Insulin stimulated glucose uptake : the influence of hyperglycemia and protein kinase C inhibition

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dc.contributor.advisor Craig, Bruce W. en_US
dc.contributor.author Lim, Kang-Il en_US
dc.date.accessioned 2011-06-03T19:39:32Z
dc.date.available 2011-06-03T19:39:32Z
dc.date.created 2002 en_US
dc.date.issued 2002
dc.identifier LD2489.Z78 2002 .L56 en_US
dc.identifier.uri http://cardinalscholar.bsu.edu/handle/handle/187219
dc.description.abstract The glucose toxicity has been recognized over the last several years as a factor contributing to both impaired insulin secretion and insulin resistance in patients with diabetes. However, the molecular mechanisms that underlie the changes in glucose transport activity induced by hyperglycemia have not been fully understood. The purpose of the present investigation is to determine if acute hyperglycemia affects an activation of glucose transport and also if hyperglycemic-induced change in insulinstimulated glucose transport is mediated via a PKC-dependent signaling system. Animals were anesthetized, and the soleus (SOL) muscles were isolated and clamped at their resting length. After a 10 minute recovery period the muscles were transferred to preincubation vials containing KHB supplemented with 4 or 16 mmol of glucose and 16 mmol/1 mannitol with or without insulin and/or inhibitors for 30 minutes. Following an incubation series to prepare the muscle, the muscle was incubated in radioactive 3-0- [3H] methylglucose and [14C] mannitol for 10 min. in the presence/absence of insulin and inhibitors, and the amount of glucose transport was measured. A total of 100µU/ml insulin with 4 mM glucose led to increase glucose transport by 155%, whereas the same amount of insulin with 16 MM glucose led to 80% increment in glucose transport. Also, 16 mM glucose in the absence of insulin induced an increase of glucose uptake by apporoximately 50% compared with 4 MM glucose. However, the addition of insulin reduced that difference to 5.3%. The conventional PKC inhibitor GF 109203X in the muscle incubated with 16 MM glucose led to a decrease in insulin-stimulated glucose transport (1l%), whereas the inhibitor with 4 mM glucose induced a decrease in insulin-stimulated glucose transport (24%). These findings suggest that glucose can directly regulate glucose transport activity by a mechanism that possibly involves a facilitated GLUT1 transporter activity. In addition to the mass action of glucose, the hyperglycemic-induced increase in insulin stimulated glucose transport may be partially mediated via a PKC-dependent signaling system.
dc.description.sponsorship School of Physical Education
dc.format.extent viii, 49 leaves : ill. ; 28 cm. en_US
dc.source Virtual Press en_US
dc.subject.lcsh Glucose -- Analysis. en_US
dc.subject.lcsh Glucose -- Physiological transport. en_US
dc.subject.lcsh Blood sugar -- Analysis. en_US
dc.subject.lcsh Hyperglycemia. en_US
dc.subject.lcsh Protein kinase C. en_US
dc.title Insulin stimulated glucose uptake : the influence of hyperglycemia and protein kinase C inhibition en_US
dc.description.degree Thesis (M.S.)
dc.identifier.cardcat-url http://liblink.bsu.edu/catkey/1236582 en_US


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  • Master's Theses [5454]
    Master's theses submitted to the Graduate School by Ball State University master's degree candidates in partial fulfillment of degree requirements.

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