| * Inhibition of Fructose 1,6-Bisphosphatase Reduces Excessive Endogenous Glucose Production and Attenuates Hyperglycemia in Zucker Diabetic Fa |
| * Metallothionein and Catalase Sensitize to Diabetes in Nonobese Diabetic Mice |
| * Glucose Regulates Foxo1 Through Insulin Receptor Signaling in the Pancreatic Islet -cell |
| * Induction of Tolerance in Type 1 Diabetes via Both CD4+CD25+ T Regulatory Cells and T Regulatory Type 1 Cells |
| * Islet Inflammation and Fibrosis in a Spontaneous Model of Type 2 Diabetes, the GK Rat |
| * The Role of Phosphoinositide 3-Kinase/Akt Signaling in Low-Dose MercuryeCInduced Mouse Pancreatic -Cell Dysfunction In Vitro and In Vivo |
| * Peroxisome ProliferatoreCActivated Receptor Improves Pancreatic Adaptation to Insulin Resistance in Obese Mice and Reduces Lipotoxicity in |
| * Cognitive Performance, Psychological Well-Being, and Brain Magnetic Resonance Imaging in Older Patients With Type 1 Diabetes |
| * Nutritional Supplementation With trans-10, cis-12eCConjugated Linoleic Acid Induces Inflammation of White Adipose Tissue |
| * Lipid Storage Compartment to Endocrine Organ |
| * Decreased Muscle Strength and Quality in Older Adults With Type 2 Diabetes |
| * Hyperglycemia Stimulates Coagulation, Whereas Hyperinsulinemia Impairs Fibrinolysis in Healthy Humans |
| * Deletion of p66Shc Longevity Gene Protects Against Experimental Diabetic Glomerulopathy by Preventing Diabetes-Induced Oxidative Stress |
| * The Intrauterine Environment as Reflected by Birth Size and Twin and Zygosity Status Influences Insulin Action and Intracellular Glucose Met |
| * Decreased Muscle Strength and Quality in Older Adults With Type 2 Diabetes |
| * Thiazolidinediones Ameliorate Diabetic Nephropathy via Cell CycleeCDependent Mechanisms |
| * Apoptosis Signal-Regulating Kinase 1 Mediates Cellular Senescence Induced by High Glucose in Endothelial Cells |
| * Altered Endothelial Nitric Oxide Synthase Targeting and Conformation and Caveolin-1 Expression in the Diabetic Kidney |
| * Diabetic Nephropathy Is Associated With Gene Expression Levels of Oxidative Phosphorylation and Related Pathways |
| * Poly(ADP-Ribose) Polymerase Inhibition Alleviates Experimental Diabetic Sensory Neuropathy |
| * Salutary Effect of Pigment EpitheliumeCDerived Factor in Diabetic Nephropathy |
| * Reversal of Type 1 Diabetes by Engineering a Glucose Sensor in Skeletal Muscle |
| * Adiponectin Suppression of High-GlucoseeCInduced Reactive Oxygen Species in Vascular Endothelial Cells |
| * Risk Factors for Renal Dysfunction in Type 2 Diabetes |
| * Mutations at the Same Residue (R50) of Kir6.2 (KCNJ11) That Cause Neonatal Diabetes Produce Different Functional Effects |
| * Chronic Inhibition of Dipeptidyl Peptidase-4 With a Sitagliptin Analog Preserves Pancreatic -Cell Mass and Function in a Rodent Model of Typ |
| * Gene Transfer of an Engineered Transcription Factor Promoting Expression of VEGF-A Protects Against Experimental Diabetic Neuropathy |
| * Functional Effects of Mutations at F35 in the NH2-terminus of Kir6.2 (KCNJ11), Causing Neonatal Diabetes, and Response to Sulfonylurea Thera |
| * Genome-Wide Linkage of Plasma Adiponectin Reveals a Major Locus on Chromosome 3q Distinct From the Adiponectin Structural Gene |
| * Clinicogenetic Studies of Maturity-Onset Diabetes of the Young to Unraveling Complex Mechanisms of Glucokinase Regulation |
| * Exercise-Induced Phosphorylation of the Novel Akt Substrates AS160 and Filamin A in Human Skeletal Muscle |
| * Combination of HLA-A24, -DQA103, and -DR9 Contributes to Acute-Onset and Early Complete -Cell Destruction in Type 1 Diabetes |
| * Kir6.2 Mutations Associated With Neonatal Diabetes Reduce Expression of ATP-Sensitive K+ channels |
| * The Experimental Type 2 Diabetes Therapy Glycogen Phosphorylase Inhibition Can Impair Aerobic Muscle Function During Prolonged Contraction |
| * Activation of AMP-Activated Protein Kinase Within the Ventromedial Hypothalamus Amplifies Counterregulatory Hormone Responses in Rats With D |
| * Evidence for a Mitochondrial Regulatory Pathway Defined by Peroxisome ProliferatoreCActivated Receptor- Coactivator-1, Estrogen-Related Rece |
| * Linkage but Not Association of Calpain-10 to Type 2 Diabetes Replicated in Northern Sweden |
| * Fasting Insulin and Obesity-Related Phenotypes Are Linked to Chromosome 2p |
| * A Novel eC192c/g Mutation in the Proximal P2 Promoter of the Hepatocyte Nuclear Factor-4 Gene (HNF4A) Associates With Late-Onset Diabetes |
| * HLA Genotyping Supports a Nonautoimmune Etiology in Patients Diagnosed With Diabetes Under the Age of 6 Months |
| * The Variable Number of Tandem Repeats Upstream of the Insulin Gene Is a Susceptibility Locus for Latent Autoimmune Diabetes in Adults |
| * Significant Linkage of BMI to Chromosome 10p in the U.K. Population and Evaluation of GAD2 as a Positional Candidate |
| * Reduced Access to Insulin-Sensitive Tissues in Dogs With Obesity Secondary to Increased Fat Intake |
| * Time-Dependent Effects of Free Fatty Acids on Glucose Effectiveness in Type 2 Diabetes |
| * A Hepatocyte Nuclear Factor-4 Gene (HNF4A) P2 Promoter Haplotype Linked With Late-Onset Diabetes |
| * Lymphocytic Infiltration and Immune Activation in Metallothionein PromotereCExendin-4 (MT-Exendin) Transgenic Mice |
| * Downregulation of Electron Transport Chain Genes in Visceral Adipose Tissue in Type 2 Diabetes Independent of Obesity and Possibly Involving |
| * Increased Infiltration of Macrophages in Omental Adipose Tissue Is Associated With Marked Hepatic Lesions in Morbid Human Obesity |