GlutaredoxinV1, Main, Exploration, bibRecord, 000375

Differential expression of islet glutaredoxin 1 and 5 with high reactive oxygen species production in a mouse model of diabesity.

Identifieur interne : 000375 ( Main/Exploration ); précédent : 000374; suivant : 000376

Differential expression of islet glutaredoxin 1 and 5 with high reactive oxygen species production in a mouse model of diabesity.

Auteurs : Sebastian Friedrich Petry [Allemagne] ; Fatemeh Sharifpanah [Allemagne] ; Heinrich Sauer [Allemagne] ; Thomas Linn [Allemagne]

Source :

PloS one [ 1932-6203 ] ; 2017.

RBID : pubmed:28542222

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Blood Glucose (MeSH), Body Weight (MeSH), Cell Proliferation (physiology), Diabetes Mellitus, Experimental (metabolism), Diabetes Mellitus, Experimental (pathology), Diabetes Mellitus, Type 2 (metabolism), Diabetes Mellitus, Type 2 (pathology), Fasting (MeSH), Gene Expression Profiling (MeSH), Glutaredoxins (metabolism), Immunohistochemistry (MeSH), Insulin (metabolism), Islets of Langerhans (metabolism), Islets of Langerhans (pathology), Male (MeSH), Mice (MeSH), RNA, Messenger (MeSH), Reactive Oxygen Species (metabolism), Real-Time Polymerase Chain Reaction (MeSH).
MESH :
- chemical , metabolism : Glutaredoxins, Insulin, Reactive Oxygen Species.
- chemical : Blood Glucose, RNA, Messenger.
- metabolism : Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 2, Islets of Langerhans.
- pathology : Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 2, Islets of Langerhans.
- physiology : Cell Proliferation.
- Animals, Body Weight, Fasting, Gene Expression Profiling, Immunohistochemistry, Male, Mice, Real-Time Polymerase Chain Reaction.

Abstract

The onset and progression of diabetes mellitus type 2 is highly contingent on the amount of functional beta-cell mass. An underlying cause of beta-cell decay in diabetes is oxidative stress, which markedly affects the insulin producing pancreatic cells due to their poor antioxidant defence capacity. Consequently, disturbances of cellular redox signaling have been implicated to play a major role in beta-cell loss in diabetes mellitus type 2. There is evidence suggesting that the glutaredoxin (Grx) system exerts a protective role for pancreatic islets, but the exact mechanisms have not yet been elucidated. In this study, a mouse model for diabetes mellitus type 2 was used to gain further insight into the significance of Grx for the islets of Langerhans in the diabetic metabolism. We have observed distinct differences in the expression levels of Grx in pancreatic islets between obese, diabetic db mice and lean, non-diabetic controls. This finding is the first report about a decrease of Grx expression levels in pancreatic islets of diabetic mice which was accompanied by declining insulin secretion, increase of reactive oxygen species (ROS) production level, and cell cycle alterations. These data demonstrate the essential role of the Grx system for the beta-cell during metabolic stress which may provide a new target for diabetes mellitus type 2 treatment.

DOI: 10.1371/journal.pone.0176267
PubMed: 28542222
PubMed Central: PMC5443478

Affiliations:

Allemagne

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000340
to stream Main, to step Curation: 000340

Le document en format XML

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<term>Diabetes Mellitus, Experimental (metabolism)</term>
<term>Diabetes Mellitus, Experimental (pathology)</term>
<term>Diabetes Mellitus, Type 2 (metabolism)</term>
<term>Diabetes Mellitus, Type 2 (pathology)</term>
<term>Fasting (MeSH)</term>
<term>Gene Expression Profiling (MeSH)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Immunohistochemistry (MeSH)</term>
<term>Insulin (metabolism)</term>
<term>Islets of Langerhans (metabolism)</term>
<term>Islets of Langerhans (pathology)</term>
<term>Male (MeSH)</term>
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<term>Diabète de type 2 (métabolisme)</term>
<term>Diabète expérimental (anatomopathologie)</term>
<term>Diabète expérimental (métabolisme)</term>
<term>Espèces réactives de l'oxygène (métabolisme)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Glycémie (MeSH)</term>
<term>Ilots pancréatiques (anatomopathologie)</term>
<term>Ilots pancréatiques (métabolisme)</term>
<term>Immunohistochimie (MeSH)</term>
<term>Insuline (métabolisme)</term>
<term>Jeûne (MeSH)</term>
<term>Mâle (MeSH)</term>
<term>Poids (MeSH)</term>
<term>Prolifération cellulaire (physiologie)</term>
<term>Réaction de polymérisation en chaine en temps réel (MeSH)</term>
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<term>Reactive Oxygen Species</term>
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<term>Diabetes Mellitus, Type 2</term>
<term>Islets of Langerhans</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Diabète de type 2</term>
<term>Diabète expérimental</term>
<term>Espèces réactives de l'oxygène</term>
<term>Glutarédoxines</term>
<term>Ilots pancréatiques</term>
<term>Insuline</term>
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<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Diabetes Mellitus, Experimental</term>
<term>Diabetes Mellitus, Type 2</term>
<term>Islets of Langerhans</term>
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<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Prolifération cellulaire</term>
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<term>Body Weight</term>
<term>Fasting</term>
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<term>Real-Time Polymerase Chain Reaction</term>
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<term>Immunohistochimie</term>
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<front><div type="abstract" xml:lang="en">The onset and progression of diabetes mellitus type 2 is highly contingent on the amount of functional beta-cell mass. An underlying cause of beta-cell decay in diabetes is oxidative stress, which markedly affects the insulin producing pancreatic cells due to their poor antioxidant defence capacity. Consequently, disturbances of cellular redox signaling have been implicated to play a major role in beta-cell loss in diabetes mellitus type 2. There is evidence suggesting that the glutaredoxin (Grx) system exerts a protective role for pancreatic islets, but the exact mechanisms have not yet been elucidated. In this study, a mouse model for diabetes mellitus type 2 was used to gain further insight into the significance of Grx for the islets of Langerhans in the diabetic metabolism. We have observed distinct differences in the expression levels of Grx in pancreatic islets between obese, diabetic db mice and lean, non-diabetic controls. This finding is the first report about a decrease of Grx expression levels in pancreatic islets of diabetic mice which was accompanied by declining insulin secretion, increase of reactive oxygen species (ROS) production level, and cell cycle alterations. These data demonstrate the essential role of the Grx system for the beta-cell during metabolic stress which may provide a new target for diabetes mellitus type 2 treatment.</div>
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Differential expression of islet glutaredoxin 1 and 5 with high reactive oxygen species production in a mouse model of diabesity.

Differential expression of islet glutaredoxin 1 and 5 with high reactive oxygen species production in a mouse model of diabesity.

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