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Sambeat, Audrey; Ratajczak, Joanna; Joffraud, Magali; Sanchez-Garcia, José L; Giner, Maria P; Valsesia, Armand; Giroud-Gerbetant, Judith; Valera-Alberni, Miriam; Cercillieux, Angelique; Boutant, Marie; Kulkarni, Sameer S; Moco, Sofia; Canto, Carles
Nature communications, 09/2019, Letnik: 10, Številka: 1Journal Article
Supplementation with the NAD precursor nicotinamide riboside (NR) ameliorates and prevents a broad array of metabolic and aging disorders in mice. However, little is known about the physiological role of endogenous NR metabolism. We have previously shown that NR kinase 1 (NRK1) is rate-limiting and essential for NR-induced NAD synthesis in hepatic cells. To understand the relevance of hepatic NR metabolism, we generated whole body and liver-specific NRK1 knockout mice. Here, we show that NRK1 deficiency leads to decreased gluconeogenic potential and impaired mitochondrial function. Upon high-fat feeding, NRK1 deficient mice develop glucose intolerance, insulin resistance and hepatosteatosis. Furthermore, they are more susceptible to diet-induced liver DNA damage, due to compromised PARP1 activity. Our results demonstrate that endogenous NR metabolism is critical to sustain hepatic NAD levels and hinder diet-induced metabolic damage, highlighting the relevance of NRK1 as a therapeutic target for metabolic disorders.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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