Exenatide inhibits beta-cell apoptosis by decreasing thioredoxin-interacting protein.

Chen J, Couto FM, Minn AH, Shalev A

Biochemical and biophysical research communications13 Jun 2006Cited by 81 (Europe PMC)

PMID16782054DOI10.1016/j.bbrc.2006.06.027PepBankPUB-16782054

Publisher page PubMedAsk about this study

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 study11

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

01AnimalAnimal study (in vivo)Mechanism
In wild-type mice receiving exenatide, TXNIP expression decreased.
In plain wordsIn mice, exenatide reduced TXNIP expression.
Peptide
Exenatide (exendin-4)
Outcome
DecreaseTXNIP expression
Study
Mousen: not reported in source
Wild-type mice
Outcome group
Receptor activity and mechanism · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
This reduction was observed in INS-1 cells, mouse, and human islets as well as in wild-type mice receiving Ex-4 and was accompanied by decreased expression of the apoptotic factors caspase-3 and Bax.
1 context sentence(design, population, supporting numbers)
Summary · context
We found that Ex-4 protects INS-1 beta-cells against oxidative stress-induced apoptosis (TUNEL) and also reduces expression (mRNA and protein) of thioredoxin-interacting protein (TXNIP), a pro-apoptotic factor involved in beta-cell glucose toxicity and oxidative stress.
Report a problemFND-1678205406
02AnimalAnimal study (in vivo)Mechanism
In wild-type mice receiving exenatide, TXNIP reduction accompanied decreased caspase-3 expression.
In plain wordsIn mice receiving exenatide, lower TXNIP accompanied lower expression of the cell-death factor caspase-3.
Peptide
Exenatide (exendin-4)
Outcome
DecreaseCaspase-3 expression
Study
Mousen: not reported in source
Wild-type mice
Outcome group
Receptor activity and mechanism · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
This reduction was observed in INS-1 cells, mouse, and human islets as well as in wild-type mice receiving Ex-4 and was accompanied by decreased expression of the apoptotic factors caspase-3 and Bax.
Report a problemFND-1678205408
03AnimalAnimal study (in vivo)Mechanism
In wild-type mice receiving exenatide, TXNIP reduction accompanied decreased Bax expression.
In plain wordsIn mice receiving exenatide, lower TXNIP accompanied lower expression of the cell-death factor Bax.
Peptide
Exenatide (exendin-4)
Outcome
DecreaseBax expression
Study
Mousen: not reported in source
Wild-type mice
Outcome group
Receptor activity and mechanism · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
This reduction was observed in INS-1 cells, mouse, and human islets as well as in wild-type mice receiving Ex-4 and was accompanied by decreased expression of the apoptotic factors caspase-3 and Bax.
Report a problemFND-1678205410
04LabEx vivo tissueMechanism
In mouse islets, exenatide reduced TXNIP expression.
In plain wordsIn lab tests with mouse islets, exenatide reduced TXNIP expression.
Peptide
Exenatide (exendin-4)
Outcome
DecreaseTXNIP expression
Study
Mousen: not reported in source
Mouse islets
Outcome group
Receptor activity and mechanism · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
This reduction was observed in INS-1 cells, mouse, and human islets as well as in wild-type mice receiving Ex-4 and was accompanied by decreased expression of the apoptotic factors caspase-3 and Bax.
1 context sentence(design, population, supporting numbers)
Summary · context
We found that Ex-4 protects INS-1 beta-cells against oxidative stress-induced apoptosis (TUNEL) and also reduces expression (mRNA and protein) of thioredoxin-interacting protein (TXNIP), a pro-apoptotic factor involved in beta-cell glucose toxicity and oxidative stress.
Report a problemFND-1678205404
05LabEx vivo tissueMechanism
In human islets, exenatide reduced TXNIP expression.
In plain wordsIn lab tests with human islets, exenatide reduced TXNIP expression.
Peptide
Exenatide (exendin-4)
Outcome
DecreaseTXNIP expression
Study
Humann: not reported in source
Human islets
Outcome group
Receptor activity and mechanism · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
This reduction was observed in INS-1 cells, mouse, and human islets as well as in wild-type mice receiving Ex-4 and was accompanied by decreased expression of the apoptotic factors caspase-3 and Bax.
1 context sentence(design, population, supporting numbers)
Summary · context
We found that Ex-4 protects INS-1 beta-cells against oxidative stress-induced apoptosis (TUNEL) and also reduces expression (mRNA and protein) of thioredoxin-interacting protein (TXNIP), a pro-apoptotic factor involved in beta-cell glucose toxicity and oxidative stress.
Report a problemFND-1678205405
06LabIn vitro (cells)Mechanism
In INS-1 beta-cells, exenatide protected against oxidative stress-induced apoptosis.
In plain wordsIn cells, exenatide reduced cell death caused by oxidative stress.
Peptide
Exenatide (exendin-4)
Outcome
DecreaseOxidative stress-induced apoptosis
Study
n: not reported in source
INS-1 beta-cells
Outcome group
Receptor activity and mechanism · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
We found that Ex-4 protects INS-1 beta-cells against oxidative stress-induced apoptosis (TUNEL) and also reduces expression (mRNA and protein) of thioredoxin-interacting protein (TXNIP), a pro-apoptotic factor involved in beta-cell glucose toxicity and oxidative stress.
Report a problemFND-1678205401
07LabIn vitro (cells)Mechanism
In INS-1 beta-cells, exenatide reduced TXNIP mRNA expression.
In plain wordsIn cells, exenatide reduced expression of the TXNIP gene.
Peptide
Exenatide (exendin-4)
Outcome
DecreaseTXNIP mRNA expression
Study
n: not reported in source
INS-1 beta-cells
Outcome group
Receptor activity and mechanism · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
We found that Ex-4 protects INS-1 beta-cells against oxidative stress-induced apoptosis (TUNEL) and also reduces expression (mRNA and protein) of thioredoxin-interacting protein (TXNIP), a pro-apoptotic factor involved in beta-cell glucose toxicity and oxidative stress.
Report a problemFND-1678205402
08LabIn vitro (cells)Mechanism
In INS-1 beta-cells, exenatide reduced TXNIP protein expression.
In plain wordsIn cells, exenatide reduced TXNIP protein levels.
Peptide
Exenatide (exendin-4)
Outcome
DecreaseTXNIP protein expression
Study
n: not reported in source
INS-1 beta-cells
Outcome group
Receptor activity and mechanism · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
We found that Ex-4 protects INS-1 beta-cells against oxidative stress-induced apoptosis (TUNEL) and also reduces expression (mRNA and protein) of thioredoxin-interacting protein (TXNIP), a pro-apoptotic factor involved in beta-cell glucose toxicity and oxidative stress.
Report a problemFND-1678205403
09LabOther designMechanism
In the reported cellular and islet models, exenatide-associated TXNIP reduction accompanied decreased caspase-3 expression.
In plain wordsIn lab tests, lower TXNIP during exenatide treatment accompanied lower expression of caspase-3, a cell-death factor.
Peptide
Exenatide (exendin-4)
Outcome
DecreaseCaspase-3 expression
Study
n: not reported in source
INS-1 cells and mouse and human islets
Outcome group
Receptor activity and mechanism · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
This reduction was observed in INS-1 cells, mouse, and human islets as well as in wild-type mice receiving Ex-4 and was accompanied by decreased expression of the apoptotic factors caspase-3 and Bax.
Report a problemFND-1678205407
10LabOther designMechanism
In the reported cellular and islet models, exenatide-associated TXNIP reduction accompanied decreased Bax expression.
In plain wordsIn lab tests, lower TXNIP during exenatide treatment accompanied lower expression of Bax, a cell-death factor.
Peptide
Exenatide (exendin-4)
Outcome
DecreaseBax expression
Study
n: not reported in source
INS-1 cells and mouse and human islets
Outcome group
Receptor activity and mechanism · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
This reduction was observed in INS-1 cells, mouse, and human islets as well as in wild-type mice receiving Ex-4 and was accompanied by decreased expression of the apoptotic factors caspase-3 and Bax.
Report a problemFND-1678205409

Studies that did not test the peptide alone1

In this study, Exenatide (exendin-4) 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 Exenatide (exendin-4).

11LabNot a test of Exenatide (exendin-4) aloneIn vitro (cells)Mechanism
In INS-1 cells, stable TXNIP overexpression completely blunted the anti-apoptotic effect of exenatide.
In plain wordsIn cells, extra TXNIP gene expression blocked exenatide's protection against cell death.
Peptide
Exenatide (exendin-4)
Outcome
DecreaseTXNIP overexpression and anti-apoptotic effect
Study
n: not reported in source
INS-1 beta-cells
Outcome group
Receptor activity and mechanism · Metabolic and weight
Source sentences
Summary
To determine whether Ex-4-mediated TXNIP reduction is critical for this inhibition of apoptosis, we stably overexpressed TXNIP in INS-1 cells, which completely blunted the anti-apoptotic Ex-4 effects.
In this study, Exenatide (exendin-4) 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 Exenatide (exendin-4).
Report a problemFND-1678205411

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
22 Oct 2026, 02:26 UTC
Study results updated
Version 1
21 Oct 2026, 18:59 UTC
First added · source update from Europe PMC

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