Skip to content

Study · Animal study (in vivo) · rat and mouse · 2024

10 results

Glycolysis-Mediated Activation of v-ATPase by Nicotinamide Mononucleotide Ameliorates Lipid-Induced Cardiomyopathy by Repressing the CD36-TLR4 Axis.

Wang S, Han Y, Liu R, Hou M, Neumann D, Zhang J, Wang F, Li Y, Zhao X, Schianchi F, Dai C, Liu L and 6 more

Show all authors

Nabben M, Glatz JFC, Wu X, Lu X, Li X, Luiken JJFP

Circulation research7 Feb 2024Cited by 44 (Europe PMC)

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study10

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    During myocardial lipid overload, NMN preserved endosomal acidification.

    In plain wordsIn rats and mice with lipid overload, NMN preserved endosomal acidity.

    Outcome
    IncreaseEndosomal acidification
    Study

    rats/micen: not reported in source

    High-fat diet-induced cardiomyopathy
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN successfully preserved endosomal acidification during myocardial lipid overload by maintaining v-ATPase activity and subsequently prevented CD36-mediated lipid accumulation, CD36-TLR4 interaction toward inflammation, fibrosis, cardiac dysfunction, and whole-body insulin resistance.
    1 context sentence
    Summary · context
    Rats/mice on cardiomyopathy-inducing high-fat diets were supplemented with NMN and for comparison with a cocktail of lysine/leucine/arginine (mTORC1 [mechanistic target of rapamycin complex 1]-mediated v-ATPase reassembly).
  2. 02AnimalAnimal study (in vivo)Mechanism

    During myocardial lipid overload, NMN maintained v-ATPase activity.

    In plain wordsIn rats and mice with lipid overload, NMN maintained v-ATPase activity.

    Outcome
    Increasev-ATPase activity
    Study

    rats/micen: not reported in source

    High-fat diet-induced cardiomyopathy
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN successfully preserved endosomal acidification during myocardial lipid overload by maintaining v-ATPase activity and subsequently prevented CD36-mediated lipid accumulation, CD36-TLR4 interaction toward inflammation, fibrosis, cardiac dysfunction, and whole-body insulin resistance.
    1 context sentence
    Summary · context
    Rats/mice on cardiomyopathy-inducing high-fat diets were supplemented with NMN and for comparison with a cocktail of lysine/leucine/arginine (mTORC1 [mechanistic target of rapamycin complex 1]-mediated v-ATPase reassembly).
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    During myocardial lipid overload, NMN prevented CD36-mediated lipid accumulation.

    In plain wordsIn rats and mice with lipid overload, NMN prevented CD36-mediated lipid accumulation.

    Outcome
    DecreaseCD36-mediated lipid accumulation
    Study

    rats/micen: not reported in source

    High-fat diet-induced cardiomyopathy
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN successfully preserved endosomal acidification during myocardial lipid overload by maintaining v-ATPase activity and subsequently prevented CD36-mediated lipid accumulation, CD36-TLR4 interaction toward inflammation, fibrosis, cardiac dysfunction, and whole-body insulin resistance.
    1 context sentence
    Summary · context
    Rats/mice on cardiomyopathy-inducing high-fat diets were supplemented with NMN and for comparison with a cocktail of lysine/leucine/arginine (mTORC1 [mechanistic target of rapamycin complex 1]-mediated v-ATPase reassembly).
  4. 04AnimalAnimal study (in vivo)Mechanism

    During myocardial lipid overload, NMN prevented CD36-TLR4 interaction toward inflammation.

    In plain wordsIn rats and mice with lipid overload, NMN prevented inflammatory CD36-TLR4 interaction.

    Outcome
    DecreaseCD36-TLR4 interaction
    Study

    rats/micen: not reported in source

    High-fat diet-induced cardiomyopathy
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN successfully preserved endosomal acidification during myocardial lipid overload by maintaining v-ATPase activity and subsequently prevented CD36-mediated lipid accumulation, CD36-TLR4 interaction toward inflammation, fibrosis, cardiac dysfunction, and whole-body insulin resistance.
    1 context sentence
    Summary · context
    Rats/mice on cardiomyopathy-inducing high-fat diets were supplemented with NMN and for comparison with a cocktail of lysine/leucine/arginine (mTORC1 [mechanistic target of rapamycin complex 1]-mediated v-ATPase reassembly).
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    During myocardial lipid overload, NMN prevented inflammation.

    In plain wordsIn rats and mice with lipid overload, NMN prevented inflammation.

    Outcome
    DecreaseInflammation
    Study

    rats/micen: not reported in source

    High-fat diet-induced cardiomyopathy
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN successfully preserved endosomal acidification during myocardial lipid overload by maintaining v-ATPase activity and subsequently prevented CD36-mediated lipid accumulation, CD36-TLR4 interaction toward inflammation, fibrosis, cardiac dysfunction, and whole-body insulin resistance.
    1 context sentence
    Summary · context
    Rats/mice on cardiomyopathy-inducing high-fat diets were supplemented with NMN and for comparison with a cocktail of lysine/leucine/arginine (mTORC1 [mechanistic target of rapamycin complex 1]-mediated v-ATPase reassembly).
  6. 06AnimalAnimal study (in vivo)Efficacy outcome

    During myocardial lipid overload, NMN prevented fibrosis.

    In plain wordsIn rats and mice with lipid overload, NMN prevented fibrosis.

    Outcome
    DecreaseFibrosis
    Study

    rats/micen: not reported in source

    High-fat diet-induced cardiomyopathy
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN successfully preserved endosomal acidification during myocardial lipid overload by maintaining v-ATPase activity and subsequently prevented CD36-mediated lipid accumulation, CD36-TLR4 interaction toward inflammation, fibrosis, cardiac dysfunction, and whole-body insulin resistance.
    1 context sentence
    Summary · context
    Rats/mice on cardiomyopathy-inducing high-fat diets were supplemented with NMN and for comparison with a cocktail of lysine/leucine/arginine (mTORC1 [mechanistic target of rapamycin complex 1]-mediated v-ATPase reassembly).
  7. 07AnimalAnimal study (in vivo)Efficacy outcome

    During myocardial lipid overload, NMN prevented cardiac dysfunction.

    In plain wordsIn rats and mice with lipid overload, NMN prevented heart dysfunction.

    Outcome
    DecreaseCardiac dysfunction
    Study

    rats/micen: not reported in source

    High-fat diet-induced cardiomyopathy
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN successfully preserved endosomal acidification during myocardial lipid overload by maintaining v-ATPase activity and subsequently prevented CD36-mediated lipid accumulation, CD36-TLR4 interaction toward inflammation, fibrosis, cardiac dysfunction, and whole-body insulin resistance.
    1 context sentence
    Summary · context
    Rats/mice on cardiomyopathy-inducing high-fat diets were supplemented with NMN and for comparison with a cocktail of lysine/leucine/arginine (mTORC1 [mechanistic target of rapamycin complex 1]-mediated v-ATPase reassembly).
  8. 08AnimalAnimal study (in vivo)Efficacy outcome

    During myocardial lipid overload, NMN prevented whole-body insulin resistance.

    In plain wordsIn rats and mice with lipid overload, NMN prevented whole-body insulin resistance.

    Outcome
    DecreaseWhole-body insulin resistance
    Study

    rats/micen: not reported in source

    High-fat diet-induced cardiomyopathy
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN successfully preserved endosomal acidification during myocardial lipid overload by maintaining v-ATPase activity and subsequently prevented CD36-mediated lipid accumulation, CD36-TLR4 interaction toward inflammation, fibrosis, cardiac dysfunction, and whole-body insulin resistance.
    1 context sentence
    Summary · context
    Rats/mice on cardiomyopathy-inducing high-fat diets were supplemented with NMN and for comparison with a cocktail of lysine/leucine/arginine (mTORC1 [mechanistic target of rapamycin complex 1]-mediated v-ATPase reassembly).

Studies that did not test the peptide alone2

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. 09AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Efficacy outcome

    In high-fat diet models, lysine/leucine/arginine/NMN treatment reversed or prevented increases in C18:1-enriched diacylglycerols.

    In plain wordsIn rats and mice, the grouped supplement treatments reversed or prevented diet-induced increases in C18:1-enriched diacylglycerols.

    Outcome
    DecreaseC18:1-enriched diacylglycerols
    Study

    rats/micen: not reported in source

    High-fat diet-induced cardiomyopathy
    Outcome group
    Lipids · Cardiovascular

    Source sentences

    Summary
    Lipidomics revealed C18:1-enriched diacylglycerols as lipid class prominently increased by high-fat diet and subsequently reversed/preserved by lysine/leucine/arginine/NMN treatment.
    1 context sentence
    Summary · context
    Rats/mice on cardiomyopathy-inducing high-fat diets were supplemented with NMN and for comparison with a cocktail of lysine/leucine/arginine (mTORC1 [mechanistic target of rapamycin complex 1]-mediated v-ATPase reassembly).

    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).

  2. 10AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism

    In inhibitor and heart-specific v-ATPase-knockout studies, results confirmed v-ATPase dependence of the supplements' beneficial actions.

    In plain wordsIn rats and mice, inhibitor and gene deletion studies confirmed v-ATPase involvement in the supplements' benefits.

    Outcome
    Not applicablev-ATPase dependence of beneficial actions
    Study

    rats/micen: not reported in source

    High-fat diet-induced cardiomyopathy
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    Studies with mTORC1/v-ATPase inhibitors and heart-specific v-ATPase-knockout mice further confirmed the pivotal roles of v-ATPase in these beneficial actions.
    1 context sentence
    Summary · context
    Rats/mice on cardiomyopathy-inducing high-fat diets were supplemented with NMN and for comparison with a cocktail of lysine/leucine/arginine (mTORC1 [mechanistic target of rapamycin complex 1]-mediated v-ATPase reassembly).

    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.