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- Title
Hyperglycemia activates glucose transport in rat skeletal muscle via a Ca(2+)-dependent mechanism.
- Authors
Nolte, Lorraine A.; Rincón, Jorge; Wahlström, Erica Odegaard; Craig, Bruce W.; Zierath, Juleen R.; Wallberg-Henriksson, Harriet; Nolte, L A; Rincón, J; Wahlström, E O; Craig, B W; Zierath, J R; Wallberg-Henriksson, H
- Abstract
We investigated the acute effect of hyperglycemia on 3-O-methylglucose transport in isolated rat epitrochlearis muscles. High levels of glucose (20 mmol/l) induced an approximately twofold increase in the rate of glucose transport when compared with muscles exposed to a low level of glucose (8 mmol/l) (P < 0.001). The hyperglycemic effect was additive to the effects of both insulin and exercise on the glucose transport rates. Dantrolene (25 mumol/l), a potent inhibitor of Ca2+ release from the sarcoplasmic reticulum, blocked the ability of hyperglycemia to increase glucose transport by 73% (P < 0.01). Although dantrolene had no effect on the non-insulin-stimulated or the insulin-stimulated glucose transport rates during normoglycemic conditions, the effect of exercise was completely blocked in the presence of dantrolene (P < 0.01). Inhibition of phosphatidylinositol (PI) 3-kinase by wortmannin (500 nmol/l) had no effect on the activation of glucose transport by hyperglycemia, whereas the insulin-stimulated glucose transport was completely abolished (P < 0.001). These findings suggest that hyperglycemia activates glucose transport by a Ca(2+)-dependent activation of glucose transport does not involve the activation of PI 3-kinase and is separate from the mass-action effect of glucose on glucose transport.
- Publication
Diabetes, 1995, Vol 44, Issue 11, p1345
- ISSN
0012-1797
- Publication type
journal article
- DOI
10.2337/diabetes.44.11.1345