Contribution of systemic inflammation to permanence of k_atp-induced neonatal diabetes in mice

Keyphrases

• Systemic Inflammation 100%
• Neonatal Diabetes 100%
• Remission 66%
• Insulin Sensitivity 66%
• Diabetes 66%
• Gain-of-function 66%
• Disease Severity 33%
• Divergence 33%
• Inflammation 33%
• Gain-of-function mutation 33%
• Blood Glucose 33%
• Disease Outcome 33%
• Glibenclamide 33%
• Insulin 33%
• Glucagon 33%
• Glucose Production 33%
• Glucagon-like 33%
• Treatment Efficacy 33%
• ATP-sensitive Potassium Channel 33%
• Patient Phenotype 33%
• Diabetes Management 33%
• Disease Treatment 33%
• Leptin 33%
• Serum Cytokines 33%
• Liver Glucose Production 33%
• Enhanced Sensitivity 33%
• Permanent Neonatal Diabetes 33%
• Diabetes Remission 33%
• Meloxicam 33%
• Gene Induction 33%
• Diabetes Progression 33%
• Severe Insulin Resistance 33%
• Diabetes Induction 33%
• Remitters 33%
• Disease Pathways 33%

Neuroscience

• Gluconeogenesis 100%
• Adenosine Triphosphate 50%
• Glibenclamide 50%
• Glucagon 50%
• Adenosine Triphosphate Sensitive Potassium Channel 50%
• Leptin 50%
• Anti-Inflammatory 50%
• Glucagon-Like Peptide-1 50%
• Gene Induction 50%
• Gain of Function Mutation 50%
• Meloxicam 50%