ROS signaling, oxidative stress and Nrf2 in pancreatic beta-cell function
This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H 2O 2, act as metabolic signaling molecules for glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells. Particular emphasis is placed on the potential inhibitory ro...
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| Published in | Toxicology and applied pharmacology Vol. 244; no. 1; pp. 77 - 83 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.04.2010
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| Subjects | |
| Online Access | Get full text |
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| Abstract | This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H
2O
2, act as metabolic signaling molecules for glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells. Particular emphasis is placed on the potential inhibitory role of endogenous antioxidants, which rise in response to oxidative stress, in glucose-triggered ROS and GSIS. We propose that cellular adaptive response to oxidative stress challenge, such as nuclear factor E2-related factor 2 (Nrf2)-mediated antioxidant induction, plays paradoxical roles in pancreatic beta-cell function. On the one hand, induction of antioxidant enzymes protects beta-cells from oxidative damage and possible cell death, thus minimizing oxidative damage-related impairment of insulin secretion. On the other hand, the induction of antioxidant enzymes by Nrf2 activation blunts glucose-triggered ROS signaling, thus resulting in reduced GSIS. These two premises are potentially relevant to impairment of beta-cells occurring in the late and early stage of Type 2 diabetes, respectively. In addition, we summarized our recent findings that persistent oxidative stress due to absence of uncoupling protein 2 activates cellular adaptive response which is associated with impaired pancreatic beta-cell function. |
|---|---|
| AbstractList | This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H
2
O
2
, act as metabolic signaling molecules for glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells. Particular emphasis is placed on the potential inhibitory role of endogenous antioxidants, which rise in response to oxidative stress, in glucose-triggered ROS and GSIS. We propose that cellular adaptive response to oxidative stress challenge, such as nuclear factor E2-related factor 2 (Nrf2)-mediated antioxidant induction, plays paradoxical roles in pancreatic beta-cell function. On the one hand, induction of antioxidant enzymes protects beta-cells from oxidative damage and possible cell death, thus minimizing oxidative damage-related impairment of insulin secretion. On the other hand, the induction of antioxidant enzymes by Nrf2 activation blunts glucose-triggered ROS signaling, thus resulting in reduced GSIS. These two premises are potentially relevant to impairment of beta-cells occurring in the late and early stage of Type 2 diabetes, respectively. In addition, we summarized our recent findings that persistent oxidative stress due to absence of uncoupling protein 2 activates cellular adaptive response which is associated with impaired pancreatic beta-cell function. This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H2O2, act as metabolic signaling molecules for glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells. Particular emphasis is placed on the potential inhibitory role of endogenous antioxidants, which rise in response to oxidative stress, in glucose-triggered ROS and GSIS. We propose that cellular adaptive response to oxidative stress challenge, such as nuclear factor E2-related factor 2 (Nrf2)-mediated antioxidant induction, plays paradoxical roles in pancreatic beta-cell function. On the one hand, induction of antioxidant enzymes protects beta-cells from oxidative damage and possible cell death, thus minimizing oxidative damage-related impairment of insulin secretion. On the other hand, the induction of antioxidant enzymes by Nrf2 activation blunts glucose-triggered ROS signaling, thus resulting in reduced GSIS. These two premises are potentially relevant to impairment of beta-cells occurring in the late and early stage of Type 2 diabetes, respectively. In addition, we summarized our recent findings that persistent oxidative stress due to absence of uncoupling protein 2 activates cellular adaptive response which is associated with impaired pancreatic beta-cell function. This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H 2O 2, act as metabolic signaling molecules for glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells. Particular emphasis is placed on the potential inhibitory role of endogenous antioxidants, which rise in response to oxidative stress, in glucose-triggered ROS and GSIS. We propose that cellular adaptive response to oxidative stress challenge, such as nuclear factor E2-related factor 2 (Nrf2)-mediated antioxidant induction, plays paradoxical roles in pancreatic beta-cell function. On the one hand, induction of antioxidant enzymes protects beta-cells from oxidative damage and possible cell death, thus minimizing oxidative damage-related impairment of insulin secretion. On the other hand, the induction of antioxidant enzymes by Nrf2 activation blunts glucose-triggered ROS signaling, thus resulting in reduced GSIS. These two premises are potentially relevant to impairment of beta-cells occurring in the late and early stage of Type 2 diabetes, respectively. In addition, we summarized our recent findings that persistent oxidative stress due to absence of uncoupling protein 2 activates cellular adaptive response which is associated with impaired pancreatic beta-cell function. This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H(2)O(2), act as metabolic signaling molecules for glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells. Particular emphasis is placed on the potential inhibitory role of endogenous antioxidants, which rise in response to oxidative stress, in glucose-triggered ROS and GSIS. We propose that cellular adaptive response to oxidative stress challenge, such as nuclear factor E2-related factor 2 (Nrf2)-mediated antioxidant induction, plays paradoxical roles in pancreatic beta-cell function. On the one hand, induction of antioxidant enzymes protects beta-cells from oxidative damage and possible cell death, thus minimizing oxidative damage-related impairment of insulin secretion. On the other hand, the induction of antioxidant enzymes by Nrf2 activation blunts glucose-triggered ROS signaling, thus resulting in reduced GSIS. These two premises are potentially relevant to impairment of beta-cells occurring in the late and early stage of Type 2 diabetes, respectively. In addition, we summarized our recent findings that persistent oxidative stress due to absence of uncoupling protein 2 activates cellular adaptive response which is associated with impaired pancreatic beta-cell function.This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H(2)O(2), act as metabolic signaling molecules for glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells. Particular emphasis is placed on the potential inhibitory role of endogenous antioxidants, which rise in response to oxidative stress, in glucose-triggered ROS and GSIS. We propose that cellular adaptive response to oxidative stress challenge, such as nuclear factor E2-related factor 2 (Nrf2)-mediated antioxidant induction, plays paradoxical roles in pancreatic beta-cell function. On the one hand, induction of antioxidant enzymes protects beta-cells from oxidative damage and possible cell death, thus minimizing oxidative damage-related impairment of insulin secretion. On the other hand, the induction of antioxidant enzymes by Nrf2 activation blunts glucose-triggered ROS signaling, thus resulting in reduced GSIS. These two premises are potentially relevant to impairment of beta-cells occurring in the late and early stage of Type 2 diabetes, respectively. In addition, we summarized our recent findings that persistent oxidative stress due to absence of uncoupling protein 2 activates cellular adaptive response which is associated with impaired pancreatic beta-cell function. This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H{sub 2}O{sub 2}, act as metabolic signaling molecules for glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells. Particular emphasis is placed on the potential inhibitory role of endogenous antioxidants, which rise in response to oxidative stress, in glucose-triggered ROS and GSIS. We propose that cellular adaptive response to oxidative stress challenge, such as nuclear factor E2-related factor 2 (Nrf2)-mediated antioxidant induction, plays paradoxical roles in pancreatic beta-cell function. On the one hand, induction of antioxidant enzymes protects beta-cells from oxidative damage and possible cell death, thus minimizing oxidative damage-related impairment of insulin secretion. On the other hand, the induction of antioxidant enzymes by Nrf2 activation blunts glucose-triggered ROS signaling, thus resulting in reduced GSIS. These two premises are potentially relevant to impairment of beta-cells occurring in the late and early stage of Type 2 diabetes, respectively. In addition, we summarized our recent findings that persistent oxidative stress due to absence of uncoupling protein 2 activates cellular adaptive response which is associated with impaired pancreatic beta-cell function. This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H(2)O(2), act as metabolic signaling molecules for glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells. Particular emphasis is placed on the potential inhibitory role of endogenous antioxidants, which rise in response to oxidative stress, in glucose-triggered ROS and GSIS. We propose that cellular adaptive response to oxidative stress challenge, such as nuclear factor E2-related factor 2 (Nrf2)-mediated antioxidant induction, plays paradoxical roles in pancreatic beta-cell function. On the one hand, induction of antioxidant enzymes protects beta-cells from oxidative damage and possible cell death, thus minimizing oxidative damage-related impairment of insulin secretion. On the other hand, the induction of antioxidant enzymes by Nrf2 activation blunts glucose-triggered ROS signaling, thus resulting in reduced GSIS. These two premises are potentially relevant to impairment of beta-cells occurring in the late and early stage of Type 2 diabetes, respectively. In addition, we summarized our recent findings that persistent oxidative stress due to absence of uncoupling protein 2 activates cellular adaptive response which is associated with impaired pancreatic beta-cell function. |
| Author | Andersen, Melvin E. Pi, Jingbo Zhang, Qiang Hou, Yongyong Corkey, Barbara E. Fu, Jingqi Collins, Sheila Woods, Courtney G. |
| AuthorAffiliation | b Division of Computational Biology, The Hamner Institutes for Health Sciences, Research Triangle Park, NC 27709 d ExxonMobil Biomedical Sciences Incorporated, Annandale, NJ, 08801 USA a Division of Translational Biology, The Hamner Institutes for Health Sciences, Research Triangle Park, NC 27709 c School of Public Health, China Medical University, Shenyang, 110001, China e Obesity Research Center, Boston University School of Medicine, Boston, MA 02118 f Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27710 |
| AuthorAffiliation_xml | – name: f Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27710 – name: a Division of Translational Biology, The Hamner Institutes for Health Sciences, Research Triangle Park, NC 27709 – name: d ExxonMobil Biomedical Sciences Incorporated, Annandale, NJ, 08801 USA – name: c School of Public Health, China Medical University, Shenyang, 110001, China – name: b Division of Computational Biology, The Hamner Institutes for Health Sciences, Research Triangle Park, NC 27709 – name: e Obesity Research Center, Boston University School of Medicine, Boston, MA 02118 |
| Author_xml | – sequence: 1 givenname: Jingbo surname: Pi fullname: Pi, Jingbo email: jpi@thehamner.org organization: Division of Translational Biology, The Hamner Institutes for Health Sciences, 6 Davis Drive, Research Triangle Park, NC 27709, USA – sequence: 2 givenname: Qiang surname: Zhang fullname: Zhang, Qiang organization: Division of Computational Biology, The Hamner Institutes for Health Sciences, Research Triangle Park, NC 27709, USA – sequence: 3 givenname: Jingqi surname: Fu fullname: Fu, Jingqi organization: Division of Translational Biology, The Hamner Institutes for Health Sciences, 6 Davis Drive, Research Triangle Park, NC 27709, USA – sequence: 4 givenname: Courtney G. surname: Woods fullname: Woods, Courtney G. organization: Division of Computational Biology, The Hamner Institutes for Health Sciences, Research Triangle Park, NC 27709, USA – sequence: 5 givenname: Yongyong surname: Hou fullname: Hou, Yongyong organization: Division of Translational Biology, The Hamner Institutes for Health Sciences, 6 Davis Drive, Research Triangle Park, NC 27709, USA – sequence: 6 givenname: Barbara E. surname: Corkey fullname: Corkey, Barbara E. organization: Obesity Research Center, Boston University School of Medicine, Boston, MA 02118, USA – sequence: 7 givenname: Sheila surname: Collins fullname: Collins, Sheila organization: Division of Translational Biology, The Hamner Institutes for Health Sciences, 6 Davis Drive, Research Triangle Park, NC 27709, USA – sequence: 8 givenname: Melvin E. surname: Andersen fullname: Andersen, Melvin E. organization: Division of Computational Biology, The Hamner Institutes for Health Sciences, Research Triangle Park, NC 27709, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19501608$$D View this record in MEDLINE/PubMed https://www.osti.gov/biblio/21344909$$D View this record in Osti.gov |
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| Snippet | This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H
2O
2, act as metabolic signaling... This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H(2)O(2), act as metabolic signaling... This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H2O2, act as metabolic signaling... This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H{sub 2}O{sub 2}, act as metabolic... This review focuses on the emerging evidence that reactive oxygen species (ROS) derived from glucose metabolism, such as H 2 O 2 , act as metabolic signaling... |
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| SubjectTerms | 60 APPLIED LIFE SCIENCES ALDEHYDES Animals Antioxidant ANTIOXIDANTS Antioxidants - metabolism Antioxidants - therapeutic use APOPTOSIS BODY CARBOHYDRATES CHEMICAL REACTIONS DAMAGE Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - metabolism DIGESTIVE SYSTEM DRUGS ENDOCRINE GLANDS ENZYMES GLANDS GLUCOSE Glucose - metabolism GLUTATHIONE HEXOSES HORMONES Humans HYDROGEN COMPOUNDS HYDROGEN PEROXIDE Hypoglycemic Agents - pharmacology INSULIN Insulin - metabolism Insulin secretion Insulin-Secreting Cells - drug effects Insulin-Secreting Cells - enzymology Insulin-Secreting Cells - metabolism Ion Channels - metabolism METABOLISM Mitochondrial Proteins - metabolism MONOSACCHARIDES NF-E2-Related Factor 2 - metabolism Nrf2 ORGANIC COMPOUNDS ORGANS OXIDATION Oxidative Stress OXIDOREDUCTASES OXYGEN COMPOUNDS PANCREAS Pancreatic beta-cells PEPTIDE HORMONES PEPTIDES PEROXIDES POLYPEPTIDES PROTEINS RADIOPROTECTIVE SUBSTANCES Reactive Oxygen Species - metabolism RESPONSE MODIFYING FACTORS ROS SACCHARIDES Signal Transduction - drug effects STRESSES SUPEROXIDE DISMUTASE Ucp2 Uncoupling Protein 2 |
| Title | ROS signaling, oxidative stress and Nrf2 in pancreatic beta-cell function |
| URI | https://dx.doi.org/10.1016/j.taap.2009.05.025 https://www.ncbi.nlm.nih.gov/pubmed/19501608 https://www.proquest.com/docview/733787932 https://www.proquest.com/docview/745713301 https://www.osti.gov/biblio/21344909 https://pubmed.ncbi.nlm.nih.gov/PMC2837798 |
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