Table 3.
Cellular and Molecular Mechanisms of Pancreatic Steatosis and Pancreatic Cancer
| a) | |
|---|---|
| Mechanisms of pancreatic steatosis | |
| Cellular mechanisms | Molecule mechanisms |
| Imbalance in endoplasmic reticulum | Changes in core circadian genes |
| Proinflammatory environments | • Phase shift in CLOCK, Per2, and REV-ERB-α |
| • ↑ Triglycerides, free fatty acids, cholesterol, total fat | • Decreased amplitude in Per2 and BMAL-1 |
| • ↑ IL-1β, TNF-α, IL-6, TGF-β, α-SMA | |
| • ↓ IL-10 | |
| b) | |
|---|---|
| Mechanisms of pancreatic steatosis leading to pancreatic cancer | |
| Cellular mechanisms | Molecule mechanisms |
| Adipokines such as adiponectin and leptin | Impairment of cellular immunity |
| Proinflammatory cytokines/chemokines | ↑ Transcriptional upregulation of genes involved in… |
| Stellate cell activation | • Angiogenesis |
| Supply of glutamine | • Inflammation |
| Impairment of cellular immunity | • Anti-apoptosis |
| • Repression of interferon-inducible genes | |
| • Cell migration and invasion | |
a) Cellular and molecular mechanisms of pancreatic steatosis. b) Cellular and molecular mechanisms of pancreatic steatosis. α-SMA=α-smooth muscle actin. BMAL-1=brain and muscle Arnt-like protein-1. CCK=cholecystokinin. CLOCK=clock circadian regulator. IL-1β=interleukin-1β. IL-6=interleukin-6. IL-10=interleukin-10. Per2=period circadian regulator 2. TNF-α=tumour necrosis factor-α. TNFβ=tumour necrosis factor-β.