Study summary · research use only
NAD(+) repletion with niacin counteracts cancer cachexia
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study used different mouse models of cancer cachexia along with human muscle tissue from cancer patients to examine nicotinamide adenine dinucleotide (NAD+) metabolism. The authors report that depletion of NAD+ and downregulation of Nrk2, an NAD+ biosynthetic enzyme, were common features of severe cachexia across the mouse models. Treating cachectic mice with the NAD+ precursor vitamin B3 niacin was associated with restored tissue NAD+ levels, changes in mitochondrial metabolism measures, and reduced cancer- and chemotherapy-induced cachexia. In human muscle samples, NRK2 was downregulated in cancer patients, and low NRK2 expression correlated with metabolic abnormalities. The authors describe NAD+ metabolism as a potential therapy target for cachectic cancer patients based on these findings.
Abstract
Cachexia is a debilitating wasting syndrome and highly prevalent comorbidity in cancer patients. It manifests especially with energy and mitochondrial metabolism aberrations that promote tissue wasting. We recently identified nicotinamide adenine dinucleotide (NAD+) loss to associate with muscle mitochondrial dysfunction in cancer hosts. In this study we confirm that depletion of NAD+ and downregulation of Nrk2, an NAD+ biosynthetic enzyme, are common features of severe cachexia in different mouse models. Testing NAD+ repletion therapy in cachectic mice reveals that NAD+ precursor, vitamin B3 niacin, efficiently corrects tissue NAD+ levels, improves mitochondrial metabolism and ameliorates cancer- and chemotherapy-induced cachexia. In a clinical setting, we show that muscle NRK2 is downregulated in cancer patients. The low expression of NRK2 correlates with metabolic abnormalities underscoring the significance of NAD+ in the pathophysiology of human cancer cachexia. Overall, our results propose NAD+ metabolism as a therapy target for cachectic cancer patients.
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