Mechanisms of High Insulin and High Glucose-Induced Skeletal Muscle Insulin Resistance: Focus on Regulation by Adiponectin

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dc.contributor.advisorSweeney, Gary
dc.creatorAhlstrom, Penny Felicia Ulrika
dc.date.accessioned2016-09-20T16:29:14Z
dc.date.available2016-09-20T16:29:14Z
dc.date.copyright2015-09-15
dc.date.issued2016-09-20
dc.date.updated2016-09-20T16:29:14Z
dc.degree.disciplineBiology
dc.degree.levelMaster's
dc.degree.nameMSc - Master of Science
dc.description.abstractSkeletal muscle insulin resistance is known to play an important role in the pathogenesis of diabetes, however the cellular processes involved are poorly defined. Autophagy, ER stress, the UPR and oxidative stress are being studied in insulin resistance but the exact role they play and their interrelationships are yet to be established. Adiponectin is a known insulin sensitizer with anti-diabetic properties but there is limited knowledge of the mechanism by which it exerts its insulin sensitizing effect in skeletal muscle. Through several well-established assays I have demonstrated that impaired autophagy caused ER stress and that UPR activation, specifically peIf2, activated autophagy. Adiponectin alleviated ER stress by restoring autophagy, and a correlation between autophagy induction and insulin sensitization by adiponectin was observed. Alleviating oxidative stress with NAC improved insulin sensitivity independent of ER stress and autophagy, and there appeared to be a correlation between downregulating the UPR and improved insulin sensitivity.
dc.identifier.urihttp://hdl.handle.net/10315/32120
dc.language.isoen
dc.rightsAuthor owns copyright, except where explicitly noted. Please contact the author directly with licensing requests.
dc.subjectEndocrinology
dc.subject.keywordsDiabetes
dc.subject.keywordsType 2 diabetes
dc.subject.keywordsInsulin resistance
dc.subject.keywordsInsulin sensitivity
dc.subject.keywordsSkeletal muscle
dc.subject.keywordsL6
dc.subject.keywordsMyotubes
dc.subject.keywordsMT
dc.subject.keywordsMyoblasts
dc.subject.keywordsMB
dc.subject.keywordsEndoplasmic reticulum
dc.subject.keywordsER
dc.subject.keywordsEndoplasmic reticulum stress
dc.subject.keywordsER stress
dc.subject.keywordsUnfolded protein response
dc.subject.keywordsUPR
dc.subject.keywordsOxidative stress
dc.subject.keywordsReactive oxygen species
dc.subject.keywordsROS
dc.subject.keywordsInsulin sensitizer
dc.subject.keywordsInsulin sensitizing
dc.subject.keywordsAnti-diabetic
dc.subject.keywordsAdiponectin
dc.subject.keywordsAdipokine
dc.subject.keywordsAdipocyte
dc.subject.keywordsAutophagy
dc.subject.keywordsGlucose
dc.subject.keywordsHigh glucose
dc.subject.keywordsHyperglycemia
dc.subject.keywordsHIHG
dc.subject.keywordsInsulin
dc.subject.keywordsHigh insulin
dc.subject.keywordsHyperinsulinemia
dc.subject.keywordsJNK
dc.subject.keywordsAutophagic flux
dc.subject.keywordsAtg5K130R
dc.subject.keywordsRapamycin
dc.subject.keywordsBafilomycin
dc.subject.keywordsTunicamycin
dc.subject.keywordsN-acetyl cysteine
dc.subject.keywordsNAC
dc.subject.keywordsSalubrinal
dc.subject.keywordsGRP78
dc.subject.keywordsGRP78mCherry
dc.titleMechanisms of High Insulin and High Glucose-Induced Skeletal Muscle Insulin Resistance: Focus on Regulation by Adiponectin
dc.typeElectronic Thesis or Dissertation

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