现在位置：百拇书刊 > 国外期刊 > 糖尿病学杂志 > 2006年.第4期 《糖尿病学杂志》.2006年.第4期  * Inhibition of Glucose-Stimulated Activation of Extracellular SignaleCRegulated Protein Kinases 1 and 2 by Epinephrine in Pancreatic -Cells  * Sustained Exposure to High Glucose Concentrations Modifies Glucose Signaling and the Mechanics of Secretory Vesicle Fusion in Primary Rat Pa  * 5-Aminoimidazole-4-Carboxamide-1--D-Ribofuranoside and Metformin Inhibit Hepatic Glucose Phosphorylation by an AMP-Activated Protein Kinasee  * Contribution of Aldose Reductase to Diabetic Hyperproliferation of Vascular Smooth Muscle Cells  * ZO-1 Expression and Phosphorylation in Diabetic Nephropathy  * Accelerated Diabetic Nephropathy in Mice Lacking the Peroxisome ProliferatoreCActivated Receptor  * Insulin Treatment Ameliorates Impaired Corneal Reepithelialization in Diabetic Rats  * Clustering of Insulin Resistance With Vascular Dysfunction and Low-Grade Inflammation in Type 2 Diabetes  * Endothelial Glycocalyx Damage Coincides With Microalbuminuria in Type 1 Diabetes  * Opposite Effect of JAK2 on Insulin-Dependent Activation of Mitogen-Activated Protein Kinases and Akt in Muscle Cells  * Genetic Mapping of Disposition Index and Acute Insulin Response Loci on Chromosome 11q  * Diabetes Reduces Basal Retinal Insulin Receptor Signaling  * Genetic and Functional Analysis of the Nkt1 Locus Using Congenic NOD Mice  * The PPARG Pro12Ala Polymorphism Is Associated With a Decreased Risk of Developing Hyperglycemia Over 6 Years and Combines With the Effect of  * Fish Oil Regulates Adiponectin Secretion by a Peroxisome ProliferatoreCActivated Receptor-eCDependent Mechanism in Mice  * EIF4A2 Is a Positional Candidate Gene at the 3q27 Locus Linked to Type 2 Diabetes in French Families  * 1 Centre National de Recherche (CNRS) Unitee Mixte de Recherche (UMR) 8147, Universitee Paris 5, Paris, France  * Characterization of Peripheral Circadian Clocks in Adipose Tissues  * Group 1B Phospholipase A2eCMediated Lysophospholipid Absorption Directly Contributes to Postprandial Hyperglycemia  * 1 Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut  * Insulin Signaling in Human Visceral and Subcutaneous Adipose Tissue In Vivo  * Gonadal Hormones Determine Sensitivity to Central Leptin and Insulin  * Combined Interleukin-6 and Interleukin-1 Deficiency Causes Obesity in Young Mice  * Atorvastatin Fails to Prevent the Development of Autoimmune Diabetes Despite Inhibition of Pathogenic -CelleCSpecific CD8 T-Cells  * Decreased In Vitro Type 1 Immune Response Against Coxsackie Virus B4 in Children With Type 1 Diabetes  * Evidence From Glut2-Null Mice That Glucose Is a Critical Physiological Regulator of Feeding  * Blockade of GABAA Receptors in the Ventromedial Hypothalamus Further Stimulates Glucagon and Sympathoadrenal but Not the Hypothalamo-Pituita  * Coordinate Changes in Plasma Glucose and Pancreatic -Cell Function in Latino Women at High Risk for Type 2 Diabetes  * CD4+CD25+ Regulatory T-Cells Inhibit the Islet Innate Immune Response and Promote Islet Engraftment  * Brain Magnetic Resonance Imaging Correlates of Impaired Cognition in Patients With Type 2 Diabetes  * Survival Benefits of Intensive Insulin Therapy in Critical Illness  * Cognitive and Neural Hippocampal Effects of Long-Term Moderate Recurrent Hypoglycemia  * Antecedent Hypercortisolemia Is Not Primarily Responsible for Generating Hypoglycemia-Associated Autonomic Failure  * Widespread and Stable Pancreatic Gene Transfer by Adeno-Associated Virus Vectors via Different Routes  * The Natural Course of -Cell Function in Nondiabetic and Diabetic Individuals  * Mechanisms of Time-Dependent Potentiation of Insulin Release  * Protection of INS-1 Cells From Free Fatty AcideCInduced Apoptosis by Targeting hOGG1 to Mitochondria  * Postprandial Suppression of Glucagon Secretion Depends on Intact Pulsatile Insulin Secretion  * Genistein Acutely Stimulates Insulin Secretion in Pancreatic -Cells Through a cAMP-Dependent Protein Kinase Pathway  * Blockers of the Delayed-Rectifier Potassium Current in Pancreatic -Cells Enhance Glucose-Dependent Insulin Secretion