Diabetes

Diabetes is one of the world’s major metabolic diseases, involving defects in insulin secretion and/or insulin resistance. We provide research-grade antibodies and small-molecule tools to study mechanisms, complications, and therapeutic strategies.

Focus areas: insulin signaling, hepatic gluconeogenesis, immuno-metabolism, β-cell stress

Diabetes-related antibodies (curated)

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Hot topics & directions

  • Peripheral insulin resistance: GLUT4 trafficking, IRS–PI3K–AKT branch integrity.
  • Hepatic IR & gluconeogenesis: FOXO1/gluconeogenic program vs lipogenic coupling.
  • β-cell stress: ER stress, inflammation, mitochondria feeding back to insulin secretion.
  • Immuno-metabolism: adipose immune infiltration as a second hit to insulin sensitivity.

Related targets

Insulin signaling
INSR, IGF1R, IRS1/2, PIK3CA/CB, PDK1, AKT1/2/3, PTEN, TBC1D4 (AS160), FOXO1
Metabolic switches
PRKAA1/2 (AMPK), MTOR (mTORC1), ULK1, SREBF1, ACACA, FASN
Inflammation & immunity
JAK/STAT, NF-κB, NLRP3 inflammasome axis (model-dependent)
Incretin axis (in vivo)
GLP1R, GIPR, GCGR

Key signaling pathways

  1. Insulin/IGF-1 → IRS → PI3K–PDK1–AKT
    Glucose uptake & anabolism; often paired with GLUT4 trafficking readouts.
  2. PI3K–AKT–mTORC1
    Nutrient-replete anabolic hub; couples to autophagy suppression & protein synthesis.
  3. AMPK
    Energy stress & reprogramming; often antagonistic/balanced with mTORC1.
  4. MAPK stress axes
    Stress/inflammation/proliferation; crosstalk with insulin needs evidence.

Tool compounds (research use)

Commonly used for mechanistic studies; follow your lab SOP, compound datasheets, and ethics approvals.

CompoundTargets / pathwaysExperimental notes
LY294002PI3K (upstream of PI3K–AKT)Common for insulin signaling branch validation; mind cytotoxicity/off-targets—use dose/time matrices.
MK-2206AKT1/2/3Useful for AKT-dependent metabolic phenotypes; watch feedback loops (RTK/MAPK) confounding interpretation.
RapamycinmTORC1 (FKBP12–Raptor)Classic autophagy/synthetic metabolism tool; prolonged treatment may engage mTORC2 feedback—pair controls.
AICARAMPK-activating tool compoundCommon for energy-stress reprogramming studies; support with phospho-readouts and upstream kinase controls.
MetforminMitochondrial complex I / AMPK axis (model-dependent)Often used as a chronic positive control; in vitro dose windows vary strongly by cell type.
RuxolitinibJAK1/2Useful for cytokine/immune-metabolism crosstalk; mind immunosuppression in in vivo IR models.
MG132ProteasomeFor proteostasis/degradation dependency; high cytotoxicity—tightly window doses.