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Study · Animal study (in vivo) · mouse · 2023

4 results

Adenosine monophosphate-activated protein kinase is elevated in human cachectic muscle and prevents cancer-induced metabolic dysfunction in mice.

Raun SH, Ali MS, Han X, Henríquez-Olguín C, Pham TCP, Meneses-Valdés R, Knudsen JR, Willemsen ACH, Larsen S, Jensen TE, Langen R, Sylow L

Journal of cachexia, sarcopenia and muscle16 May 2023Cited by 29 (Europe PMC)

PMID37194385 (opens in a new tab)PMCIDPMC10401533 (opens in a new tab)DOI10.1002/jcsm.13238 (opens in a new tab)PepBankPUB-37194385
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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. Results still quote short attributed sentences.

Results from this study4

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In tumour-bearing mice, chronic AICAR elevated hexokinase II protein content compared with no AICAR.

    In plain wordsIn mice with tumours, AICAR increased hexokinase II protein compared with no AICAR.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseHexokinase II protein content
    Study

    mousen = 19

    male Lewis lung carcinoma-bearing mice
    Comparator
    tumour-bearing mice without AICAR
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 13 daysAs given in this study (mouse).

    Source sentences

    Summary
    Lastly, chronic AICAR treatment elevated hexokinase II protein content and normalized phosphorylation of p70S6Kthr389 (mTORC1 substrate) and ACCser212 (AMPK substrate) and rescued cancer-induced insulin intolerance.
    1 context sentence
    Summary · context
    Moreover, male LLC-tumour-bearing mice were treated with (n = 10)/without (n = 9) 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) to activate AMPK for 13 days.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In tumour-bearing mice, chronic AICAR normalized p70S6K thr389 phosphorylation compared with no AICAR.

    In plain wordsIn mice with tumours, AICAR normalized p70S6K phosphorylation compared with no AICAR.

    Peptide
    AICAR (acadesine)
    Outcome
    Direction not reportedp70S6K thr389 phosphorylation
    Study

    mousen = 19

    male Lewis lung carcinoma-bearing mice
    Comparator
    tumour-bearing mice without AICAR
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 13 daysAs given in this study (mouse).

    Source sentences

    Summary
    Lastly, chronic AICAR treatment elevated hexokinase II protein content and normalized phosphorylation of p70S6Kthr389 (mTORC1 substrate) and ACCser212 (AMPK substrate) and rescued cancer-induced insulin intolerance.
    1 context sentence
    Summary · context
    Moreover, male LLC-tumour-bearing mice were treated with (n = 10)/without (n = 9) 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) to activate AMPK for 13 days.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In tumour-bearing mice, chronic AICAR normalized ACC ser212 phosphorylation compared with no AICAR.

    In plain wordsIn mice with tumours, AICAR normalized ACC phosphorylation compared with no AICAR.

    Peptide
    AICAR (acadesine)
    Outcome
    Direction not reportedACC ser212 phosphorylation
    Study

    mousen = 19

    male Lewis lung carcinoma-bearing mice
    Comparator
    tumour-bearing mice without AICAR
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 13 daysAs given in this study (mouse).

    Source sentences

    Summary
    Lastly, chronic AICAR treatment elevated hexokinase II protein content and normalized phosphorylation of p70S6Kthr389 (mTORC1 substrate) and ACCser212 (AMPK substrate) and rescued cancer-induced insulin intolerance.
    1 context sentence
    Summary · context
    Moreover, male LLC-tumour-bearing mice were treated with (n = 10)/without (n = 9) 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) to activate AMPK for 13 days.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In tumour-bearing mice, chronic AICAR rescued cancer-induced insulin intolerance compared with no AICAR.

    In plain wordsIn mice with tumours, AICAR reversed cancer-induced insulin intolerance compared with no AICAR.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseInsulin intolerance
    Study

    mousen = 19

    male Lewis lung carcinoma-bearing mice
    Comparator
    tumour-bearing mice without AICAR
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated · 13 daysAs given in this study (mouse).

    Source sentences

    Summary
    Lastly, chronic AICAR treatment elevated hexokinase II protein content and normalized phosphorylation of p70S6Kthr389 (mTORC1 substrate) and ACCser212 (AMPK substrate) and rescued cancer-induced insulin intolerance.
    1 context sentence
    Summary · context
    Moreover, male LLC-tumour-bearing mice were treated with (n = 10)/without (n = 9) 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) to activate AMPK for 13 days.

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.

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