The Serine Kinase C-Jun N-Terminal Kinase (JNK) Contributes to Oxidant-Induced Insulin Resistance in Isolated Rat Skeletal Muscle

Persistent Link:
http://hdl.handle.net/10150/244754
Title:
The Serine Kinase C-Jun N-Terminal Kinase (JNK) Contributes to Oxidant-Induced Insulin Resistance in Isolated Rat Skeletal Muscle
Author:
Santos, Fernando Reyes; Diamond-Stanic, Maggie K.; Prasannarong, Mujalin; Henriksen, Erik J.
Issue Date:
May-2012
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
Insulin resistance of the mammalian skeletal muscle glucose transport system, one cause of which is oxidative stress, leads to the development of type 2 diabetes. While the direct contributions to insulin resistance of certain stress-activated serine kinases have been described previously, the specific contribution of c-Jun N-terminal kinase (JNK) is not fully understood. Therefore, we assessed the role of JNK in insulin resistance caused by in vitro exposure to the oxidant hydrogen peroxide (H₂O₂). Soleus muscles from lean Zucker rats were incubated in low levels (~30 μM) of H₂O₂ in the absence or presence of insulin for up to 6 hr. Decreases in insulin-stimulated glucose transport activity (ISGTA) were observed at all time points and were associated with similar diminutions in insulin stimulation of Akt Ser⁴⁶⁷ phosphorylation. Phosphorylation (Thr¹⁸³/Tyr¹⁸⁵) of JNK isoforms (JNK1 and JNK2/3) was increased by H₂O₂ in the absence and presence of insulin at all time points. To determine the specific contribution of JNK to oxidant-induced insulin resistance, the JNK inhibitor SP600125 was used. ISGTA in the presence of H₂O₂ was improved when the inhibitor was added during the 6-hr incubation. These results indicate that JNK contributes to oxidative stress-induced insulin resistance in mammalian skeletal muscle.
Type:
text; Electronic Thesis
Degree Name:
B.S.H.S.
Degree Level:
bachelors
Degree Program:
Honors College; Physiology
Degree Grantor:
University of Arizona

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleThe Serine Kinase C-Jun N-Terminal Kinase (JNK) Contributes to Oxidant-Induced Insulin Resistance in Isolated Rat Skeletal Muscleen_US
dc.creatorSantos, Fernando Reyesen_US
dc.contributor.authorSantos, Fernando Reyesen_US
dc.contributor.authorDiamond-Stanic, Maggie K.en_US
dc.contributor.authorPrasannarong, Mujalinen_US
dc.contributor.authorHenriksen, Erik J.en_US
dc.date.issued2012-05-
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractInsulin resistance of the mammalian skeletal muscle glucose transport system, one cause of which is oxidative stress, leads to the development of type 2 diabetes. While the direct contributions to insulin resistance of certain stress-activated serine kinases have been described previously, the specific contribution of c-Jun N-terminal kinase (JNK) is not fully understood. Therefore, we assessed the role of JNK in insulin resistance caused by in vitro exposure to the oxidant hydrogen peroxide (H₂O₂). Soleus muscles from lean Zucker rats were incubated in low levels (~30 μM) of H₂O₂ in the absence or presence of insulin for up to 6 hr. Decreases in insulin-stimulated glucose transport activity (ISGTA) were observed at all time points and were associated with similar diminutions in insulin stimulation of Akt Ser⁴⁶⁷ phosphorylation. Phosphorylation (Thr¹⁸³/Tyr¹⁸⁵) of JNK isoforms (JNK1 and JNK2/3) was increased by H₂O₂ in the absence and presence of insulin at all time points. To determine the specific contribution of JNK to oxidant-induced insulin resistance, the JNK inhibitor SP600125 was used. ISGTA in the presence of H₂O₂ was improved when the inhibitor was added during the 6-hr incubation. These results indicate that JNK contributes to oxidative stress-induced insulin resistance in mammalian skeletal muscle.en_US
dc.typetexten_US
dc.typeElectronic Thesisen_US
thesis.degree.nameB.S.H.S.en_US
thesis.degree.levelbachelorsen_US
thesis.degree.disciplineHonors Collegeen_US
thesis.degree.disciplinePhysiologyen_US
thesis.degree.grantorUniversity of Arizonaen_US
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