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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

FieldValue
PM IDBRS6(PM2)
FM OwnershipBRS6(FM1)
Dose Target / RequirementRepeated activity + dietary fibre pattern; not achieved through one nutrient
Coverage TimingDaily
Response TypeHours–Builds
Functional LatencySame day–Weeks

12. References

  1. Mikus et al. (2012)
  2. Colberg et al. (2016)

13. Missing Entities

  • None flagged from this row-level pass