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Identification of a novel glucose transporter-like protein-GLUT-12.
Facilitative glucose transporters exhibit variable hexose affinity and tissue-specific expression. These characteristics contribute to specialized metabolic properties of cells. Here we describe theExpand
Acute Effects of Atypical Antipsychotics on Whole-Body Insulin Resistance in Rats: Implications for Adverse Metabolic Effects
OLAN and CLOZ can thus rapidly induce marked insulin resistance, which could contribute to the hyperglycemia and ketoacidosis reported for patients receiving those therapies. Expand
Altered metabolism causes cardiac dysfunction in perfused hearts from diabetic (db/db) mice.
Findings strongly support a causative role of impaired metabolism in the cardiomyopathy observed in db/db diabetic hearts. Expand
Nitric Oxide Stimulates Skeletal Muscle Glucose Transport Through a Calcium/Contraction– and Phosphatidylinositol-3-Kinase–Independent Pathway
The results indicate that NO/cGMP can markedly stimulate skeletal muscle glucose transport by increasing GLUT4 levels at the cell surface by a mechanism that does not depend on activation of PI-3-K. Expand
Enhanced peripheral glucose utilization in transgenic mice expressing the human GLUT4 gene.
The data demonstrate that high level expression of hGLUT4 increases systemic glucose clearance and muscle glucose utilization in vivo and also results in marked compensatory lipolysis and muscle glycogenolysis during a fast. Expand
Distribution of GLUT3 glucose transporter protein in human tissues.
It is concluded that a major role of GLUT3 in humans is as the brain neuronal glucose transporter. Expand
Glycemic improvement in diabetic db/db mice by overexpression of the human insulin-regulatable glucose transporter (GLUT4).
It is demonstrated that GLUT4 upregulation overcomes the glucose transporter translocation defect and alleviates insulin resistance in genetically diabetic mice, thus resulting in markedly improved glycemic control. Expand
Effects of overexpression of human GLUT4 gene on maternal diabetes and fetal growth in spontaneous gestational diabetic C57BLKS/J Lepr(db/+) mice.
The results suggest that the single mutant db allele effects susceptibility to GDM through abnormalities in insulin receptor signaling, defective insulin secretion, and greater nutrient availability, and GLUT4 overexpression markedly improves insulin-signaling in GDM, resulting in increased insulin secretion and improved glycemic control. Expand
Transgenic mice expressing the human GLUT4/muscle-fat facilitative glucose transporter protein exhibit efficient glycemic control.
Data demonstrate that increased expression of the humanGLUT4 gene in vivo results in a constitutively high level of cell surface GLUT4 protein expression and more efficient metabolic control over fluctuations in plasma glucose concentrations. Expand
Inhibitory effects of antipsychotics on carbachol-enhanced insulin secretion from perifused rat islets: role of muscarinic antagonism in antipsychotic-induced diabetes and hyperglycemia.
It is demonstrated that low concentrations of olanzapine and clozapine can markedly and selectively impair cholinergic-stimulated insulin secretion by blocking muscarinic M3 receptors, which could be one of the contributing factors to their higher risk for producing hyperglycemia and diabetes in humans. Expand