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Study · In vitro (cells) · 2016

2 results

Acute Exercise Improves Insulin Clearance and Increases the Expression of Insulin-Degrading Enzyme in the Liver and Skeletal Muscle of Swiss Mice.

Kurauti MA, Freitas-Dias R, Ferreira SM, Vettorazzi JF, Nardelli TR, Araujo HN, Santos GJ, Carneiro EM, Boschero AC, Rezende LF, Costa-Júnior JM

PloS one28 Jul 2016Cited by 27 (Europe PMC)

PMID27467214 (opens in a new tab)PMCIDPMC4965115 (opens in a new tab)DOI10.1371/journal.pone.0160239 (opens in a new tab)PepBankPUB-27467214
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Summary

The effects of exercise on insulin clearance and IDE expression are not yet fully elucidated. Here, we have explored the effect of acute exercise on insulin clearance and IDE expression in lean mice. Male Swiss mice were subjected to a single bout of exercise on a speed/angle controlled treadmill for 3-h at approximately 60-70% of maximum oxygen consumption. As expected, acute exercise reduced glycemia and insulinemia, and increased insulin tolerance. The activity of AMPK-ACC, but not of IR-Akt, pathway was increased in the liver and skeletal muscle of trained mice. In an apparent contrast to the reduced insulinemia, glucose-stimulated insulin secretion was increased in isolated islets of these mice. However, insulin clearance was increased after acute exercise and was accompanied by increased expression of the insulin-degrading enzyme (IDE), in the liver and skeletal muscle. Finally, C2C12, but not HEPG2 cells, incubated at different concentrations of 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) for 3-h, showed increased expression of IDE. In conclusion, acute exercise increases insulin clearance, probably due to an augmentation of IDE expression in the liver and skeletal muscle. The elevated IDE expression, in the skeletal muscle, seems to be mediated by activation of AMPK-ACC pathway, in response to exercise. We believe that the increase in the IDE expression, comprise a safety measure to maintain glycemia at or close to physiological levels, turning physical exercise more effective and safe.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study2

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

  1. 01LabIn vitro (cells)Mechanism

    In C2C12 cells, AICAR incubation increased insulin-degrading enzyme expression.

    In plain wordsIn cells, AICAR increased insulin-degrading enzyme expression in C2C12 cells.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseInsulin-degrading enzyme expression
    Study

    n: not reported in source

    C2C12 cells
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 3-hAs given in this study.

    Source sentences

    Summary
    Finally, C2C12, but not HEPG2 cells, incubated at different concentrations of 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) for 3-h, showed increased expression of IDE.
  2. 02LabIn vitro (cells)Mechanism

    In HEPG2 cells, AICAR incubation did not increase insulin-degrading enzyme expression.

    In plain wordsIn cells, AICAR did not increase insulin-degrading enzyme expression in HEPG2 cells.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeInsulin-degrading enzyme expression
    Study

    n: not reported in source

    HEPG2 cells
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 3-hAs given in this study.

    Source sentences

    Summary
    Finally, C2C12, but not HEPG2 cells, incubated at different concentrations of 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) for 3-h, showed increased expression of IDE.

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Version history

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  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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