Skip to content

Study · Animal study (in vivo) · mouse · 2019

7 results

Investigating RNA expression profiles altered by nicotinamide mononucleotide therapy in a chronic model of alcoholic liver disease.

Assiri MA, Ali HR, Marentette JO, Yun Y, Liu J, Hirschey MD, Saba LM, Harris PS, Fritz KS

Human genomics10 Dec 2019Cited by 20 (Europe PMC)

PMID31823815 (opens in a new tab)PMCIDPMC6902345 (opens in a new tab)DOI10.1186/s40246-019-0251-1 (opens in a new tab)PepBankPUB-31823815
Download PDFPubMedAsk about this study
Jump to 7 results

Summary

BackgroundChronic alcohol consumption is a significant cause of liver disease worldwide. Several biochemical mechanisms have been linked to the initiation and progression of alcoholic liver disease (ALD) such as oxidative stress, inflammation, and metabolic dysregulation, including the disruption of NAD+/NADH. Indeed, an ethanol-mediated reduction in hepatic NAD+ levels is thought to be one factor underlying ethanol-induced steatosis, oxidative stress, steatohepatitis, insulin resistance, and inhibition of gluconeogenesis. Therefore, we applied a NAD+ boosting supplement to investigate alterations in the pathogenesis of early-stage ALD.MethodsTo examine the impact of NAD+ therapy on the early stages of ALD, we utilized nicotinamide mononucleotide (NMN) at 500 mg/kg intraperitoneal injection every other day, for the duration of a Lieber-DeCarli 6-week chronic ethanol model in mice. Numerous strategies were employed to characterize the effect of NMN therapy, including the integration of RNA-seq, immunoblotting, and metabolomics analysis.ResultsOur findings reveal that NMN therapy increased hepatic NAD+ levels, prevented an ethanol-induced increase in plasma ALT and AST, and changed the expression of 25% of the genes that were modulated by ethanol metabolism. These genes were associated with a number of pathways including the MAPK pathway. Interestingly, our analysis revealed that NMN treatment normalized Erk1/2 signaling and prevented an induction of Atf3 overexpression.ConclusionsThese findings reveal previously unreported mechanisms by which NMN supplementation alters hepatic gene expression and protein pathways to impact ethanol hepatotoxicity in an early-stage murine model of ALD. Overall, our data suggest further research is needed to fully characterize treatment paradigms and biochemical implications of NAD+-based interventions.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study7

6 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Mechanism

    In mice with chronic ethanol exposure, NMN increased hepatic NAD+ levels.

    In plain wordsIn mice exposed to ethanol, NMN increased liver NAD+ levels.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseHepatic NAD+
    Study

    mousen: not reported in source

    Lieber-DeCarli chronic ethanol model
    Outcome group
    Mitochondrial function · Liver
    Studied dose
    500 mg/kg every other day · intraperitoneal · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Our findings reveal that NMN therapy increased hepatic NAD+ levels, prevented an ethanol-induced increase in plasma ALT and AST, and changed the expression of 25% of the genes that were modulated by ethanol metabolism.
    1 context sentence
    Summary · context
    To examine the impact of NAD+ therapy on the early stages of ALD, we utilized nicotinamide mononucleotide (NMN) at 500 mg/kg intraperitoneal injection every other day, for the duration of a Lieber-DeCarli 6-week chronic ethanol model in mice.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice, NMN prevented the ethanol-induced increase in plasma ALT.

    In plain wordsIn mice, NMN prevented an ethanol-induced increase in the liver injury marker ALT.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreasePlasma ALT
    Study

    mousen: not reported in source

    Lieber-DeCarli chronic ethanol model
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    500 mg/kg every other day · intraperitoneal · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Our findings reveal that NMN therapy increased hepatic NAD+ levels, prevented an ethanol-induced increase in plasma ALT and AST, and changed the expression of 25% of the genes that were modulated by ethanol metabolism.
    1 context sentence
    Summary · context
    To examine the impact of NAD+ therapy on the early stages of ALD, we utilized nicotinamide mononucleotide (NMN) at 500 mg/kg intraperitoneal injection every other day, for the duration of a Lieber-DeCarli 6-week chronic ethanol model in mice.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice, NMN prevented the ethanol-induced increase in plasma AST.

    In plain wordsIn mice, NMN prevented an ethanol-induced increase in the liver injury marker AST.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreasePlasma AST
    Study

    mousen: not reported in source

    Lieber-DeCarli chronic ethanol model
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    500 mg/kg every other day · intraperitoneal · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Our findings reveal that NMN therapy increased hepatic NAD+ levels, prevented an ethanol-induced increase in plasma ALT and AST, and changed the expression of 25% of the genes that were modulated by ethanol metabolism.
    1 context sentence
    Summary · context
    To examine the impact of NAD+ therapy on the early stages of ALD, we utilized nicotinamide mononucleotide (NMN) at 500 mg/kg intraperitoneal injection every other day, for the duration of a Lieber-DeCarli 6-week chronic ethanol model in mice.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In ethanol-exposed mice, NMN changed expression of 25% of genes modulated by ethanol metabolism.

    In plain wordsIn mice exposed to ethanol, NMN changed expression of 25% of genes affected by ethanol metabolism.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    Direction not reportedEthanol-modulated gene expression
    Study

    mousen: not reported in source

    Lieber-DeCarli chronic ethanol model
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    500 mg/kg every other day · intraperitoneal · 6 weeksAs given in this study (mouse).

    Measurements

    Genes with changed expression
    25%
    genes modulated by ethanol metabolism

    Source sentences

    Summary
    Our findings reveal that NMN therapy increased hepatic NAD+ levels, prevented an ethanol-induced increase in plasma ALT and AST, and changed the expression of 25% of the genes that were modulated by ethanol metabolism.
    1 context sentence
    Summary · context
    To examine the impact of NAD+ therapy on the early stages of ALD, we utilized nicotinamide mononucleotide (NMN) at 500 mg/kg intraperitoneal injection every other day, for the duration of a Lieber-DeCarli 6-week chronic ethanol model in mice.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In ethanol-exposed mice, NMN normalized Erk1/2 signaling.

    In plain wordsIn mice exposed to ethanol, NMN normalized Erk1/2 signaling.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    Not applicableErk1/2 signaling
    Study

    mousen: not reported in source

    Lieber-DeCarli chronic ethanol model
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    500 mg/kg every other day · intraperitoneal · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Interestingly, our analysis revealed that NMN treatment normalized Erk1/2 signaling and prevented an induction of Atf3 overexpression.
    1 context sentence
    Summary · context
    To examine the impact of NAD+ therapy on the early stages of ALD, we utilized nicotinamide mononucleotide (NMN) at 500 mg/kg intraperitoneal injection every other day, for the duration of a Lieber-DeCarli 6-week chronic ethanol model in mice.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In ethanol-exposed mice, NMN prevented induction of Atf3 overexpression.

    In plain wordsIn mice exposed to ethanol, NMN prevented excessive Atf3 expression.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseAtf3 overexpression
    Study

    mousen: not reported in source

    Lieber-DeCarli chronic ethanol model
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    500 mg/kg every other day · intraperitoneal · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Interestingly, our analysis revealed that NMN treatment normalized Erk1/2 signaling and prevented an induction of Atf3 overexpression.
    1 context sentence
    Summary · context
    To examine the impact of NAD+ therapy on the early stages of ALD, we utilized nicotinamide mononucleotide (NMN) at 500 mg/kg intraperitoneal injection every other day, for the duration of a Lieber-DeCarli 6-week chronic ethanol model in mice.

Studies that did not test the peptide alone1

In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking NMN (nicotinamide mononucleotide).

  1. 07Computer modelNot a test of NMN (nicotinamide mononucleotide) aloneIn silicoMechanism

    Gene analysis associated NMN-responsive ethanol-modulated genes with pathways including MAPK.

    In plain wordsComputer analysis linked genes affected by NMN and ethanol to pathways that included MAPK.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    Not applicableMAPK pathway association
    Study

    mousen: not reported in source

    Lieber-DeCarli chronic ethanol model
    Outcome group
    Receptor activity and mechanism · Liver

    Source sentences

    Summary
    These genes were associated with a number of pathways including the MAPK pathway.
    2 context sentences
    Summary · context
    Our findings reveal that NMN therapy increased hepatic NAD+ levels, prevented an ethanol-induced increase in plasma ALT and AST, and changed the expression of 25% of the genes that were modulated by ethanol metabolism.
    Summary · context
    To examine the impact of NAD+ therapy on the early stages of ALD, we utilized nicotinamide mononucleotide (NMN) at 500 mg/kg intraperitoneal injection every other day, for the duration of a Lieber-DeCarli 6-week chronic ethanol model in mice.

    In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

PepBank is a research reference. Talk to a doctor before you use any peptide.