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KIN 404 SECTION 3:TEST 3 NOTES- Regulation of energy storage.docx

9 Pages
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Department
Kinesiology
Course Code
KIN 404
Professor
Russ Tupling

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Description
Current understanding of the signaling pathways involved in GLUT4 translocation with insulin or contraction In the fasted statetheres no glucose so theres no muscle glucose uptake eithero GSV are sequestered inside the cell due to the action of AS160 protein which contains a RAB protein domain that binds GTPo When AS160 is activated thats when insulin is not present therefore fasted state and it promotes the hydrolysis of GTP to RABbound GDP This is what prevents the GSV from translocating to the cell surface membrane In the fed state o Insulin binds to the alpha subunits of IR leading to a conformational change in the receptor which leads to the auto phosphorylation of tyrosine residues and the activation of the kinase associated with the betasubunitso Kinase of the IR recruits and phosphorylates IRS1 muscle specific isoform o Phosphorylated IRS1 recruits and binds to the p85 regulatory subunit of PI3K which activates the p110 catalytic subunit of the enzymeo Activation of PI3K increases the production of PIP3 within plasma membrane which initiates recruitment and activation of PDK1 enzyme PIP3 is involved in signaling cascades and NEEDS to be present to activate PDK1 o Akt PKB is recruited in association with PDK1 and is phosphorylated by PDK1 but full activation of Akt requires additional phosphorylation by the RictormTOR kinaseo PKD1 also activates PKC which along with Akt can phosphorylate AS160 and inhibit the GTPase activity of RAB which leads to increased movement and fusion of GLUT4 storage vesicles GSVActivation of Akt and aPKC leads to the phosphorylation of AS160 RAB GTP cannot be converted to RAB GDP RAB GTP then promotes GSV translocation Insulin is inhibiting AS160s inhibition o AS160 becomes phosphorylated in response not only to insulin but also to contractile activity and pharmacological activation of AMPK with AICARo Therefore AMPK is a potential therapeutic target for insulin resistance and T2DM because it is not involved in any pathway but can still phosphorylate AS160 directly AS160 is the convergence point for both pathways The different effects of the pathways and their additive effect could be because there are different isoforms for each pathwaySummary of acute regulation of FA transport by insulin and muscle contraction Following contraction by both insulin and exercise different transport proteins are transported and incorporated into the cell membrane Therefore its not only GLUT4 but also FATCD36 and FABP as wello FATCD36Fatty acid translocasesequestered in cell like GLUT4 in healthy condition
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