A Tbc1d1 ^Ser231Ala-knockin mutation partially impairs AICAR- but not exercise-induced muscle glucose uptake in mice.

Chen Q, Xie B, Zhu S, Rong P, Sheng Y, Ducommun S, Chen L, Quan C, Li M, Sakamoto K, MacKintosh C, Chen S, Wang HY

Diabetologia8 Nov 2016Cited by 39 (Europe PMC)

PMID27826658DOI10.1007/s00125-016-4151-9PepBankPUB-27826658

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 study5

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

Studies that did not test the peptide alone5

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).

01AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism
In mice, muscle-specific AMPK deletion prevented AICAR-induced hypoglycaemia.
In plain wordsIn mice, muscle AMPK deletion prevented the blood sugar reduction seen with AICAR in controls.
Peptide
AICAR (acadesine)
Outcome
DecreaseHypoglycaemia after AMPK deletion
Study
mousen: not reported in source
AMPK deletion or Tbc1d1 Ser231Ala knockin
Comparator
Wild-type mice stimulated with AICAR
Outcome group
Receptor activity and mechanism · Metabolic and weight
Source sentences
Summary
Skeletal muscle-specific deletion of Ampkα1/a2 in mice prevented AICAR-induced hypoglycaemia and muscle glucose uptake.
1 context sentence(design, population, supporting numbers)
Summary · context
Whole-body glucose homeostasis and muscle glucose uptake were assayed in mice bearing a Tbc1d1 ^Ser231Ala-knockin mutation or harbouring skeletal muscle-specific Ampkα1/α2 (also known as Prkaa1/2) double-knockout mutations in response to an AMPK-activating agent, 5-aminoimidazole-4-carboxa…
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).
Report a problemFND-2782665801
02AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism
In mice, muscle-specific AMPK deletion prevented AICAR-induced muscle glucose uptake.
In plain wordsIn mice, muscle AMPK deletion prevented the muscle glucose uptake seen with AICAR in controls.
Peptide
AICAR (acadesine)
Outcome
DecreaseMuscle glucose uptake after AMPK deletion
Study
mousen: not reported in source
AMPK deletion or Tbc1d1 Ser231Ala knockin
Comparator
Wild-type mice stimulated with AICAR
Outcome group
Receptor activity and mechanism · Metabolic and weight
Source sentences
Summary
Skeletal muscle-specific deletion of Ampkα1/a2 in mice prevented AICAR-induced hypoglycaemia and muscle glucose uptake.
1 context sentence(design, population, supporting numbers)
Summary · context
Whole-body glucose homeostasis and muscle glucose uptake were assayed in mice bearing a Tbc1d1 ^Ser231Ala-knockin mutation or harbouring skeletal muscle-specific Ampkα1/α2 (also known as Prkaa1/2) double-knockout mutations in response to an AMPK-activating agent, 5-aminoimidazole-4-carboxa…
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).
Report a problemFND-2782665802
03AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism
In mice, the Tbc1d1 Ser231Ala knockin mutation attenuated AICAR-induced glucose lowering.
In plain wordsIn mice, the Tbc1d1 mutation weakened AICAR's blood sugar reduction compared with controls.
Peptide
AICAR (acadesine)
Outcome
DecreaseGlucose lowering after Tbc1d1 mutation
Study
mousen: not reported in source
AMPK deletion or Tbc1d1 Ser231Ala knockin
Comparator
Wild-type mice stimulated with AICAR
Outcome group
Receptor activity and mechanism · Metabolic and weight
Source sentences
Summary
The Tbc1d1 ^Ser231Ala-knockin mutation also attenuated the glucose-lowering effect of AICAR in mice.
1 context sentence(design, population, supporting numbers)
Summary · context
Whole-body glucose homeostasis and muscle glucose uptake were assayed in mice bearing a Tbc1d1 ^Ser231Ala-knockin mutation or harbouring skeletal muscle-specific Ampkα1/α2 (also known as Prkaa1/2) double-knockout mutations in response to an AMPK-activating agent, 5-aminoimidazole-4-carboxa…
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).
Report a problemFND-2782665803
04LabNot a test of AICAR (acadesine) aloneEx vivo tissueMechanism
In isolated mouse muscle, the Tbc1d1 Ser231Ala knockin mutation reduced glucose uptake during submaximal AICAR stimulation.
In plain wordsIn lab tests, muscle from mutant mice absorbed less glucose than control muscle after submaximal AICAR stimulation.
Peptide
AICAR (acadesine)
Outcome
DecreaseMuscle glucose uptake after Tbc1d1 mutation
Study
mousen: not reported in source
Isolated muscle from Tbc1d1 Ser231Ala knockin mice
Comparator
Wild-type isolated muscle stimulated with AICAR
Outcome group
Receptor activity and mechanism · Metabolic and weight
Source sentences
Summary
Glucose uptake and cell surface GLUT4 content were significantly lower in muscle isolated from the Tbc1d1 ^Ser231Ala-knockin mice upon stimulation with a submaximal dose of AICAR.
1 context sentence(design, population, supporting numbers)
Summary · context
Whole-body glucose homeostasis and muscle glucose uptake were assayed in mice bearing a Tbc1d1 ^Ser231Ala-knockin mutation or harbouring skeletal muscle-specific Ampkα1/α2 (also known as Prkaa1/2) double-knockout mutations in response to an AMPK-activating agent, 5-aminoimidazole-4-carboxa…
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).
Report a problemFND-2782665804
05LabNot a test of AICAR (acadesine) aloneEx vivo tissueMechanism
In isolated mouse muscle, the Tbc1d1 Ser231Ala knockin mutation reduced cell surface GLUT4 during submaximal AICAR stimulation.
In plain wordsIn lab tests, muscle from mutant mice had less surface GLUT4 than control muscle after submaximal AICAR stimulation.
Peptide
AICAR (acadesine)
Outcome
DecreaseCell surface GLUT4 after Tbc1d1 mutation
Study
mousen: not reported in source
Isolated muscle from Tbc1d1 Ser231Ala knockin mice
Comparator
Wild-type isolated muscle stimulated with AICAR
Outcome group
Receptor activity and mechanism · Metabolic and weight
Source sentences
Summary
Glucose uptake and cell surface GLUT4 content were significantly lower in muscle isolated from the Tbc1d1 ^Ser231Ala-knockin mice upon stimulation with a submaximal dose of AICAR.
1 context sentence(design, population, supporting numbers)
Summary · context
Whole-body glucose homeostasis and muscle glucose uptake were assayed in mice bearing a Tbc1d1 ^Ser231Ala-knockin mutation or harbouring skeletal muscle-specific Ampkα1/α2 (also known as Prkaa1/2) double-knockout mutations in response to an AMPK-activating agent, 5-aminoimidazole-4-carboxa…
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).
Report a problemFND-2782665805

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.

Version 2Current
21 Oct 2026, 15:58 UTC
Study results updated
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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