Quick answer

Paired fasting insulin + glucose yields HOMA-IR — quantifying how hard your pancreas works to hold sugar steady. Elevated insulin with NORMAL glucose marks compensated resistance: the earliest metabolic warning available, decades before diabetes.

The compensation concept

Beta-cells overproduce insulin to force resistant tissues responding — glucose stays normal WHILE insulin climbs. This compensation phase lasts years-decades, offering enormous intervention windows invisible to glucose-only testing. Eventually output falters, glucose rises, diabetes announces itself late.

Calculating and interpreting HOMA-IR

HOMA-IR = (fasting glucose × fasting insulin) ÷ 405 (mg/dL units). Interpretation bands: <1.0 optimal insulin sensitivity · 1.0–1.9 average · 1.9–2.9 early resistance · >2.9 significant resistance. Fasting state non-negotiable — post-meal samples destroy the calculation's validity.

Who benefits from testing

Central-weight-gain strugglers, PCOS patients (near-universal resistance), family-history-heavy diabetes backgrounds, acanthosis nigricans carriers, hypertension/metabolic-cluster members, and anyone tracking longevity metrics seriously. Also monitors INTERVENTION efficacy — resistance measurably reverses with weight/exercise within 8–12 weeks.

Downstream companions worth adding

Resistance travels with entourage: triglycerides rise, HDL falls, liver fat accumulates (ALT bumps), uric acid climbs, inflammatory markers hum. Testing the cluster contextualizes HOMA-IR and identifies which downstream dominoes already toppled.

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Frequently asked questions

My glucose is 92 but insulin is 22 — fine?

HOMA-IR ≈ 5.0 — significantly resistant despite 'normal' glucose. This is precisely the compensated phase the test exposes.

Can thin people be insulin resistant?

TOFI phenotype (thin-outside-fat-inside) exists — sedentary normal-BMI individuals with visceral/hepatic fat register resistance identically.