NDLI: Disruption of Sur2-containing K(ATP) channels enhances insulin-stimulated glucose uptake in skeletal muscle.

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Disruption of Sur2-containing K(ATP) channels enhances insulin-stimulated glucose uptake in skeletal muscle.

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Disruption of Sur2-containing K(ATP) channels enhances insulin-stimulated glucose uptake in skeletal muscle.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Hansen, P. A. Pu, J. Makielski, J. C. Burant, C. F. Chutkow, W. A. Valdivia, C. R. Samuel, V.
Description	Author Affiliation: Chutkow WA ( Department of Medicine, University of Chicago, Chicago, IL 60637, USA.);
Abstract	ATP-sensitive potassium channels (K(ATP)) are involved in a diverse array of physiologic functions including protection of tissue against ischemic insult, regulation of vascular tone, and modulation of insulin secretion. To improve our understanding of the role of K(ATP) in these processes, we used a gene-targeting strategy to generate mice with a disruption in the muscle-specific K(ATP) regulatory subunit, SUR2. Insertional mutagenesis of the Sur2 locus generated homozygous null (Sur2(-/-)) mice and heterozygote (Sur2(+/-)) mice that are viable and phenotypically similar to their wild-type littermates to 6 weeks of age despite, respectively, half or no SUR2 mRNA expression or channel activity in skeletal muscle or heart. Sur2(-/-) animals had lower fasting and fed serum glucose, exhibited improved glucose tolerance during a glucose tolerance test, and demonstrated a more rapid and severe hypoglycemia after administration of insulin. Enhanced glucose use was also observed during in vivo hyperinsulinemic euglycemic clamp studies during which Sur2(-/-) mice required a greater glucose infusion rate to maintain a target blood glucose level. Enhanced insulin action was intrinsic to the skeletal muscle, as in vitro insulin-stimulated glucose transport was 1.5-fold greater in Sur2(-/-) muscle than in wild type. Thus, membrane excitability and K(ATP) activity, to our knowledge, seem to be new components of the insulin-stimulated glucose uptake mechanism, suggesting possible future therapeutic approaches for individuals suffering from diabetes mellitus.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	20
Volume Number	98
Language	English
Publisher	National Academy of Sciences
Publisher Date	2001-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	ATP-Binding Cassette Transporters Glucose Metabolism Insulin Pharmacology Muscle Proteins Muscle, Skeletal Physiology Potassium Channels, Inwardly Rectifying Potassium Channels Receptors, Drug Analysis Of Variance Animals Biological Transport Blood Glucose Deoxyglucose Pharmacokinetics Exons Glucose Clamp Technique Glucose Tolerance Test Glucose Transporter Type 4 Blood Introns Mice Mice, Knockout Monosaccharide Transport Proteins Genetics Drug Effects Polymerase Chain Reaction Deficiency RNA, Messenger Signal Transduction Sodium-Potassium-Exchanging ATPase Sulfonylurea Receptors Triglycerides Weight Gain Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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