Skip to content

Study · In vitro (cells) · rat · 2010

17 results

Disruption of AMPKalpha1 signaling prevents AICAR-induced inhibition of AS160/TBC1D4 phosphorylation and glucose uptake in primary rat adipocytes.

Gaidhu MP, Perry RL, Noor F, Ceddia RB

Molecular endocrinology (Baltimore, Md.)25 May 2010Cited by 23 (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 study17

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

  1. 01LabIn vitro (cells)Mechanism

    In primary rat adipocytes, AICAR increased AMPK activation.

    In plain wordsIn cells from rats, AICAR increased AMPK activation.

    Outcome
    IncreaseAMPK activation
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 1 hAs given in this study (rat).

    Source sentences

    Summary
    AICAR increased AMPK activation without affecting basal and insulin-stimulated Akt1/2 phosphorylation on Thr(308) and Ser(473) residues.
    1 context sentence
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.
  2. 02LabIn vitro (cells)Mechanism

    In primary rat adipocytes, AICAR did not affect basal Akt1/2 phosphorylation at Thr(308).

    In plain wordsIn cells from rats, AICAR did not affect basal Akt1/2 phosphorylation at Thr(308).

    Outcome
    No significant changeBasal Akt1/2 Thr(308) phosphorylation
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 1 hAs given in this study (rat).

    Source sentences

    Summary
    AICAR increased AMPK activation without affecting basal and insulin-stimulated Akt1/2 phosphorylation on Thr(308) and Ser(473) residues.
    1 context sentence
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.
  3. 03LabIn vitro (cells)Mechanism

    In primary rat adipocytes, AICAR did not affect insulin-stimulated Akt1/2 phosphorylation at Thr(308).

    In plain wordsIn cells from rats, AICAR did not affect insulin-stimulated Akt1/2 phosphorylation at Thr(308).

    Outcome
    No significant changeInsulin-stimulated Akt1/2 Thr(308) phosphorylation
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 1 hAs given in this study (rat).

    Source sentences

    Summary
    AICAR increased AMPK activation without affecting basal and insulin-stimulated Akt1/2 phosphorylation on Thr(308) and Ser(473) residues.
    1 context sentence
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.
  4. 04LabIn vitro (cells)Mechanism

    In primary rat adipocytes, AICAR did not affect basal Akt1/2 phosphorylation at Ser(473).

    In plain wordsIn cells from rats, AICAR did not affect basal Akt1/2 phosphorylation at Ser(473).

    Outcome
    No significant changeBasal Akt1/2 Ser(473) phosphorylation
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 1 hAs given in this study (rat).

    Source sentences

    Summary
    AICAR increased AMPK activation without affecting basal and insulin-stimulated Akt1/2 phosphorylation on Thr(308) and Ser(473) residues.
    1 context sentence
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.
  5. 05LabIn vitro (cells)Mechanism

    In primary rat adipocytes, AICAR did not affect insulin-stimulated Akt1/2 phosphorylation at Ser(473).

    In plain wordsIn cells from rats, AICAR did not affect insulin-stimulated Akt1/2 phosphorylation at Ser(473).

    Outcome
    No significant changeInsulin-stimulated Akt1/2 Ser(473) phosphorylation
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 1 hAs given in this study (rat).

    Source sentences

    Summary
    AICAR increased AMPK activation without affecting basal and insulin-stimulated Akt1/2 phosphorylation on Thr(308) and Ser(473) residues.
    1 context sentence
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.
  6. 06LabIn vitro (cells)Mechanism

    In primary rat adipocytes, AMPK activation by AICAR suppressed AS160/TBC1D4 phosphorylation.

    In plain wordsIn cells from rats, AMPK activation by AICAR reduced AS160/TBC1D4 phosphorylation.

    Outcome
    DecreaseAS160/TBC1D4 phosphorylation
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 1 hAs given in this study (rat).

    Source sentences

    Summary
    However, AMPK activation suppressed the phosphorylation of AS160/TBC1D4 and its interaction with the 14-3-3 signal transduction-regulatory protein,
    2 context sentences
    Summary · context
    AICAR increased AMPK activation without affecting basal and insulin-stimulated Akt1/2 phosphorylation on Thr(308) and Ser(473) residues.
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.
  7. 07LabIn vitro (cells)Mechanism

    In primary rat adipocytes, AMPK activation by AICAR suppressed AS160/TBC1D4 interaction with the 14-3-3 protein.

    In plain wordsIn cells from rats, AMPK activation by AICAR reduced AS160/TBC1D4 interaction with the 14-3-3 protein.

    Outcome
    DecreaseAS160 interaction with 14-3-3 protein
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 1 hAs given in this study (rat).

    Source sentences

    Summary
    However, AMPK activation suppressed the phosphorylation of AS160/TBC1D4 and its interaction with the 14-3-3 signal transduction-regulatory protein,
    2 context sentences
    Summary · context
    AICAR increased AMPK activation without affecting basal and insulin-stimulated Akt1/2 phosphorylation on Thr(308) and Ser(473) residues.
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.
  8. 08LabIn vitro (cells)Mechanism

    In primary rat adipocytes, AMPK activation by AICAR reduced basal plasma membrane glucose transporter 4 content.

    In plain wordsIn cells from rats, AMPK activation by AICAR reduced basal glucose transporter 4 content at the cell surface.

    Outcome
    DecreaseBasal membrane GLUT4 content
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 1 hAs given in this study (rat).

    Source sentences

    Summary
    which was accompanied by significant reductions in plasma membrane glucose transporter 4 content and glucose uptake under basal and insulin-stimulated conditions.
    2 context sentences
    Summary · context
    AICAR increased AMPK activation without affecting basal and insulin-stimulated Akt1/2 phosphorylation on Thr(308) and Ser(473) residues.
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.
  9. 09LabIn vitro (cells)Mechanism

    In primary rat adipocytes, AMPK activation by AICAR reduced insulin-stimulated plasma membrane glucose transporter 4 content.

    In plain wordsIn cells from rats, AMPK activation by AICAR reduced insulin-stimulated glucose transporter 4 content at the cell surface.

    Outcome
    DecreaseInsulin-stimulated membrane GLUT4 content
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 1 hAs given in this study (rat).

    Source sentences

    Summary
    which was accompanied by significant reductions in plasma membrane glucose transporter 4 content and glucose uptake under basal and insulin-stimulated conditions.
    2 context sentences
    Summary · context
    AICAR increased AMPK activation without affecting basal and insulin-stimulated Akt1/2 phosphorylation on Thr(308) and Ser(473) residues.
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.
  10. 10LabIn vitro (cells)Mechanism

    In primary rat adipocytes, AMPK activation by AICAR reduced basal glucose uptake.

    In plain wordsIn cells from rats, AMPK activation by AICAR reduced basal glucose uptake.

    Outcome
    DecreaseBasal glucose uptake
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 1 hAs given in this study (rat).

    Source sentences

    Summary
    which was accompanied by significant reductions in plasma membrane glucose transporter 4 content and glucose uptake under basal and insulin-stimulated conditions.
    2 context sentences
    Summary · context
    AICAR increased AMPK activation without affecting basal and insulin-stimulated Akt1/2 phosphorylation on Thr(308) and Ser(473) residues.
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.
  11. 11LabIn vitro (cells)Mechanism

    In primary rat adipocytes, AMPK activation by AICAR reduced insulin-stimulated glucose uptake.

    In plain wordsIn cells from rats, AMPK activation by AICAR reduced insulin-stimulated glucose uptake.

    Outcome
    DecreaseInsulin-stimulated glucose uptake
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 1 hAs given in this study (rat).

    Source sentences

    Summary
    which was accompanied by significant reductions in plasma membrane glucose transporter 4 content and glucose uptake under basal and insulin-stimulated conditions.
    2 context sentences
    Summary · context
    AICAR increased AMPK activation without affecting basal and insulin-stimulated Akt1/2 phosphorylation on Thr(308) and Ser(473) residues.
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.
  12. 12LabIn vitro (cells)Mechanism

    In primary rat adipocytes, AICAR did not alter glycogen synthase kinase 3alpha phosphorylation.

    In plain wordsIn cells from rats, AICAR did not change glycogen synthase kinase 3alpha phosphorylation.

    Outcome
    No significant changeGlycogen synthase kinase 3alpha phosphorylation
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 1 hAs given in this study (rat).

    Source sentences

    Summary
    Phosphorylation of Akt substrates glycogen synthase kinase 3alpha and -beta were unaltered by AICAR, indicating that the AMPK-regulatory effects were specific to the AS160/TBC1D4 signaling pathway.
    1 context sentence
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.
  13. 13LabIn vitro (cells)Mechanism

    In primary rat adipocytes, AICAR did not alter glycogen synthase kinase 3beta phosphorylation.

    In plain wordsIn cells from rats, AICAR did not change glycogen synthase kinase 3beta phosphorylation.

    Outcome
    No significant changeGlycogen synthase kinase 3beta phosphorylation
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated · 1 hAs given in this study (rat).

    Source sentences

    Summary
    Phosphorylation of Akt substrates glycogen synthase kinase 3alpha and -beta were unaltered by AICAR, indicating that the AMPK-regulatory effects were specific to the AS160/TBC1D4 signaling pathway.
    1 context sentence
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.

Studies that did not test the peptide alone4

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. 14LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In primary rat adipocytes, kinase-dead AMPKalpha1 expression prevented the suppression of AS160/TBC1D4 phosphorylation induced by AICAR.

    In plain wordsIn cells from rats, a kinase-dead AMPKalpha1 mutant prevented the decrease in AS160/TBC1D4 phosphorylation induced by AICAR.

    Outcome
    IncreaseMutant prevention of AS160 phosphorylation suppression
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight

    Source sentences

    Summary
    Expression of the kinase-dead AMPKalpha1 mutant fully prevented the suppression of AS160/TBC1D4 phosphorylation, plasma membrane glucose transporter 4 content, and the inhibitory effect of AICAR-induced AMPK activation on basal and insulin-stimulated glucose uptake.
    1 context sentence
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.

    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. 15LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In primary rat adipocytes, kinase-dead AMPKalpha1 expression prevented the suppression of plasma membrane GLUT4 content induced by AICAR.

    In plain wordsIn cells from rats, a kinase-dead AMPKalpha1 mutant prevented the decrease in cell-surface GLUT4 induced by AICAR.

    Outcome
    IncreaseMutant prevention of membrane GLUT4 suppression
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight

    Source sentences

    Summary
    Expression of the kinase-dead AMPKalpha1 mutant fully prevented the suppression of AS160/TBC1D4 phosphorylation, plasma membrane glucose transporter 4 content, and the inhibitory effect of AICAR-induced AMPK activation on basal and insulin-stimulated glucose uptake.
    1 context sentence
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.

    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).

  3. 16LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In primary rat adipocytes, kinase-dead AMPKalpha1 expression prevented the inhibition of basal glucose uptake induced by AICAR.

    In plain wordsIn cells from rats, a kinase-dead AMPKalpha1 mutant prevented the inhibition of basal glucose uptake induced by AICAR.

    Outcome
    IncreaseMutant prevention of basal glucose uptake inhibition
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight

    Source sentences

    Summary
    Expression of the kinase-dead AMPKalpha1 mutant fully prevented the suppression of AS160/TBC1D4 phosphorylation, plasma membrane glucose transporter 4 content, and the inhibitory effect of AICAR-induced AMPK activation on basal and insulin-stimulated glucose uptake.
    1 context sentence
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.

    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).

  4. 17LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In primary rat adipocytes, kinase-dead AMPKalpha1 expression prevented the inhibition of insulin-stimulated glucose uptake induced by AICAR.

    In plain wordsIn cells from rats, a kinase-dead AMPKalpha1 mutant prevented the inhibition of insulin-stimulated glucose uptake induced by AICAR.

    Outcome
    IncreaseMutant prevention of insulin-stimulated uptake inhibition
    Study

    ratn: not reported in source

    Primary epididymal adipocytes
    Outcome group
    Receptor activity and mechanism · Metabolic and weight

    Source sentences

    Summary
    Expression of the kinase-dead AMPKalpha1 mutant fully prevented the suppression of AS160/TBC1D4 phosphorylation, plasma membrane glucose transporter 4 content, and the inhibitory effect of AICAR-induced AMPK activation on basal and insulin-stimulated glucose uptake.
    1 context sentence
    Summary · context
    Rat epididymal adipocytes were exposed to 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) for 1 h.

    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.

PepBank is a research reference. Talk to a doctor before you use any peptide.