Abstract

PurposeVitamin B3 provides nicotinamide adenine dinucleotide (NAD+), an essential coenzyme in oxidoreductase reactions. Severe vitamin B3 deficiency leads to the disease Pellagra, while mild vitamin B3 deficiency has been linked to age-related and metabolic diseases. Mild vitamin B3 deficiency is understudied, especially in females. Therefore, we examined how female mice responded to a diet that induced mild vitamin B3 deficiency in male mice.MethodsFemale C57BL/6RccHsd mice were subjected for 18 weeks to a diet without vitamin B3 and low but sufficient tryptophan (0.115%) (0NR) and were compared to control female mice on the same diet with the reference dose of vitamin B3 (30NR, 30 mg nicotinamide riboside/ kg diet).ResultsIn the female mice, no differences between the two dietary groups were found in liver nicotinamide mononucleotide (NMN) levels, body composition, whole body energy and substrate metabolism measured by indirect calorimetry, or liver triacylglycerol metabolism. Expression of seven genes that previously were shown to respond to mild vitamin B3 deficiency in male white adipose tissue were not differentially expressed between the female dietary groups, neither was insulin sensitivity.ConclusionWe concluded that the female 0NR mice were not vitamin B3 deficient; the role of age, sex and health status is discussed. Demonstrated by clear differences between females and males, the latter showing mild deficiency under the same conditions, this study highlights the importance of studying both sexes.

Highlights

  • Oxidised nicotinamide adenine dinucleotide ­(NAD+) is essential as a coenzyme in oxidoreductase reactions, and it functions as a consumed ligand in, for example, sirtuinand poly(ADP-ribose) polymerase-related activities [1, 2]

  • In a recent study in male C57BL/6JRccHsd mice, we found that mild vitamin ­B3 deficiency emerged after 18 weeks on a diet without vitamin ­B3

  • We investigated the expression of seven genes in the white adipose tissue of the female mice that were previously found to be responsive to mild vitamin ­B3 deficiency in males

Read more

Summary

Introduction

Oxidised nicotinamide adenine dinucleotide ­(NAD+) is essential as a coenzyme in oxidoreductase reactions, and it functions as a consumed ligand in, for example, sirtuinand poly(ADP-ribose) polymerase-related activities [1, 2]. Dietary intake of vitamin ­B3, which exists in various forms, and de novo synthesis from the essential amino acid tryptophan, via the kynurenine pathway, are of essence to produce ­NAD+. Vitamin ­B3 has gained interest since it was shown that an increased intake improved health, for example, in hypercholesterolaemic patients. Using a partly different pathway compared to nicotinic acid expected to result in less side effects, NR supplementation showed a potent increase in (mitochondrial) ­NAD+ levels in vitro and in vivo [10]. The liver of mice fed a high-fat diet supplemented with a high dose of NR (400 mg/kg/day) showed a 40% reduction in triacylglycerol content, and decreased cholesterol levels were found, resulting in an improved lipid profile in the NR supplemented mice [10]

Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call