The disrupted cross-talk in adipose tissue, hepatocytes, skeletal muscles and pancreatic islets leads to insulin resistance in type 2 diabetes. Permanent nutrient excess induces hypertrophy of adipocytes and low grade chronic inflammation accompanied by pro-inflammatory cytokines secretion and disrupt insulin signaling (IRS-1/PI3K/AKT axis). This causes increased glucogenesis by hepatocytes, decline in peripheral glucose uptake, and pancreatic β-cells compensates by increasing insulin secretion. Prolonged exposure to these conditions leads to functional exhaustion of β-cell and insulin resistance.
Diabetes II modelling set components
$550.00
$250.00
Price range: $250.00 through $290.00
Assays validated
- Insulin-stimulated glucose uptake assays (muscle/adipocytes)
- Hepatic glucose production assays
- Lipid accumulation (steatosis) assays in hepatocytes
- β-cell insulin secretion (GSIS – glucose-stimulated insulin secretion)