NAD + Supplementation by Nicotinamide Riboside Alters Function of Murine Hematopoietic Stem Cells from Impaired Environments
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ABSTRACT:
PROVIDER: PRJNA615893 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11435227_1.fastq.gz | Fastqsanger.gz | |||
| SRR11435227_2.fastq.gz | Fastqsanger.gz | |||
| SRR11435228_1.fastq.gz | Fastqsanger.gz | |||
| SRR11435228_2.fastq.gz | Fastqsanger.gz | |||
| SRR11435229_1.fastq.gz | Fastqsanger.gz |
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Project description:In clinical trials, oral supplementation with nicotinamide riboside (NR) fails to increase muscle mitochondrial respiratory capacity and insulin sensitivity, but also does not increase muscle NAD+ levels. This study tests the feasibility of chronically elevating skeletal muscle NAD+ in mice and investigates the putative effects on mitochondrial respiratory capacity, insulin sensitivity, and gene expression. Accordingly, to improve bioavailability to skeletal muscle, we developed an experimental model for administering NR repeatedly through a jugular vein catheter. Mice on a Western diet were treated with various combinations of NR, pterostilbene (PT), and voluntary wheel running, but metabolic effects of NR and PT treatment were modest. We conclude that chronic elevation of skeletal muscle NAD+ by intravenous injection of NR is possible but does not affect muscle respiratory capacity or insulin sensitivity in either sedentary or physically active mice. Our data have implications for NAD+ precursor supplementation regimes.
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Project description:During aging, general cellular processes such as autophagic clearance, DNA repair, mitochondrial health, metabolism, nicotinamide adenine dinucleotide (NAD+) levels, and immunological responses become compromised. Urolithin A (UA) and NAD+ supplementation stimulate mitophagy, reduce pathological plaque load, and inflammation while improving learning in models of Alzheimer’s disease (Hou et al 2021; Fang et al 2019). Here we have performed a During aging, general cellular processes such as autophagic clearance, DNA repair, mitochondrial health, metabolism, nicotinamide adenine dinucleotide (NAD+) levels, and immunological responses become compromised. Urolithin A (UA) and NAD+ supplementation stimulate mitophagy, reduce pathological plaque load, and inflammation while improving learning in models of Alzheimer’s disease (Hou et al 2021; Fang et al 2019). Here we have performed a pairwise analysis of UA and nicotinamide riboside (NR) to investigate how these compounds modulate inflammation. The role of microglia in driving neuroinflammation is becoming more recognized in several neurodegenerative diseases, yet the effects of these drugs on microglia cells have not been thoroughly investigated. As both UA and NR are recognized as safe dietary supplements, their function in normal cells is equally important to understand as in a disease state. Here we investigated the effects of UA and NR in the human microglia cell line, HMC3.
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