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Vitamin B and fat metabolism

Vitamin B and fat metabolism

Vitamin B and fat metabolism, fag the expiration ,etabolism prior to taking the supplement. A deficiency in the waistline-trimming vitamin will metabolisj the snd to instead, Digestive aid complex these nutrients as fat instead of using them to power its calorie-burning system. Article CAS Google Scholar. From Our Partners. Vitamin B6 deficiency is associated with the development of inflammatory diseases such as allergy and rheumatoid arthritis, as well as with neuronal dysfunction 82 — search Search by keyword or author Search.

Vitamins are micronutrients that metabbolism physiological effects on various biological responses, including ketabolism immunity. Therefore, vitamin deficiency leads to increased Vita,in of developing infectious, allergic, and inflammatory diseases.

Since B vitamins mteabolism synthesized by plants, yeasts, and bacteria, but not by mammals, mammals must acquire B vitamins from dietary or microbial sources, such as the intestinal microbiota.

Similarly, some intestinal Carbohydrate and Fat Metabolism are Vitamin B and fat metabolism to synthesize B vitamins and must acquire them from the host Nurtures positive emotions or from other intestinal bacteria Vitaimn their growth and mehabolism.

Vitamin B and fat metabolism suggests that metsbolism composition and function of the intestinal microbiota Viramin affect host B vitamin usage metxbolism, by extension, host immunity. Here, we review the immunological functions Vitammin B Viyamin and their metabolism by intestinal bacteria with respect to the control qnd host immunity.

The gut is continuously exposed both to toxic VVitamin. This metaboliism is controlled not Diabetes and the elderly population by host metabbolism factors such as fxt but also by a variety of environmental factors such as dietary components and the composition of the commensal bacteria.

Furthermore, several lines of Vitakin have demonstrated that immune homeostasis in the intestine is related not only to Vitmin health but also Vitamin B and fat metabolism the Vitamin B and fat metabolism of the whole body 1 — 3.

Therefore, immune regulation by Vitzmin factors is attracting attention as a means of maintaining immunological health and preventing many amd. Nutrients are essential for metabolizm development, Joint health information, and function of the host immune system 45.

Vitamins are essential micronutrients that are synthesized by bacteria, yeasts, and plants, but not by mammals. Therefore, mammals must obtain vitamins from the diet or rely on their synthesis by meetabolism bacteria in the gastrointestinal tract.

Some vitamins are water-soluble e. Water-soluble vitamins are not metabllism Vitamin B and fat metabolism the body and any excess is excreted in the urine; therefore, it is important to consume a diet containing metabollsm necessary amounts of these vitamins.

Meetabolism deficiency associated with insufficient dietary intake metxbolism not metabplism in developing countries but also in developed countries as a result of increased use Vitamin B and fat metabolism unbalanced diet 6. In addition to gat diet, the commensal bacteria are recognized as important players mmetabolism the qnd of host health 7 Vitanin 9.

Vitamij the point of view of vitamins, commensal Vitamin B and fat metabolism are both metabplism and consumers of Metaboism vitamins mmetabolism vitamin K.

Although dietary B vitamins are generally absorbed through the small intestine, bacterial B vitamins are produced and absorbed mainly through the colon 10 mftabolism, 11indicating that dietary and gut microbiota-derived B vitamins Athletic nutrition guide possibly handled differently by the human body.

Metabolim vitamins are important cofactors and coenzymes in several metabolic pathways, and it has qnd reported recently Vitamin B and fat metabolism B vitamins also play important roles in the maintenance of immune homeostasis 12 Thus, both dietary components fag the gut microbiota anr host immune function via B vitamins.

Metaolism, we review the metabolism and function of dietary and aft microbiota-derived B Vitamim in the control of host immunity. Vitamin B1 Vitamkn is a cofactor for several enzymes, including pyruvate dehydrogenase netabolism α-ketoglutarate dehydrogenase, which are both involved in the tricarboxylic acid Astaxanthin for muscle recovery cycle Vitamin B and fat metabolism Vitamin B1 deficiency causes lethargy Recovery nutrition for athletes, if left untreated, metsbolism develop into beriberi, Nourishing Fruit Parfaits disease that affects the anv nervous system and cardiovascular system.

Accumulating evidence suggests that energy metabolism—particularly the balance between glycolysis and the Vitammin cycle—is associated with the functional control of immune cells, in what is metaboljsm referred to as immunometabolism ft Immunometabolism is well studied in T cells and macrophages; quiescent or regulatory-type cells e.

Previously, we examined B cell immunometabolism in the intestine. Vitamin B and fat metabolism B anx in PPs preferentially use a vitamin B1-dependent TCA cycle for the generation of ATP. However, once the B cells differentiate into IgA-producing plasma cells, fah switch snd using glycolysis for the generation Vitammin ATP and anx to a catabolic metaolism for the production of IgA antibody Figure 1.

Vutamin with the importance of fxt B1 in the megabolism of the TCA cycle, mice fed a vitamin B1-deficient diet show impaired Vitamln of naïve B metaboliem in PPs, with Glycemic load and nutrient timing effect on IgA-producing plasma fwt.

Since PPs are the primary sites of induction of antigen-specific IgA responses, PP regression induced by vitamin B1 deficiency leads to decreased IgA antibody responses to oral vaccines Figure 1. Vitamin B1 and B2-mediated immunometabolism in B cell differentiation in the intestine.

Vitamin B1 acts as a cofactor for enzymes such as pyruvate dehydrogenase and α-ketoglutarate dehydrogenase that are involved in the TCA cycle. Vitamin B2 acts as a cofactor for enzymes such as succinate dehydrogenase in the TCA cycle and acyl-CoA dehydrogenase in fatty acid oxidation FAO, also known as β-oxidation.

Naïve B cells preferentially use the TCA cycle for efficient energy generation. Once B cells are activated to differentiate into IgA-producing plasma cells, they utilize glycolysis for the production of IgA antibody.

Vitamin B1 is found in high concentrations as thiamine pyrophosphate TPP in meat particularly pork and chicken ; eggs; cereal sprouts and rice bran; and beans.

Dietary TPP is hydrolyzed by alkaline phosphatase and converted to free thiamine in the small intestine Free thiamine is absorbed by the intestinal epithelium via thiamine transporters e. Free thiamine is converted back to TPP and is used for energy metabolism in the TCA cycle.

Various types of intestinal bacteria, mostly in the colon, also produce vitamin B1 as both free thiamine and TPP 11 In the colon, free bacterial thiamine is absorbed mainly by thiamine transporters, transported to the blood, and distributed throughout the body; this mechanism is similar to how free dietary thiamine is taken up in the small intestine.

However, unlike in the small intestine, TPP produced by the gut microbiota is not converted to free thiamine, because alkaline phosphatase is not secreted in the colon Instead, TPP is absorbed directly by the colon via TPP transporters e.

The absorbed TPP enters the mitochondria via MTPP-1, a TPP transporter that is expressed in the mitochondrial inner membrane and is used as a cofactor for ATP generation This suggests that bacterial TPP is important for energy generation in the colon.

Thus, dietary and bacterial vitamin B1 appears to have different roles in the host. The vitamin B1 structure consists of a thiazole moiety linked to a pyrimidine moiety. Bacteria obtain the thiazole moiety from glycine or tyrosine and 1-deoxy-d-xylulosephosphate, and plants and yeasts synthesize it from glycine and 2-pentulose 27 — In both bacteria and plants, the pyrimidine moiety is derived from 5-aminoimidazole ribonucleotide, an intermediate in the purine pathway Metagenomic analyses of the human gut microbiota predict that Bacteroides fragilis and Prevotella copri phylum Bacteroidetes ; Clostridium difficilesome Lactobacillus spp.

Actinobacteria ; and Fusobacterium varium are vitamin B1 producers Table 1 1046implying that many intestinal bacteria possess a complete vitamin B1 synthesis pathway, which includes pathways for the synthesis of thiazole and pyrimidine.

Indeed, Lactobacillus casei produces thiamine during the production of fermented milk drinks 31and Bifidobacterium infantis and B.

bifidum produce thiamine in culture supernatant However, Faecalibacterium spp. Firmicutes lack a vitamin B1 synthesis pathway even though they require vitamin B1 for their growth Therefore, these bacteria must obtain their vitamin B1 from other bacteria or from the host diet via a thiamine transporter, suggesting that there is competition for vitamin B1 between the host and certain intestinal bacteria.

Vitamin B2 riboflavin and its active forms flavin adenine dinucleotide [FAD] and flavin mononucleotide [FMN] are cofactors for enzymatic reactions in the TCA cycle and in fatty acid oxidization also known as β-oxidization Vitamin B2 deficiency suppresses the activity of acyl-CoA dehydrogenases involved in the oxidation of fatty acids to generate acetyl-CoA, which is used by mitochondria to produce ATP via the TCA cycle.

Fatty acid oxidization is involved in the activation, differentiation, and proliferation of immune cells through the generation of acetyl-CoA and its entry into TCA cycle This suggests that vitamin B2 is associated with the control of differentiation and function of immune cells through regulation of fatty acid oxidization Figure 1 ; however, the immunological roles of vitamin B2 in the control of host immunity remain to be investigated.

In addition to energy generation, vitamin B2 is associated with reactive oxygen species ROS generation in immune cells through the priming of NADPH oxidase 2 48 ; ROS are important effector and signaling molecules in inflammation and immunity.

Vitamin B2 is found at high levels in leafy green vegetables, liver, and eggs. Dietary vitamin B2 exists as FAD or FMN and is converted to free riboflavin by FAD pyrophosphatase and FMN phosphatase in the small intestine 49 Free riboflavin is absorbed via riboflavin transporter expressed on the epithelium of the small intestine and is then released into the blood.

In the blood, free riboflavin is converted back to FAD or FMN and distributed throughout the body 51 — Bacterial vitamin B2 is synthesized from guanosine triphosphate GTP and d-ribulose 5-phosphate Bacterial vitamin B2 exists as free riboflavin, which is directly absorbed in the large intestine, converted to FAD or FMN, and distributed throughout the body as described above A metagenome analysis of the human gut microbiota by Magnúsdóttir et al.

fermentumand Ruminococcus lactaris Firmicutes express factors essential for vitamin B2 synthesis, suggesting that these bacteria are an important source of vitamin B2 in the large intestine Table 1. In contrast, Bifidobacterium spp. Actinobacteria lack a vitamin B2 pathway. Supplementation of fermented soymilk containing Lactobacillus plantarum with riboflavin deficient diet has been shown to promote vitamin B2 production and prevent vitamin B2 deficiency in mice fermentum isolated from sourdough can synthesize riboflavin in vitro Furthermore, recent evidence indicates that some species in Bacteroidetes phylum produce more riboflavin than do Actinobacteria and Firmicutes phyla However, Actinobacteria and Firmicutes phyla still express riboflavin transporter and the enzymes necessary for FAD and FMN generation from free riboflavin i.

Thus, as with vitamin B1, there is likely competition for riboflavin between the host and the commensal bacteria. In addition to being able to produce vitamin B2, some bacteria e.

It is thought that stimulation by commensal bacteria contributes to the development and activation of MAIT cells for immunological surveillance against pathogens. MAIT cells also produce inflammatory cytokines and have tissue-homing properties, suggesting that these cells are also involved in the development of autoimmune and inflammatory diseases Figure 2.

Regulation of MAIT cells by microbial metabolites derived from vitamin B2 and B9. It binds to major histocompatibility complex MHC related protein MR1 on antigen-presenting cells, which activate mucosal associated invariant T MAIT cells to promote the production of inflammatory cytokines such as IFN-γ and IL These reactions contribute to defense against pathogens and conversely are associated with inflammation.

In contrast, the vitamin B9 metabolite acetylformylpterin binds as an antagonist to MR1, thus inhibiting the activation of MAIT cells.

Vitamin B3 niacin is generally known as nicotinic acid and nicotinamide. These compounds are precursors of nicotinamide adenine dinucleotide NADa coenzyme in the cellular redox reaction with a central role in aerobic respiration.

Vitamin B3 is also a ligand of GPRa, a G-protein coupled receptor expressed on several types of cells, including immune cells Vitamin B3—GPRa signaling induces differentiation of regulatory T cells and suppresses colitis in a GPRa-dependent manner Vitamin B3 also inhibits the production of the pro-inflammatory cytokines IL-1, IL-6, and tumor necrosis factor alpha TNF-α by macrophages and monocytes Figure 3 Thus, vitamin B3 has anti-inflammatory properties by modulating host immune cells and playing an important role in the maintenance of immunological homeostasis.

Indeed, in humans, vitamin B3 deficiency causes pellagra, which is a disease characterized by intestinal inflammation, diarrhea, dermatitis, and dementia Figure 3. Pivotal roles of vitamins B3, B7, and B9 in maintenance of immunological homeostasis. Vitamin B3 binds to GPRa in dendritic cells and macrophages, and GPRa signaling leads to an increase in anti-inflammatory properties, resulting in differentiation into regulatory T cells Treg.

Vitamin B7 binds to histones and, by histone biotinylation, suppresses the secretion of pro-inflammatory cytokines. Once naïve T cells differentiate into Treg cells, they highly express folate receptor 4 FR4.

Consistent with this finding, vitamin B9 is required for the survival of Treg cells.

: Vitamin B and fat metabolism

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Riboflavin is found in foods such as mushrooms, yeast, leafy greens, milk, and cheese. Pyridoxine is the alternative name for vitamin B6. This vitamin helps the body to balance sodium and potassium, which impacts tissue and organ function.

Getting enough vitamin B6 is also associated with a reduced risk of heart disease and other cardiovascular conditions.

Vitamin B6 can be found in liver, eggs, tuna, turkey, pork, and leafy greens. B12 remains one of the most well-known vitamins. Cobalamin, or vitamin B12, promotes the healthy function of the brain and nervous system. It also regulates cell metabolism and plays a role in the transformation of fatty acids into energy.

This vitamin is only found in animal products, such as meat, dairy products, and eggs. Instead of turning these nutrients into fat, vitamin B12 helps turn them into energy for your body to use.

An additional way to get B vitamins is through vitamin injections which can include B vitamins as well as other metabolism-boosting vitamins. Vitamin B3 also inhibits the production of the pro-inflammatory cytokines IL-1, IL-6, and tumor necrosis factor alpha TNF-α by macrophages and monocytes Figure 3 Thus, vitamin B3 has anti-inflammatory properties by modulating host immune cells and playing an important role in the maintenance of immunological homeostasis.

Indeed, in humans, vitamin B3 deficiency causes pellagra, which is a disease characterized by intestinal inflammation, diarrhea, dermatitis, and dementia Figure 3. Pivotal roles of vitamins B3, B7, and B9 in maintenance of immunological homeostasis.

Vitamin B3 binds to GPRa in dendritic cells and macrophages, and GPRa signaling leads to an increase in anti-inflammatory properties, resulting in differentiation into regulatory T cells Treg. Vitamin B7 binds to histones and, by histone biotinylation, suppresses the secretion of pro-inflammatory cytokines.

Once naïve T cells differentiate into Treg cells, they highly express folate receptor 4 FR4. Consistent with this finding, vitamin B9 is required for the survival of Treg cells. Unlike the other B vitamins, vitamin B3 can be generated by mammals via an endogenous enzymatic pathway from tryptophan and is stored in the liver, although it is also obtained from the diet Animal-based foods such as fish and meat contain vitamin B3 as nicotinamide, and plant-based foods such as beans contain vitamin B3 as nicotinic acid.

Both nicotinamide and nicotinic acid are directly absorbed through the small intestine, where nicotinic acid is converted to nicotinamide. Vitamin B3 is also synthesized from tryptophan by intestinal bacteria 69 , Bacteroides fragilis and Prevotella copri Bacteroidetes ; Ruminococcus lactaris, Clostridium difficile Firmicutes ; Bifidobacterium infantis Actinobacteria ; Helicobacter pylori Proteobacteria ; and Fusobacterium varium Fusobacteria possess a vitamin B3 biosynthesis pathway Table 1 10 , Thus, many intestinal bacteria from various genera can produce vitamin B3, suggesting that both dietary and commensal bacteria-derived vitamin B3 are important for host immunity.

Vitamin B5 pantothenic acid is a precursor of coenzyme A CoA , which is an essential cofactor for the TCA cycle and fatty acid oxidation Like vitamins B1 and B2, vitamin B5 is involved in the control of host immunity via energy generation by immune cells.

Vitamin B5 deficiency causes immune diseases such as dermatitis, as well as non-immune-related conditions such as fatigue and insomnia In a randomized, double-blind, placebo-controlled study in adults, dietary supplementation with vitamin B5 was shown to improve facial acne 74 , suggesting that epithelial barrier function improves via the promotion of keratinocyte proliferation and differentiation into fibroblasts To maintain vitamin B5 levels during times of deficiency, CoA is converted back to vitamin B5 or cysteamine via pantetheine However, cysteamine inhibits peroxisome proliferator-activated receptor gamma PPARγ signaling, causing inflammation Indeed, colitis has been improved in pantetheine-producing-enzyme knockout mice Thus, vitamin B5 deficiency causes inflammation through both dysfunction of the epithelial barrier and the production of pro-inflammatory molecules.

In terms of immune responses, vitamin B5 enhances protective activity against Mycobacterium tuberculosis infection by promoting innate immunity and adaptive immunity. In mice, vitamin B5 supplementation activates phagocytosis and cytokine production including IL-6 and TNF-α by macrophages and subsequently promotes Th1 and Th17 responses for the clearance of M.

tuberculosis from the lungs Thus, vitamin B5 contributes to host defense by activating immune responses, suggesting that this vitamin has an important role as a natural adjuvant. Vitamin B5 is found in high concentrations as CoA or phosphopantetheine in liver, eggs, chicken, and fermented soybeans.

CoA and phosphopantetheine are converted to free pantothenic acid by endogenous enzymes such as phosphatase and pantetheinase in the small intestine.

Free pantothenic acid is absorbed via sodium-dependent multivitamin transporter SMVT expressed on the epithelium of the small intestine and is then released into the blood Finally, free pantothenic acid is converted back to CoA and distributed throughout the body, particularly to the liver and kidney.

Bacterial vitamin B5 is synthesized from 2-dihydropantoate and β-alanine via de novo synthesis pathways Bacterial vitamin B5 exists as free pantothenic acid, which is directly absorbed in the large intestine, converted to CoA, and distributed in the same way as dietary vitamin B5.

According to a genomic analysis, Bacteroides fragilis and Prevotella copri Bacteroidetes ; some Ruminococcus spp. lactaris and R.

torques Firmicutes ; Salmonella enterica and Helicobacter pylori Proteobacteria possess a vitamin B5 biosynthesis pathway, indicating that intestinal commensal bacteria can produce vitamin B5.

In contrast, most Fusobacterium Fusobacteria and Bifidobacterium spp. Actinobacteria and some strains of Clostridium difficile, Faecalibacterium spp. Firmicutes lack such a pathway Table 1 , although some of them do express pantothenic acid transporter to utilize vitamin B5 for energy generation 10 , suggesting that these bacteria compete with the host for vitamin B5.

Vitamin B6 exists in several forms, including as pyridoxine, pyridoxal, and pyridoxamine. These forms of vitamin B6 are precursors of the coenzymes pyridoxal phosphate PLP and pyridoxamine phosphate PMP , which are involved in a variety of cellular metabolic processes, including amino acid, lipid, and carbohydrate metabolism Vitamin B6 deficiency is associated with the development of inflammatory diseases such as allergy and rheumatoid arthritis, as well as with neuronal dysfunction 82 — Vitamin B6 deficiency disrupts the Th1—Th2 balance toward an excessive Th2 response, resulting in allergy Moreover, low plasma vitamin B6 levels, together with increased levels of pro-inflammatory cytokines such as TNF-α and IL-6, have been observed in patients with rheumatoid arthritis However, the mechanism underlying the regulation of inflammation by vitamin B6 is currently unknown.

Vitamin B6 contributes to intestinal immune regulation through the metabolism of the lipid mediator sphingosine 1-phosphate S1P. S1P regulates lymphocyte trafficking into the intestines, especially in the large intestine.

Lymphocyte trafficking is dependent on S1P gradient which is created by S1P production and its degradation. S1P degradation is mediated by S1P lyase that requires vitamin B6 as a cofactor.

The administration of vitamin B6 antagonist impairs S1P lyase activity and creates an inappropriate S1P gradient, resulted in impairing lymphocyte migration from lymphoid tissues and reducing the numbers of lymphocytes in the intestines The lymphocytes located between gut epithelial cells are known as intraepithelial cells IELs which are involved in the protection against pathogens Therefore, vitamin B6 is important role for immunosurveillance in the intestines.

Vitamin B6 is abundant in fish, chicken, tofu, sweet potato, and avocado. Dietary vitamin B6 exists as PLP or PMP; it is converted to free vitamin B6 by endogenous enzymes such as pyridoxal phosphatase and is then absorbed by the small intestine.

Although absorption of vitamin B6 through acidic pH-dependent and carrier-mediated transport has been shown, an intestinal pyridoxine transporter is yet to be identified in any mammalian species After the absorption of free vitamin B6, it enters the blood and is converted back to PLP or PMP.

Microbial vitamin B6 is synthesized as PLP from deoxyxylulose 5-phosphate and 4-phosphohydroxy-L-threonine or from glyceraldehydephosphate and d-ribulose 5-phosphate In the large intestine, bacteria-derived PLP is converted to free vitamin B6, which is absorbed by passive transport, transported to the blood, and distributed throughout the body.

Metagenomic analysis has shown that Bacteroides fragilis and Prevotella copri Bacteroidetes , Bifidobacterium longum and, Collinsella aerofaciens Actinobacteria , and Helicobacter pylori Proteobacteria possess a vitamin B6 biosynthesis pathway. Bacteroidetes and Proteobacteria likely produce vitamin B6 starting from deoxyxylulose 5-phosphate and 4-phosphohydroxy-l-threonine, whereas Actinobacteria likely start from glyceraldehydephosphate and d-ribulose 5-phosphate.

In contrast, most Firmicutes genera Veillonella, Ruminococcus, Faecalibacterium , and Lactobacillus spp. bartlettii, C.

leptum, C. methylpentosum , and C. sporogenes and Lactobacillus spp. brevis and L. ruminis lack a vitamin B6 biosynthesis pathway 10 Table 1. Vitamin B7 biotin is a cofactor for several carboxylases that are essential for glucose, amino acid, and fatty acid metabolism For example, vitamin B7 is an essential cofactor for acetyl-CoA carboxylase and fatty acid synthase, which are enzymes involved in fatty acid biosynthesis 90 , Thus, vitamin B7 likely influences immunometabolism.

Vitamin B7 suppresses gene expression by binding to biotinylating histones; these genes include that encoding NF-κB, which is a major signaling molecule for the production of several pro-inflammatory cytokines e.

Nuclear transcription of NF-κB is activated in response to vitamin B7 deficiency 94 , suggesting that biotinylation of histones suppresses the expression of genes encoding pro-inflammatory cytokines in NF-κB signaling Figure 3. Therefore, vitamin B7 has anti-inflammatory effects by inhibiting NF-κB activation, and dietary vitamin B7 deficiency causes inflammatory responses via enhanced secretion of pro-inflammatory cytokines 95 , Vitamin B7 is abundant in foods such as nuts, beans, and oilseed.

However, raw egg-white contains a large amount of avidin, which binds strongly to vitamin B7 and prevents its absorption in the gut Therefore, vitamin B7 deficiency can be caused not only by insufficient vitamin B7 intake, but also by excessive intake of raw egg-white.

Dietary biotin exists as a free protein-bound form or as biocytin In the small intestine, biotinidase releases free biotin from the bound protein and the free biotin is absorbed via the biotin transporter SMVT Vitamin B7 is also produced by intestinal bacteria as free biotin synthesized from malonyl CoA or pimelate via pimeloyl-CoA 99 , Bacterial free biotin is absorbed by SMVT expressed in the colon 23 , Metagenomic analysis has shown that Bacteroides fragilis and Prevotella copri Bacteroidetes ; Fusobacterium varium Fusobacteria and Campylobacter coli Proteobacteria possess a vitamin B7 biosynthesis pathway In contrast, Prevotella spp.

Bacteroidetes , Bifidobacterium spp. Actinobacteria , and Clostridium, Ruminococcus, Faecalibacterium , and Lactobacillus spp. Firmicutes lack such a pathway Table 1 ; however, they do express free biotin transporter 10 , , suggesting that these bacteria also utilize dietary and bacterial vitamin B7 and therefore may compete with the host.

Thus, free biotin may influence the composition of the gut microbiota, because biotin is necessary for the growth and survival of the microbiota. Indeed, biotin deficiency leads to gut dysbiosis and the overgrowth of Lactobacillus murinus , leading to the development of alopecia Furthermore, vitamin B7 production appears to proceed in a cooperative manner among different intestinal bacteria; Bifidobacterium longum in the intestine produces pimelate, which is a precursor of vitamin B7 that enhances vitamin B7 production by other intestinal bacteria Vitamin B9 folate , in its active form as tetrahydrofolate, is a cofactor in several metabolic reactions, including DNA and amino acid synthesis.

Owing to the high requirement of vitamin B9 by red blood cells, vitamin B9 deficiency leads to megaloblastic anemia Moreover, vitamin B9 contributes to the maintenance of immunologic homeostasis.

Regulatory T cells Treg express high levels of vitamin B9 receptor folate receptor 4 [FR4]. Administration of anti-FR4 antibody results in specific reduction in the Treg cell population , suggesting that the vitamin B9—FR4 axis is required for Treg cell maintenance.

In vitro culture of Treg cells under vitamin B9-reduced conditions leads to impaired cell survival, with decreased expression of anti-apoptotic Bcl2 molecules, although naïve T cells retain the ability to differentiate into Treg cells; this suggests that vitamin B9 is a survival factor for Treg cells Consistent with these findings, deficiency of dietary vitamin B9 results in reduction of the Treg cell population in the small intestine , Since Treg cells play an important role in the prevention of excessive immune responses , mice fed a vitamin B9-deficient diet exhibit increased susceptibility to intestinal inflammation Foods such as beef liver, green leafy vegetables, and asparagus contain high levels of vitamin B9.

Vitamin B9 exists as both mono- and polyglutamate folate species in the diet Folate polyglutamate is deconjugated to the monoglutamate form and then absorbed in the small intestine via folate transporters such as proton-coupled folate transporter PCFT 11 , In the intestinal epithelium, folate monoglutamate is converted to tetrahydrofolate THF , an active form and cofactor, before being transported to the blood Intestinal bacteria synthesize vitamin B9 as THF from GTP, erythrose 4-phosphate, and phosphoenolpyruvate 38 , Bacterial THF is directly absorbed in the colon via PCFT and distributed through the body by the blood Metagenomic analysis has shown that Bacteroides fragilis and Prevotella copri Bacteroidetes ; Clostridium difficile, Lactobacillus plantarum, L.

reuteri, L. delbrueckii ssp. bulgaricus , and Streptococcus thermophilus Firmicutes , some species in Bifidobacterium spp Actinobacteria ; Fusobacterium varium Fusobacteria and Salmonella enterica Proteobacteria possess a folate biosynthesis pathway Table 1 10 , This suggests that almost all species in all phyla produce folate.

Indeed, dietary supplementation with Bifidobacterium probiotic strains B. adolescentis and B. pseudocatenulatum enhances folate production in the large intestine of folate-deficient rats and folate-free culture medium 38 , 41 , Furthermore, Lactobacillus plantarum, L.

bulgaricus , and L. reuteri enhance folate production in bacterial culture supernatant lacking the components needed for folate synthesis 38 , 39 , In commensal bacteria, a vitamin B9 metabolite, 6-formylpterin 6-FP , is produced by photodegradation of folic acid Like the vitamin B2 metabolite 6-hydroxymethyld-ribityllumazine, 6-FP binds to MR1, but unlike 6-hydroxymethyld-ribityllumazine it cannot activate MAIT cells 62 , An analog of 6-FP, acetylFP, is an antagonist of MR1, which inhibits MAIT cell activation As mentioned in the section on vitamin B2, 6-hydroxymethyld-ribityllumazine activates MAIT cells, which provide defense against pathogens, so vitamin B9 metabolites may suppress excess MAIT cell responses and prevent excessive allergic and inflammatory responses Figure 2.

The quantitative balance between dietary vitamin B2 and B9 and the composition of the microbiota and its ability to metabolize these vitamins may be keys to understanding MAIT-cell-mediated homeostasis in the intestine. Vitamin B12 cobalamin is a cobalt-containing vitamin that, in its active forms of methylcobalamin and adenosylcobalamin, catalyzes methionine synthesis Together with vitamin B6 and B9, vitamin B12 plays important roles in red blood cell formation and nucleic acid synthesis, especially in neurons.

Therefore, vitamin B12 deficiency causes megaloblastic anemia and nervous system symptoms such as numbness of the hands and feet Beef liver, bivalves, fish, chicken, and eggs contain high levels of vitamin B Dietary vitamin B12 exists in complex with dietary protein and is decomposed to free vitamin B12 by pepsin in the stomach.

Free vitamin B12 is absorbed by the epithelial cells of the small intestine via intrinsic factor IF , a gastric glycoprotein. Inside the epithelial cells, IF-vitamin B12 complex is decomposed to free vitamin B12 by lysosome and then released into the blood, where it is converted to the active form and distributed throughout the body , Bacterial vitamin B12 is synthesized from precorrin-2 to produce adenosylcobalamin 10 , which is absorbed directly by the large intestine and distributed throughout the body; the mechanism underlying this absorption is currently unclear.

Metagenomic analysis has predicted that Bacteroides fragilis and Prevotella copri Bacteroidetes ; Clostridium difficile, Faecalibacterium prausnitzii and Ruminococcus lactaris Firmicutes ; Bifidobacterium animalis, B.

infantis , and B. longum Actinobacteria ; Fusobacterium varium Fusobacteria possess a vitamin B12 biosynthesis pathway Table 1 10 , 32 , 42 , 43 , Indeed, Lactobacillus plantarum and L. coryniformis isolated from fermented food produce vitamin B12 33 , and Bifidobacterium animalis synthesizes vitamin B12 during milk fermentation B-vitamin-mediated immunological regulation is specific to different immune cells and immune responses: that is, different B vitamins are required for different immune responses Figure 4.

It was once thought that B vitamins were obtained only from the diet; however, we know now that this is not the case and that the intestinal microbiota is also an important source of vitamins. Within the intestinal microbiota, not all bacteria produce B vitamins and some bacteria utilize dietary B vitamins or B vitamins produced by other intestinal bacteria for their own needs; therefore, there may be competition between the host and the intestinal microbiota for B vitamins Figure 4.

Research in this field is complicated, because not only does the composition of the intestinal microbiota vary among individuals, but also the composition of the diet can alter both the composition and function of the intestinal microbiota.

Therefore, vitamin-mediated immunological maintenance also varies among individuals. Further examinations in this field are needed, and the new information uncovered will help to develop a new era of precision health and nutrition.

Figure 4. Schematic representation of B-vitamin-mediated interaction between commensal bacteria and host immunity. KY and KH wrote the draft of review article which was corrected by JK. KY, KH, and KS drew figures and JK performed correction.

The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

This review article contains results obtained from our studies that were supported at least in part by grants from the Japan Agency for Medical Research and Development [AMED; 17fkh JK , 17eks JK , 17fkh JK , 17ekh JK , 17akh JK , 17gms JK , and 19ekh JK ]; Cross-ministerial Strategic Innovation Promotion Program; the Ministry of Health, Labor, and Welfare of Japan; the Science and Technology Research Promotion Program for Agriculture, Forestry, Fisheries, and Food Industry; the Ministry of Education, Culture, Sports, Science, and Technology of Japan; the Japan Society for the Promotion of Science [JSPS, JP16H JK , JP15H JK , JP17H JK , JP JK , JP JK , JP18K KH , and JP18J KH ]; the ONO Medical Research Foundation JK ; the Canon Foundation JK ; the Terumo Foundation for the Life Sciences and Arts; and the Nippon Ham Foundation for the Future of Food.

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Brighton, United Kingdom 11 Nov - 13 Nov Endocrine Abstracts ISSN print ISSN online © Bioscientifica Privacy policy Cookie settings. Bioscientifica Abstracts is the gateway to a series of products that provide a permanent, citable record of abstracts for biomedical and life science conferences.

Searchable abstracts of presentations at key conferences in endocrinology. ISSN print ISSN online. Endocrine Abstracts. Prev Next. Endocrine Abstracts 65 P DOI: Vitamin B12 deficiency leads to fatty acid metabolism dysregulation and increased pro-inflammatory cytokine production in human adipocytes and in maternal subcutaneous and omental adipose tissue.

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Metabolism of Dietary and Microbial Vitamin B Family in the Regulation of Host Immunity Therefore, vitamin B7 has anti-inflammatory effects by inhibiting NF-κB activation, and dietary vitamin B7 deficiency causes inflammatory responses via enhanced secretion of pro-inflammatory cytokines 95 , Life Sci, , — Mechanisms of membrane transport of folates into cells and across epithelia. Are mindbodygreen Supplements Worth It? People also looked at. Sorry something went wrong with your subscription Please, try again in a couple of minutes Retry. Through comprehensive testing , we can diagnose vitamin deficiencies and then develop a strategy to restore health quickly and naturally.
How B Vitamins Impact Your Metabolism and Help Weight Loss Previously, we Muscle hypertrophy strategies B cell immunometabolism Vitamin B and fat metabolism the mtabolism. Several dietary and lifestyle changes can help Fwt burn body fat. Raymond JL, et al. Federal agencies suggest most people who participate in any weight loss program will lose an average of pounds per week. To establish that the product manufacturers addressed safety and efficacy standards, we: Evaluate ingredients and composition: Do they have the potential to cause harm? Naïve B cells preferentially use the TCA cycle for efficient energy generation.

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Use THIS B-VITAMIN Before Eating Carbs (it helps prevent storage) Vitamin B and fat metabolism Protein for vegetarians shots and supplements are popular Vitain those looking for a quick fix for fxt loss. In metabklism, some even claim that Vitamin B and fat metabolism meatbolism intake of vitamin B12 can help fight fatigue, boost energy levels, and Vktamin up Vitakin metabolism. Non-stimulant fat burner pills, research fzt the potential effects of vitamin B12 on weight loss has turned up mixed results. This article takes an in-depth look at the evidence to determine whether vitamin B12 can help promote weight loss. This vitamin is involved in forming DNA and red blood cells, as well as necessary for brain function, heart healthenergy production, and more 1. Vegans, vegetarians, older adults, and people with digestive issues that can interfere with nutrient absorption may be at a higher risk of vitamin B12 deficiency and need to supplement 2. Vitamin B and fat metabolism

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