The female mouse is resistant to mild vitamin B3 deficiency
Purpose Vitamin B 3 provides nicotinamide adenine dinucleotide (NAD + ), an essential coenzyme in oxidoreductase reactions. Severe vitamin B 3 deficiency leads to the disease Pellagra, while mild vitamin B 3 deficiency has been linked to age-related and metabolic diseases. Mild vitamin B 3 deficienc...
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Veröffentlicht in: | European journal of nutrition 2022-02, Vol.61 (1), p.329-340 |
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Sprache: | eng |
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Zusammenfassung: | Purpose
Vitamin B
3
provides nicotinamide adenine dinucleotide (NAD
+
), an essential coenzyme in oxidoreductase reactions. Severe vitamin B
3
deficiency leads to the disease Pellagra, while mild vitamin B
3
deficiency has been linked to age-related and metabolic diseases. Mild vitamin B
3
deficiency is understudied, especially in females. Therefore, we examined how female mice responded to a diet that induced mild vitamin B
3
deficiency in male mice.
Methods
Female C57BL/6RccHsd mice were subjected for 18 weeks to a diet without vitamin B
3
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 B
3
(30NR, 30 mg nicotinamide riboside/ kg diet).
Results
In 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 B
3
deficiency in male white adipose tissue were not differentially expressed between the female dietary groups, neither was insulin sensitivity.
Conclusion
We concluded that the female 0NR mice were not vitamin B
3
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. |
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ISSN: | 1436-6207 1436-6215 |
DOI: | 10.1007/s00394-021-02651-8 |