Background: Postprandial hypertriglyceridaemia is an independent risk factor for cardiovascular diseases. An acute rise of insulin in the fed state suppresses hormone-sensitive lipase to inhibit free fatty acids (FFAs) mobilisation from adipose tissue, and up-regulates lipoprotein lipase to increase FFAs influx to adipose tissue from chylomicrons, that is blunted in insulin resistant states. Polycystic ovary syndrome (PCOS) is associated with insulin resistance and cardiovascular risk markers and therefore may have an exaggerated postprandial hypertriglyceridaemia akin to diabetes mellitus.
Methods: Nine patients with PCOS fulfilling all the three criteria of Rotterdam consensus statement and 7 controls were recruited after informed consent. All patients underwent a high fat meal test after an overnight fast. A 900 kcal meal was given and bloods were taken at baseline, half hourly for 3 h and hourly for a further 3 h.
Results: The age (PCOS versus controls) (mean±S.D.) (31.4±3.5 vs 31.5±6.5 year, P=0.27) and body mass index (31.4±3.5 vs 33.7±5.5 kg/m2, P=0.33) were comparable between the two groups. The free androgen index (13.8±2.4 vs 6.3±1.7, P=0.02), androstenandione (10.8±2.8 vs 7.8±2.7 nmol/l P=0.04), dihydroepiandostenedione sulphate (6.7±0.5 vs 4.8±0.8 μmol/l P=0.05) were higher in PCOS women. Fasting glucose and lipid profile including triglyceride, total cholesterol, HDL-C and LDL-C were comparable between the two groups. The median and interquartile range of triglyceride area under the curve (AUC) were significantly higher in the PCOS group (11.9, 9.0, 13.6 vs 6.4, 4.8, 7.6 mmol/l/6 h, P=0.04) but of FFAs AUC were not significantly different (1373, 1118, 1643 vs 1190, 1131, 1411 μmol/l/6 h P=NS).
Conclusion: Postprandial hypertriglyceridaemia is higher in patients with PCOS compared to normal women and could potentially contribute to their higher cardiovascular risk.