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Study · Not a test of the peptide alone · 2005

2 results

Deficiency of LKB1 in skeletal muscle prevents AMPK activation and glucose uptake during contraction.

Sakamoto K, McCarthy A, Smith D, Green KA, Grahame Hardie D, Ashworth A, Alessi DR

The EMBO journal5 May 2005Cited by 435 (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: Publisher copyright. Results still quote short attributed sentences.

Results from this study2

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

Studies that did not test the peptide alone2

In this study, AICAR (acadesine) 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 AICAR (acadesine).

  1. 01AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism

    In LKB1-lacking mouse muscle, AICAR did not increase AMPKalpha2 activity.

    In plain wordsIn lab tests, AICAR did not increase AMPKalpha2 activity in mouse muscle without LKB1.

    Outcome
    No significant changeAICAR-stimulated AMPKalpha2 activity
    Study

    mousen: not reported in source

    LKB1-deficient skeletal muscle
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    In LKB1-lacking muscle, the basal activity of the AMPKalpha2 isoform was greatly reduced and was not increased by the AMP-mimetic agent, 5-aminoimidazole-4-carboxamide riboside (AICAR), by the antidiabetic drug phenformin, or by muscle contraction.
    1 context sentence
    Summary · context
    We have used mice in which LKB1 is expressed at only approximately 10% of the normal levels in muscle and most other tissues, or that lack LKB1 entirely in skeletal muscle.

    In this study, AICAR (acadesine) 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 AICAR (acadesine).

  2. 02AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism

    In mouse muscle, LKB1 absence inhibited AICAR-stimulated glucose uptake.

    In plain wordsIn mice, loss of LKB1 reduced AICAR-stimulated muscle glucose uptake compared with LKB1-expressing muscle.

    Outcome
    DecreaseAICAR-stimulated glucose uptake
    Study

    mousen: not reported in source

    LKB1-deficient skeletal muscle
    Comparator
    LKB1-expressing muscle
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    Glucose uptake stimulated by AICAR or muscle contraction, but not by insulin, was inhibited in the absence of LKB1.
    1 context sentence
    Summary · context
    We have used mice in which LKB1 is expressed at only approximately 10% of the normal levels in muscle and most other tissues, or that lack LKB1 entirely in skeletal muscle.

    In this study, AICAR (acadesine) 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 AICAR (acadesine).

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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