Women with polycystic ovary syndrome have intrinsic insulin resistance on euglycaemic-hyperinsulaemic clamp.
Level 4 - case-series / case-control
Cross-sectional comparative study with BMI-matched controls
PubMed 23315061 · doi:10.1093/humrep/des463
What was done
A cross-sectional study evaluated 40 women with polycystic ovary syndrome (PCOS, diagnosed via Rotterdam criteria; 20 lean, 20 overweight) and 33 BMI-matched controls (19 lean, 14 overweight) in an academic clinic setting. All participants underwent a 3-month washout period off insulin sensitizers and oral contraceptive pills. Insulin sensitivity was quantified via glucose infusion rate (GIR) using a euglycaemic-hyperinsulinaemic clamp.
What was found
PCOS status and BMI independently contributed to insulin resistance (IR; main effect P < 0.001). IR was present in 75% of lean PCOS, 62% of overweight controls, and 95% of overweight PCOS. Mean (± SD) GIR values (mg min⁻¹ m⁻²) were 339 ± 76 in lean controls, 270 ± 66 in lean PCOS, 264 ± 66 in overweight controls, and 175 ± 96 in overweight PCOS. The negative relationship between BMI and GIR was more pronounced in PCOS (y = 445.1 - 7.7x, R² = 0.42, P < 0.0001) than in controls (y = 435.5 - 4.6x, R² = 0.04, P < 0.01).
Why it matters
Using gold-standard clamp methodology, this study demonstrates that insulin resistance is an intrinsic feature of Rotterdam-diagnosed PCOS in both lean and overweight women, and that excess adiposity compounds this metabolic defect more severely than in healthy controls.
Limits
The study had a modest sample size (n = 73 across four subgroups), lacked matching for body composition and age, and did not use glucose tracer techniques to fully characterize peripheral versus hepatic insulin resistance.
Cited by
- supports Approximately 80% of individuals with PCOS have insulin resistance.