BRS6(PM2) - Insulin Sensitivity & Glucose Disposal
1. Definition
Capacity to clear glucose efficiently through insulin-sensitive tissues and reduce prolonged metabolic strain.
2. Mechanistic Basis
↑ glucose disposal; ↑ insulin sensitivity; ↓ metabolic stress load
3. Dependencies
3.1 KCs (Key Constraints)
3.2 Optional BRSX Modifiers
- None listed
3.3 Co-factors
- magnesium
- chromium
- vitamin D context
4. Interventions (Core Regulatory Levers)
4.1 Dietary Modulation
fibre-rich pattern → improved metabolic response; low-UPF diet → reduced insulin demand and improved tissue insulin responsiveness
4.2 Non-Dietary Regulatory Levers
post-meal walking and regular movement → increased skeletal muscle glucose disposal; resistance training → improved insulin sensitivity and metabolic flexibility
5. Functional Outputs (Directional Effects)
↑ glucose disposal; ↑ insulin sensitivity; ↓ metabolic stress load
6. System Integration
Integrated within BRS6(FM1) to translate glycaemic input quality and activity context into stable glucose clearance dynamics.
7. Key Insight
Insulin sensitivity is strongly lifestyle-amplified: diet provides substrate quality and signalling context, while movement and training drive the dominant disposal effect.
8. Functional Mechanism Ownership
- BRS6(FM1)
9. Intervention Dominance
- Diet-Supported
10. Constraints and Failure Modes
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11. Notes
- Evidence Type: Human + mechanistic
- Evidence Notes: Diet-supported but lifestyle strongly amplifies the effect.
Mechanism Summary Table
| Field | Value |
|---|---|
| PM ID | BRS6(PM2) |
| FM Ownership | BRS6(FM1) |
| Dose Target / Requirement | Repeated activity + dietary fibre pattern; not achieved through one nutrient |
| Coverage Timing | Daily |
| Response Type | Hours–Builds |
| Functional Latency | Same day–Weeks |
12. References
13. Missing Entities
- None flagged from this row-level pass