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BRS6 — Metabolic & Neuroendocrine Regulation: circadian rhythm, autonomic tone, hormonal coordination, and energy prioritisation

BRS6(FM4) - Metabolic–Endocrine Signalling & Adaptive Regulation​

(Peripheral Metabolic Signals and Central Adaptive Responses)

Primary Mechanisms​

Key Constraints​

No shared nutritional constraint is newly established for this refocused FM. The previous glucose-pool mapping remains in architectural history pending relevance review.

1. Definition​

Coordinates peripheral metabolic–endocrine signalling and stress-responsive central regulation to communicate energy availability, metabolic state and physiological demand.

  • Regulates adipose-derived endocrine output, including adipokine secretion and local glucocorticoid responsiveness.
  • Integrates metabolic and stress-related hormonal signals with central appetite and reward regulation.
  • Supports communication between peripheral metabolic state and central neuroendocrine responses to changing physiological demands.

2. Primary Biological Effects​

Context-appropriate endocrine communication and stress-responsive appetite/reward regulation; no universal direction of adipokine change or eating response is assumed.

4. Mechanistic Basis (Integrated FM Narrative)​

4.1 Functional Rationale​

Coordinates peripheral metabolic–endocrine signalling and stress-responsive central regulation to communicate energy availability, metabolic state and physiological demand.

4.2 Evidence Summary​

Human adipose experiments distinguish endocrine synthesis, secretion and local glucocorticoid conversion. Mouse adipocyte-GR experiments support qualified stress-feedback involvement; they do not establish a corresponding human dietary pathway. Central stress-eating evidence is assessed separately in PM9. See the linked PM evidence and source assessments.

4.3 Functional Boundaries​

FM1 retains glycaemic–insulin regulation and glucose disposal. FM2 retains systemic HPA-axis rhythm and cortisol timing. FM3 retains autonomic activation and recovery. BRS3 retains inflammatory activation, redox regulation and resolution. This FM does not own whole-body allostasis or resource allocation across the six BRSs. Inflammatory signalling is a possible Cross-BRS relationship rather than the defining function.

5. Connected Mechanisms​

7. Phenome Connections​

Historical integrated outcome interpretations are preserved in the architectural history. No new Phenome confidence or outcome relationship is inferred from this scope reconciliation.

8. References​