Broskey · Nutrition & metabolism 2018 · cross-sectional comparative study · n=86

Metabolic inflexibility in women with PCOS is similar to women with type 2 diabetes.

Cited 24 times in the scientific literature.

Level 4 - case-series / case-control

Cross-sectional comparative physiological study across clinical cohorts

PubMed 30377436 · doi:10.1186/s12986-018-0312-9 · record verified 2026-08-26

What was done

Researchers evaluated metabolic flexibility (the ability to switch from fat oxidation in the fasted state to carbohydrate oxidation in the fed state) in 86 weight-stable women categorized into four groups: PCOS (n = 30), obesity without diabetes (n = 12), type 2 diabetes (T2DM, n = 27), and normal BMI controls (n = 17). All participants underwent indirect calorimetry to measure substrate oxidation alongside a hyperinsulinemic euglycemic clamp to assess insulin sensitivity. Analyses adjusted for age, ethnicity, and BMI, and women with PCOS were further stratified by insulin resistance status.

What was found

Women with PCOS demonstrated significantly lower metabolic flexibility compared to healthy women with obesity (p < 0.0001) and normal BMI controls (p < 0.0001). After adjusting for glucose disposal rate, metabolic flexibility in PCOS was similar to women with T2DM (p = 0.99). Within the PCOS group, insulin-resistant women had lower non-oxidative glucose metabolism (p = 0.0001), lower metabolic flexibility (p = 0.007), higher percent free testosterone (p = 0.04), higher free androgen index (p = 0.006), and more visceral adipose tissue (p = 0.02) compared to non-insulin-resistant women with PCOS. Absolute mean values and effect sizes were not reported in the abstract.

Why it matters

This study demonstrates that the impairment in substrate switching seen in PCOS is as severe as that in type 2 diabetes and is tightly linked to the degree of insulin resistance, visceral adiposity, and hyperandrogenism rather than body mass index alone.

Limits

The study is cross-sectional, precluding causal conclusions regarding whether androgen excess causes metabolic inflexibility or vice versa. Subgroup sample sizes were modest, particularly the obesity comparator group (n = 12), and the abstract does not report baseline clinical characteristics, absolute calorimetry metrics, or confidence intervals.

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