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Subacute toxicity study of nicotinamide mononucleotide via oral administration

ABSTRACT: Subacute toxicity study of nicotinamide mononucleotide via oral administration

PROVIDER: PRJNA662085 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12604428_1.fastq.gz	Fastqsanger.gz
	SRR12604428_2.fastq.gz	Fastqsanger.gz
	SRR12604429_1.fastq.gz	Fastqsanger.gz
	SRR12604429_2.fastq.gz	Fastqsanger.gz
	SRR12604430_1.fastq.gz	Fastqsanger.gz

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Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice

Project description:NAD+ availability decreases with age and in certain disease conditions. Nicotinamide mononucleotide (NMN), a key NAD+ intermediate, has been shown to enhance NAD+ biosynthesis and ameliorate various pathologies in mouse disease models. In this study, we conducted a 12 month-long NMN administration to regular chow-fed wild-type C57BL/6N mice during their normal aging. Orally administered NMN was quickly utilized to synthesize NAD+ in tissues. Remarkably, NMN effectively mitigates age-associated physiological decline in mice. Without any obvious toxicity or deleterious effects, NMN suppressed age-associated body weight gain, enhanced energy metabolism, promoted physical activity, improved insulin sensitivity and plasma lipid profile, and ameliorated eye function and other pathophysiologies. Consistent with these phenotypes, NMN prevented age-associated gene expression changes in key metabolic organs and enhanced mitochondrial oxidative metabolism and mitonuclear protein imbalance in skeletal muscle. These effects of NMN highlight the preventive and therapeutic potential of NAD+ intermediates as effective anti-aging interventions in humans.

2016-12-01 | GSE85718 | GEO

Subacute toxicity study of nicotinamide mononucleotide via oral administration

Project description:To investigate genome-wide gene expression changes induced by 1340mg/kg/d or 2680mg/kg/d NMN adnimistration in mice using next-generation sequencing

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Subacute Toxicity Study of Nicotinamide Mononucleotide via Oral Administration.

Project description:Nicotinamide mononucleotide (NMN), a key precursory metabolite of NAD+, has been shown to elevate the cellular level of NAD+ and ameliorate various age-related diseases. Despite these progresses, systemic evaluation pertaining to the subacute toxicity of NMN remains to be determined. Here, we examine the subacute toxicity of NMN in mice and beagle dogs. Mice were gavaged with a saturated concentration of NMN solution at the maximum intragastric dose once or twice per day for 7 days. Dogs were gavaged twice per day for 14 days. In mice, NMN administrated once per day for 7 days is well tolerated with minimal deleterious effects. Upon higher dosage, we observe slightly increased level of alamine aminotransferase, while other biomarkers remain unchanged. Consistently, administration of NMN in beagle dogs only results in mild increases in creatinine and uric acid. Together, our study highlights the safety of NMN, providing a possible safe dose range for oral administration of NMN.

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Nicotinamide Mononucleotide administration prevents doxorubicin-induced cardiotoxicity and loss in physical activity in mice.

Project description:In this study we investigated whether nicotinamide mononucleotide (NMN) could protect against Doxorubicin-induced cardiotoxicity and physical dysfunction in vivo. To assess the short- and long-term toxicity, two Doxo regimens were tested, acute and chronic. In the acute study, C57BL6/J (B6) mice were injected intraperitoneally (i.p.) once with Doxo (20 mg/kg) and NMN (180 mg/kg/day, i.p.) was administered daily for five days before and after the Doxo injection. In the chronic study, B6 mice received a cumulative dose of 20 mg/kg Doxo administered in fractionated doses for five days. NMN (500 mg/kg/day) was supplied in the mice’s drinking water beginning five days before the first injection of Doxo and continuing for 60 days after.

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Reduced Nicotinamide Mononucleotide (NMNH) Potently Enhances NAD+, Suppresses Glycolysis and Cell Growth

Project description:In the present study, we developed a chemical method to produce dihydro nicotinamide mononucleotide (NMNH), which is the reduced-form of nicotinamide mononucleotide (NMN). We demonstrated that NMNH was a better nicotinamide adenine dinucleotide (NAD+) enhancer compared to NMN both in vitro and in vivo mediated by mononucleotide adenylyltransferase (NMNAT). Additionally, NMNH increased the reduced NAD (NADH) levels in cells and in mouse liver. Metabolomic analysis revealed that NMNH inhibited glycolysis and TCA cycle. In vitro experiments demonstrated that NMNH induced cell cycle arrest and suppressed cell growth. Nevertheless, NMNH treatment did not cause observable difference in mice. Taken together, our work demonstrates that NMNH is a potent NAD+ enhancer, and suppresses glycometabolism and cell growth.

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Nicotinamide mononucleotide administration triggers macrophages reprogramming and alleviates inflammation during sepsis induced by experimental peritonitis

Project description:Peritonitis and subsequent sepsis lead to high morbidity and mortality in response to uncontrolled systemic inflammation primarily mediated by macrophages. We investigated whether the administration of a natural biosynthetic precursor of NAD+, β-nicotinamide mononucleotide (β‐NMN), could prevent clinical deterioration effects of sepsis. To this purpose, C57BL6 mice were subjected to the cecal ligation and puncture (CLP) model to provoke sepsis or were injected with thioglycolate (TGC) to induce a sterile peritonitis with recruitment and differentiation of macrophages into the inflamed peritoneal cavity. β-NMN was administered for 4 days after CLP and for 3 days post TGC treatment. Administration of β‐NMN decreased bacterial load in blood and reduced clinical signs of distress and mortality during sepsis. Transcriptomic analysis of hearts and lungs 24 hours post CLP-induction, revealed that β-NMN downregulated genes controlling immuno-inflammatory response and upregulated genes involved in bioenergetic metabolism, mitochondria biogenesis, and autophagy. In the thioglycolate model, β‐NMN treatment significantly reduced phagolysosomes acidification and inflammatory mediators secretion from bacteria-stimulated peritoneal macrophages. Transcriptomic signature of these macrophages showed that β‐NMN administration limited the pro-inflammatory M1 phenotype, induced the expression of specific markers of M2 type macrophages and significantly impacted gens involved in NAD+ metabolism.

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Nicotinamide Mononucleotide administration prevents doxorubicin-induced cardiotoxicity and loss in physical activity in mice.

Project description:Nicotinamide Mononucleotide administration prevents doxorubicin-induced cardiotoxicity and loss in physical activity in mice.

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Effect of nicotinamide mononucleotide on doxorubicin-induced cardiac injury in mice

Project description:Doxorubicin (DOX) is the cornerstone of chemotherapy regimens for many malignancies, but its clinical usage is limited by severe cardiotoxicity. Accumulating evidence suggest that nicotinamide adenine dinucleotide (NAD+) depletion contributes to DOX-induced cardiotoxicity, making NAD+ boosting an appealing strategy. Nicotinamide mononucleotide (NMN) is an NAD+ precursor that shows promising therapeutic effects in various diseases. To understand the impact of NMN on gene expression in myocardial tissue of DOX-exposed mice, a RNA-seq assay was carried out.

2023-06-03 | GSE233644 | GEO

Nicotinamide mononucleotide administration triggers macrophages reprogramming and alleviates inflammation during sepsis induced by experimental peritonitis

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