Few research have looked at the effect of insulin on substrate usage in PCOS women. There is no data on women with distinct PCOS phenotypes in specific. The study’s goal was to look at how insulin affects glucose (Gox) and lipid (Lox) oxidation, nonoxidative glucose metabolism (Gnonox), and serum free fatty acids (FFAs) in people with PCOS. 187 nondiabetic women with PCOS diagnosed using the Rotterdam criteria were included in the study. As a baseline, data from a previous sample of 20 healthy women was used. The hyperinsulinemic euglycemic clamp in conjunction with indirect calorimetry was used to acquire whole-body substrate consumption data. Liquid chromatography–mass spectrometry and equilibrium dialysis were used to analyse serum androgens. In each PCOS phenotype, hyperinsulinemia changed the rise of Gox (Gox), Gnonox, as well as the suppression of Lox (Lox) and serum FFA (percent FFA). Furthermore, Gnonox and percent FFA were lower in women with the classic phenotype compared to those with the ovulatory or normoandrogenic phenotypes, and Gox was lower in women with the classic phenotype compared to those with the ovulatory phenotype. Fat mass and free testosterone were independent predictors of Gox, Gnonox, and percent FFA in multivariable analysis, but only fat mass predicted Lox.
Insulin-mediated substrate utilisation is impaired in women with PCOS, independent of phenotype. Individuals with the traditional phenotype are more prone to this occurrence. In insulin action anomalies in glucose and lipid metabolism, free testosterone has an independent function.