Últimos Artículos de Diabetes
- Response to Comment on Shah and Ayala. Interpreting Stage-Dependent Changes in Semaglutide Response: From Patterns to Mechanisms
- CD8 + Memory T Cells Encode Obesogenic Memory in White Adipose Tissue
- Comment on Lin et al. Reconsidering Adipose Tissue Lipolysis Dysfunction: Evidence for a Distal Machinery Defect Beyond Insulin Resistance
- Issues and Events
- Comment on Uddin et al. Interpreting Retinal Hypoxia in Early Diabetes
- Comment on Shah and Ayala. Interpreting Stage-Dependent Changes in Semaglutide Response: From Patterns to Mechanisms
- Hippo–YAP Signaling Drives Epigenetic Vulnerability in the Diabetic Heart via the miR-22-3p–SIRT1 Axis: Linking Metabolic Stress to Chromatin Control
- Beyond Blood Sugar: Exploring the Contribution of Metabolic Syndrome to Peripheral Neuropathy
- Diabetes Spotlight: Jonathan Campbell, PhD—Understanding Incretins Through α-Cell–to–β-Cell Communication and Receptor Signaling Pathways
- Response to Comment on Uddin et al. Interpreting Retinal Hypoxia in Early Diabetes
- Issues and Events
- Diabetes Spotlight: Jennifer Estall, PhD—Identifying Signals Between the Pancreas and Liver
- Associations of Combined Genetic and Lifestyle Risks With Incident Type 2 Diabetes in the UK Biobank
- Tomosyn-2 Regulates Postnatal β-Cell Expansion and Insulin Secretion to Maintain Glucose Homeostasis
- IDH3A Deficiency Compromises Adaptive Thermogenesis and Exacerbates Obesity-Induced Metabolic Dysfunction via Impaired BCKDHA-Dependent BCAA Catabolism
- Cooperative Action of Cathepsin K Inhibitor and hUMSC-EVs in Attenuating Ferroptosis Sensitivity for Superior Diabetic Wound Healing
- Different Metabolic Responses to Long-term Weight Loss After Lifestyle Intervention Among Type 2 Diabetes Risk Clusters: Results From the TULIP Study
- Human iPSC-Based Modeling Identifies Epigenetic Regulation at the KCNQ1 Locus During Early Islet Development That Contributes to Lower β-Cell Mass
- Gut-Derived FGF15 Modulates Lean Mass, Bone, and Bile Acid Responses to Weight Loss
- A Self-Reinforcing LGR5–Wnt/β-Catenin–Nedd4L Circuit Drives Fibrotic Progression in Diabetic Kidney Disease