrated in Drosophila in which mutations in a gene involved in vitamin B6 metabolism known as the dPdxk gene caused hyperglycemia and DM [45,46]. In addition, studies show that reduced vitamin B6 levels may predispose people to pancreatic islet autoimmunity in T1D [47]. Qian et al. [48] demonstrated that reduced vitamin B6 may affect the T-cell composition and compromise the immune system and predispose it to autoimmune diseases. Overall, this shows that vitamin B6 may possess a protective or ameliorative effect on diabetic conditions. In a study, dietary vitamin B6 prevents endothelial disorders, insulin insensitivity, and hepatic lipid accumulation in mice treated with high fat-diets [49]. The mechanistic links between vitamin B6 deficiency and DM are summarized in Figure 4.