NAD Supplement Alleviates Intestinal Barrier Injury Induced by Ethanol Via Protecting Epithelial Mitochondrial Function.

Li W, Zhou Y, Pang N, Hu Q, Li Q, Sun Y, Ding Y, Gu Y, Xiao Y, Gao M, Ma S, Pan J, Fang EF, Zhang Z, Yang L

Nutrients30 Dec 2022Cited by 34 (Europe PMC)

PMID36615829PMCIDPMC9823589DOI10.3390/nu15010174PepBankPUB-36615829

Summary

BackgroundThe epithelial tight junction is an important intestinal barrier whose disruption can lead to the release of harmful intestinal substances into the circulation and cause damage to systemic injury. The maintenance of intestinal epithelial tight junctions is closely related to energy homeostasis and mitochondrial function. Nicotinamide riboside (NR) is a NAD booster that can enhance mitochondrial biogenesis in liver. However, whether NR can prevent ethanol-induced intestinal barrier dysfunction and the underlying mechanisms remain unclear.MethodsWe applied the mouse NIAAA model (chronic plus binge ethanol feeding) and Caco-2 cells to explore the effects of NR on ethanol-induced intestinal barrier dysfunction and the underlying mechanisms. NAD homeostasis and mitochondrial function were measured. In addition, knockdown of SirT1 in Caco-2 cells was further applied to explore the role of SirT1 in the protection of NR.ResultsWe found that ethanol increased intestinal permeability, increased the release of LPS into the circulation and destroyed the intestinal epithelial barrier structure in mice. NR supplementation attenuated intestinal barrier injury. Both in vivo and in vitro experiments showed that NR attenuated ethanol-induced decreased intestinal tight junction protein expressions and maintained NAD homeostasis. In addition, NR supplementation activated SirT1 activity and increased deacetylation of PGC-1α, and reversed ethanol-induced mitochondrial dysfunction and mitochondrial biogenesis. These effects were diminished with the knockdown of SirT1 in Caco-2 cells.ConclusionBoosting NAD by NR alleviates ethanol-induced intestinal epithelial barrier damage via protecting mitochondrial function in a SirT1-dependent manner.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study10

No result from this study comes from a test of the peptide.

Natural levels measured2

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

01AnimalEndogenous levelAnimal study (in vivo)Mechanism
In ethanol-exposed mice, NR maintained natural NAD homeostasis.
In plain wordsIn mice exposed to ethanol, NR maintained the body's own NAD balance.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
Not applicableNAD homeostasis
Study
mousen: not reported in source
NIAAA chronic plus binge ethanol model
Outcome group
Mitochondrial function · Gastrointestinal
Source sentences
Summary
Both in vivo and in vitro experiments showed that NR attenuated ethanol-induced decreased intestinal tight junction protein expressions and maintained NAD homeostasis.
1 context sentence(design, population, supporting numbers)
Summary · context
We applied the mouse NIAAA model (chronic plus binge ethanol feeding) and Caco-2 cells to explore the effects of NR on ethanol-induced intestinal barrier dysfunction and the underlying mechanisms.
This result measures the body's own NAD+ (nicotinamide adenine dinucleotide). Nobody was given the peptide. It is not evidence about taking it.
Show in the study text Report a problemFND-3661582904
02LabEndogenous levelIn vitro (cells)Mechanism
In ethanol-exposed cell experiments, NR maintained natural NAD homeostasis.
In plain wordsIn cells exposed to ethanol, NR maintained natural NAD balance.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
Not applicableNAD homeostasis
Study
n: not reported in source
Caco-2 cells
Outcome group
Mitochondrial function · Gastrointestinal
Source sentences
Summary
Both in vivo and in vitro experiments showed that NR attenuated ethanol-induced decreased intestinal tight junction protein expressions and maintained NAD homeostasis.
1 context sentence(design, population, supporting numbers)
Summary · context
We applied the mouse NIAAA model (chronic plus binge ethanol feeding) and Caco-2 cells to explore the effects of NR on ethanol-induced intestinal barrier dysfunction and the underlying mechanisms.
This result measures the body's own NAD+ (nicotinamide adenine dinucleotide). Nobody was given the peptide. It is not evidence about taking it.
Show in the study text Report a problemFND-3661582905

Studies that did not test the peptide alone8

In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).

03AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome
In ethanol-exposed mice, NR supplementation attenuated intestinal barrier injury.
In plain wordsIn mice exposed to ethanol, NR supplementation reduced intestinal barrier injury.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseIntestinal barrier injury
Study
mousen: not reported in source
NIAAA chronic plus binge ethanol model
Outcome group
Gastrointestinal protection · Gastrointestinal
Source sentences
Summary
NR supplementation attenuated intestinal barrier injury.
1 context sentence(design, population, supporting numbers)
Summary · context
We applied the mouse NIAAA model (chronic plus binge ethanol feeding) and Caco-2 cells to explore the effects of NR on ethanol-induced intestinal barrier dysfunction and the underlying mechanisms.
In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3661582901
04AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Mechanism
In ethanol-exposed mice, NR attenuated the decrease in intestinal tight junction protein expression.
In plain wordsIn mice exposed to ethanol, NR reduced the loss of intestinal tight junction protein expression.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
IncreaseIntestinal tight junction protein expression
Study
mousen: not reported in source
NIAAA chronic plus binge ethanol model
Outcome group
Gastrointestinal protection · Gastrointestinal
Source sentences
Summary
Both in vivo and in vitro experiments showed that NR attenuated ethanol-induced decreased intestinal tight junction protein expressions and maintained NAD homeostasis.
1 context sentence(design, population, supporting numbers)
Summary · context
We applied the mouse NIAAA model (chronic plus binge ethanol feeding) and Caco-2 cells to explore the effects of NR on ethanol-induced intestinal barrier dysfunction and the underlying mechanisms.
In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3661582902
05AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism
In ethanol injury experiments, NR supplementation activated SirT1 activity.
In plain wordsIn experimental ethanol injury models, NR supplementation activated SirT1 activity.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
IncreaseSirT1 activity
Study
n: not reported in source
Outcome group
Receptor activity and mechanism · Gastrointestinal
Source sentences
Summary
In addition, NR supplementation activated SirT1 activity and increased deacetylation of PGC-1α, and reversed ethanol-induced mitochondrial dysfunction and mitochondrial biogenesis.
1 context sentence(design, population, supporting numbers)
Summary · context
We applied the mouse NIAAA model (chronic plus binge ethanol feeding) and Caco-2 cells to explore the effects of NR on ethanol-induced intestinal barrier dysfunction and the underlying mechanisms.
In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3661582906
06AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism
In ethanol injury experiments, NR supplementation increased PGC-1α deacetylation.
In plain wordsIn experimental ethanol injury models, NR supplementation increased PGC-1α deacetylation.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
IncreasePGC-1α deacetylation
Study
n: not reported in source
Outcome group
Receptor activity and mechanism · Gastrointestinal
Source sentences
Summary
In addition, NR supplementation activated SirT1 activity and increased deacetylation of PGC-1α, and reversed ethanol-induced mitochondrial dysfunction and mitochondrial biogenesis.
1 context sentence(design, population, supporting numbers)
Summary · context
We applied the mouse NIAAA model (chronic plus binge ethanol feeding) and Caco-2 cells to explore the effects of NR on ethanol-induced intestinal barrier dysfunction and the underlying mechanisms.
In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3661582907
07AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism
In ethanol injury experiments, NR supplementation reversed ethanol-induced mitochondrial dysfunction.
In plain wordsIn experimental ethanol injury models, NR supplementation reversed mitochondrial dysfunction.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseMitochondrial dysfunction
Study
n: not reported in source
Outcome group
Mitochondrial function · Gastrointestinal
Source sentences
Summary
In addition, NR supplementation activated SirT1 activity and increased deacetylation of PGC-1α, and reversed ethanol-induced mitochondrial dysfunction and mitochondrial biogenesis.
1 context sentence(design, population, supporting numbers)
Summary · context
We applied the mouse NIAAA model (chronic plus binge ethanol feeding) and Caco-2 cells to explore the effects of NR on ethanol-induced intestinal barrier dysfunction and the underlying mechanisms.
In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3661582908
08AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism
In ethanol injury experiments, NR supplementation reversed ethanol-induced changes in mitochondrial biogenesis.
In plain wordsIn experimental ethanol injury models, NR supplementation reversed changes in mitochondrial biogenesis.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
Direction not reportedMitochondrial biogenesis
Study
n: not reported in source
Outcome group
Mitochondrial function · Gastrointestinal
Source sentences
Summary
In addition, NR supplementation activated SirT1 activity and increased deacetylation of PGC-1α, and reversed ethanol-induced mitochondrial dysfunction and mitochondrial biogenesis.
1 context sentence(design, population, supporting numbers)
Summary · context
We applied the mouse NIAAA model (chronic plus binge ethanol feeding) and Caco-2 cells to explore the effects of NR on ethanol-induced intestinal barrier dysfunction and the underlying mechanisms.
In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3661582909
09LabNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneIn vitro (cells)Mechanism
In ethanol-exposed cell experiments, NR attenuated the decrease in intestinal tight junction protein expression.
In plain wordsIn cells exposed to ethanol, NR reduced the loss of intestinal tight junction protein expression.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
IncreaseIntestinal tight junction protein expression
Study
n: not reported in source
Caco-2 cells
Outcome group
Gastrointestinal protection · Gastrointestinal
Source sentences
Summary
Both in vivo and in vitro experiments showed that NR attenuated ethanol-induced decreased intestinal tight junction protein expressions and maintained NAD homeostasis.
1 context sentence(design, population, supporting numbers)
Summary · context
We applied the mouse NIAAA model (chronic plus binge ethanol feeding) and Caco-2 cells to explore the effects of NR on ethanol-induced intestinal barrier dysfunction and the underlying mechanisms.
In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3661582903
10LabNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneIn vitro (cells)Mechanism
In Caco-2 cells, SirT1 knockdown diminished the reported protective effects of the NAD booster NR.
In plain wordsIn cells, SirT1 knockdown diminished the protective effects of the NAD booster NR.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseNR protective effects after SirT1 knockdown
Study
n: not reported in source
Caco-2 cells with SirT1 knockdown
Outcome group
Receptor activity and mechanism · Gastrointestinal
Source sentences
Summary
These effects were diminished with the knockdown of SirT1 in Caco-2 cells.
2 context sentences(design, population, supporting numbers)
Summary · context
In addition, NR supplementation activated SirT1 activity and increased deacetylation of PGC-1α, and reversed ethanol-induced mitochondrial dysfunction and mitochondrial biogenesis.
Summary · context
We applied the mouse NIAAA model (chronic plus binge ethanol feeding) and Caco-2 cells to explore the effects of NR on ethanol-induced intestinal barrier dysfunction and the underlying mechanisms.
In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).
Show in the study text Report a problemFND-3661582910

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.

Version 2Current
14 Oct 2026, 05:02 UTC
Study results updated
Version 1
14 Oct 2026, 01:46 UTC
First added · source update from Europe PMC

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