Niacin

Penberthy, W. Todd; Kirkland, James B.

doi:10.1002/9781119946045.ch19

Cited by 18 publications

(11 citation statements)

References 68 publications

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“…Nicotinamide riboside (NR) is a single chemical moiety containing nicotinamide and ribose (Figure 1) and, because it is a precursor of nicotinamide adenine dinucleotide (NAD+), is considered to be a form of vitamin B 3. 1 –3 Although there is no evidence of adverse effects from naturally occurring niacin in foods, it is recognized that for nutrients, there is a daily level of intake or threshold above which the risk of adverse effects increase (defined as the tolerable upper intake level (UL). 4 A UL for NR has not been established by an authoritative or regulatory body.…”

Section: Introductionmentioning

confidence: 99%

Safety assessment of nicotinamide riboside, a form of vitamin B₃

Conze¹,

Crespo-Barreto²,

Kruger³

2016

Hum Exp Toxicol

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Nicotinamide riboside (NR) is a naturally occurring form of vitamin B3 present in trace amounts in some foods. Like niacin, it has been shown to be a precursor in the biosynthesis of nicotinamide adenine dinucleotide (NAD+). The safety of Niagen™, a synthetic form of NR, was determined using a bacterial reverse mutagenesis assay (Ames), an in vitro chromosome aberration assay, an in vivo micronucleus assay, and acute, 14-day and 90-day rat toxicology studies. NR was not genotoxic. There was no mortality at an oral dose of 5000 mg/kg. Based on the results of a 14-day study, a 90-day study was performed comparing NR at 300, 1000, and 3000 mg/kg/day to an equimolar dose of nicotinamide at 1260 mg/kg/day as a positive control. Results from the study show that NR had a similar toxicity profile to nicotinamide at the highest dose tested. Target organs of toxicity were liver, kidney, ovaries, and testes. The lowest observed adverse effect level for NR was 1000 mg/kg/day, and the no observed adverse effect level was 300 mg/kg/day.

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Section: Introductionmentioning

confidence: 99%

Safety assessment of nicotinamide riboside, a form of vitamin B₃

Conze¹,

Crespo-Barreto²,

Kruger³

2016

Hum Exp Toxicol

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“…B3 vitamers are cofactors for a vast number of enzymatic redox reactions, such as the β-oxidation of fatty acids and substrate oxidation in Krebs cycle [ 45 ], as well as in the synthesis of carnitine [ 46 ]. In one-carbon metabolism, vitamin B3 is used as a reducing agent for both MTHFR and MSR [ 38 , 39 ], as well as in the conversion of choline to betaine [ 47 ].…”

Section: Discussionmentioning

confidence: 99%

Peroxisome Proliferator-Activated Receptor Activation is Associated with Altered Plasma One-Carbon Metabolites and B-Vitamin Status in Rats

et al. 2016

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Plasma concentrations of metabolites along the choline oxidation pathway have been linked to increased risk of major lifestyle diseases, and peroxisome proliferator-activated receptors (PPARs) have been suggested to be involved in the regulation of key enzymes along this pathway. In this study, we investigated the effect of PPAR activation on circulating and urinary one-carbon metabolites as well as markers of B-vitamin status. Male Wistar rats (n = 20) received for 50 weeks either a high-fat control diet or a high-fat diet with tetradecylthioacetic acid (TTA), a modified fatty acid and pan-PPAR agonist with high affinity towards PPARα. Hepatic gene expression of PPARα, PPARβ/δ and the enzymes involved in the choline oxidation pathway were analyzed and concentrations of metabolites were analyzed in plasma and urine. TTA treatment altered most biomarkers, and the largest effect sizes were observed for plasma concentrations of dimethylglycine, nicotinamide, methylnicotinamide, methylmalonic acid and pyridoxal, which were all higher in the TTA group (all p < 0.01). Hepatic Pparα mRNA was increased after TTA treatment, but genes of the choline oxidation pathway were not affected. Long-term TTA treatment was associated with pronounced alterations on the plasma and urinary concentrations of metabolites related to one-carbon metabolism and B-vitamin status in rats.

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“… 24‐30 In our study population, the top five dietary sources of vitamin B 3 are ready‐to‐eat breakfast cereal, black coffee, bread/dinner rolls, chicken (not fried) and tuna. In the human body, vitamin B 3 is metabolized into the enzymatic cofactor, nicotinamide adenine dinucleotide (NAD), which is used by over 400 enzymes for various biological functions, including posttranslational modifications of cellular proteins 39,40 . However, NAD is not completely stable, it is converted to nicotinamide adenine dinucleotide phosphate (NADP) and both NAD and NADP are involved in cellular oxidation/reduction processes that contribute to the prevention of oxidative DNA damage and maintenance of genome integrity 41,42 .…”

Section: Discussionmentioning

confidence: 99%

One‐carbon metabolism‐related micronutrients intake and risk for hepatocellular carcinoma: A prospective cohort study

Antwi

Petrick

Campbell

et al. 2020

Intl Journal of Cancer

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Deficient intake of micronutrients involved in one‐carbon metabolism (eg, choline, methionine, vitamin B12 and folic acid) leads to hepatocellular carcinoma (HCC) development in rodents, but is under‐investigated in humans. We investigated the association between one‐carbon metabolism‐related micronutrient intake and HCC risk in a prospective cohort of 494 860 participants with 16 years of follow‐up in the NIH‐AARP study. Dietary intakes and supplement use were ascertained at baseline using a food‐frequency questionnaire. Total intake (diet plus supplements) of the following one‐carbon metabolism‐related micronutrients were calculated: folate, methionine and vitamins B2 (riboflavin), B3 (niacin), B6 and B12. These micronutrients were examined both individually and simultaneously, with adjustment for covariates. Cox proportional hazard models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). Over the 16‐year follow‐up period, 647 incident HCC cases were diagnosed. When examined individually, higher total vitamin B3 intake was associated with a lower HCC risk (HRQ5 vs Q1 = 0.60; 95% CI = 0.42‐0.85; Ptrend = .008), and the association remained significant when all six micronutrients were examined simultaneously (HRQ5 vs Q1 = 0.32; 95% CI = 0.18‐0.55; Ptrend < .0001). Among participants with >3 years of follow‐up, higher total vitamin B3 intake was again associated with lower risk (HRQ5 vs Q1 = 0.37; 95% CI = 0.20‐0.68; Ptrend = .001), whereas higher total vitamin B6 intake was associated with higher risk (HRQ5 vs Q1 = 2.04; 95% CI = 1.02‐4.07; Ptrend = .04). Restricted cubic spline analyses showed a dose‐response inverse association between total vitamin B3 intake and HCC risk, and dose‐response positive association between total vitamin B6 intake and HCC risk. The study suggests that higher vitamin B3 intake is associated with lower HCC risk, whereas higher vitamin B6 intake is associated with increased risk.

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Niacin

Cited by 18 publications

References 68 publications

Safety assessment of nicotinamide riboside, a form of vitamin B₃

Safety assessment of nicotinamide riboside, a form of vitamin B₃

Peroxisome Proliferator-Activated Receptor Activation is Associated with Altered Plasma One-Carbon Metabolites and B-Vitamin Status in Rats

One‐carbon metabolism‐related micronutrients intake and risk for hepatocellular carcinoma: A prospective cohort study

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Niacin

Cited by 18 publications

References 68 publications

Safety assessment of nicotinamide riboside, a form of vitamin B3

Safety assessment of nicotinamide riboside, a form of vitamin B3

Peroxisome Proliferator-Activated Receptor Activation is Associated with Altered Plasma One-Carbon Metabolites and B-Vitamin Status in Rats

One‐carbon metabolism‐related micronutrients intake and risk for hepatocellular carcinoma: A prospective cohort study

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Safety assessment of nicotinamide riboside, a form of vitamin B₃

Safety assessment of nicotinamide riboside, a form of vitamin B₃