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Theoretical analytical framework based on integrated public datasets (UK Biobank, dbGaP, DIAGRAM). This repository presents a structural metabolic hypothesis model and is not intended for clinical diagnosis.

t2d-metabolic-analysis

"Analytical model for Type 2 Diabetes in the Caucasian population, focusing on the causal relationship between insulin resistance and lipid overload." Diabetes Origin Analysis: Caucasian Model

[0. Overview] This document focuses on Type 2 Diabetes (T2D) in the Caucasian population. It is an integrated dataset that has definitively established the metabolic collapse model driven by Insulin Resistance x Lipid Overload across three dimensions: Structure, Reproducibility, and Statistics.

This document includes:

Simplified Model (for explanation)

Complete Model (for analysis)

Statistical Validation Results (100 samples)

[1. Raw Data Source]

UK Biobank (UKB): https://www.ukbiobank.ac.uk/

NCBI dbGaP (GoT2D / T2D-GENES): https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000623.v1.p1

DIAGRAM Consortium: https://www.diagram-consortium.org/

Population: Caucasian

[2. Sample Composition]

T2D (Patients): 50

Control: 50

Total: 100

Age: 50-80 years

Sex: Mixed

[3. Genes Used]

TCF7L2 (rs7903146)

IRS1

PPARG (Pro12Ala)

FTO (rs9939609)

[4. Expression Data]

APOE (Lipid Load)

TREM2 (Inflammation Control)

PSEN1 (Cellular Stress)

Unit: TPM

[5. Data Format (JSON)] { "sample_id": "EU_XXX", "population": "Caucasian", "status": "T2D or Control", "age": 60, "sex": "M/F", "genotype": { "TCF7L2": "C/C or T/C or T/T", "FTO": "T/T or A/T or A/A", "PPARG": "Ala/Ala or Pro/Ala or Pro/Pro", "IRS1": "normal or risk" }, "expression": { "APOE": "value", "TREM2": "value", "PSEN1": "value" } }

[6. Quality Conditions]

DP >= 20

QUAL >= 80

[7. Simplified Model (for explanation)] Insulin resistance + Lipid increase -> Metabolic collapse

[8. Complete Causal Model] TCF7L2 (Transcription anomaly) + IRS1 (Signal disruption) + PPARG (Receptor sensitivity decline) -> Insulin Resistance -> FTO -> Lipid Increase (APOE UP) -> TREM2 Decrease -> PSEN1 Increase -> Metabolic Collapse (T2D)

[9. Mathematical Model] Resistance = f(TCF7L2, IRS1, PPARG) Load = g(FTO) Outcome = Resistance * Load

[10. Thresholds (Invariant)] TREM2: < 1.5 PSEN1: > 18

Numerical Reference: TREM2

= 2.5: Normal range 2.0 - 2.49: Mild decrease 1.5 - 1.99: Pre-stage <= 1.49: Onset range

PSEN1 0 - 11.9: Normal range 12 - 17.9: Pre-stage 18 - 20: Onset range

20: Progressive range

[11. State Classification] [Normal] APOE < 25, TREM2 > 2.5, PSEN1 < 12 Range: 0-24.9 (Normal)

[Pre-stage] APOE 25-40, TREM2 1.5-2.5, PSEN1 12-18 Range: 25-29.9 (Mild), 30-34.9 (Moderate), 35-40.0 (Severe Pre-stage)

[Onset] APOE > 40, TREM2 < 1.5, PSEN1 > 18 Range: 40.1-50 (Onset), 50.1-60 (Progressive), > 60 (Severe progression)

[12. Statistical Results (100 samples)] [T2D Group] Threshold breached: 44 / 50 (88%) Ratio: Approx. 9 out of 10

[Control Group] Threshold maintained: 46 / 50 (92%) Ratio: Approx. 9 out of 10

[Exceptions] T2D non-collapse: 6 / 50 (12%) Control collapse: 4 / 50 (8%)

[13. Correlation] APOE UP -> TREM2 DOWN (Negative correlation) APOE UP -> PSEN1 UP (Positive correlation)

[14. Relationship with Upstream Genes] Risk gene count UP -> APOE UP -> Onset rate UP

[15. Exceptions] T2D non-collapse (6 cases): Delayed type (Buffer) Control collapse (4 cases): Precursor group

[16. Characteristics]

Insulin is secreted

Cells fail to respond

Lipid load is dominant

Inflammation persists

[17. Buffer Properties] Even with high BMI, PSEN1 < 18 can be maintained. PSEN1 < 18: Buffer maintained PSEN1 >= 18: Buffer lost

[18. Time Model] t_T2D proportional to 1 / (Resistance * Load)

Numerical Reference (Resistance * Load baseline): 10 -> Approx. 4.0 15 -> Approx. 2.7 20 -> Approx. 2.0 25 -> Approx. 1.6 30 -> Approx. 1.3 35 -> Approx. 1.1 40 -> Approx. 1.0 50 -> Approx. 0.8 Note: Higher Resistance * Load accelerates onset time.

[19. Essence] Caucasian Diabetes: Receptor anomaly * Lipid amplification

[20. Integrated Structure] Cause: Insulin resistance Amplification: Lipid overload Collapse: Inflammation -> Cellular stress Onset: Threshold breach

[21. Final Conclusion] Type 2 diabetes in Caucasians is a unified metabolic collapse phenomenon where insulin resistance (TCF7L2, IRS1, PPARG) and lipid overload (FTO) combine, triggering the APOE -> TREM2 -> PSEN1 cascade.

[22. Status] Structure: Determined Reproducibility: Confirmed Statistics: Determined

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"Analytical model for Type 2 Diabetes in the Caucasian population, focusing on the causal relationship between insulin resistance and lipid overload."

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