Relationship between altered postprandial lipemia and insulin resistance in normolipidemic and normoglucose tolerant obese patients

OBJECTIVE: Although there are changes in the postprandial lipid responses o f obese patients, these are closely associated with high fasting triglyceri des (TG). This study of 17 normotriglyceridemic, normglucose-tolerant andro id obese subjects (body mass index, BMI = 34.3 +/- 3.1 kg/m(2)) and 33 norm al-weight controls (BMI = 21.8 +/- 1.6 kg/m(2)) was done to examine their p ostprandial responses to an oral fat loading test containing retinol (890 c alories, 85% fat) and to evaluate the possible association between clinical and biological features of obesity and/or insulin resistance and postprand ial lipemia. SUBJECTS AND MEASUREMENTS: Blood samples were taken before giving the fat l oad and at 2,3,4,5,6 and 8 h after it. Insulin sensitivity was assessed usi ng HOMA, and TG and retinyl palmitate (RP) in the plasma, chylomicrons and non-chylomicron fractions were measured each time. RESULTS: The areas under the curves (AUC) of chylomicron TG for the obese a nd controls were not different, indicating adequate lipolytic activity. By contrast, the AUC for non-chylomicron TG was significantly greater in the o bese than in the controls (512 +/- 135 vs 429 +/- 141 mmol/l min, P < 0.01) . In addition, the AUC for RP in this same fraction was significantly lower in the obese than in the controls (103 +/- 55 vs 157 +/- 88 mg/l min, P < 0.05), suggesting that the TG from endogenous lipoproteins accounted for mo st of the increase in TG in the non chylomicron fraction. Parameters relate d to obesity showed no relationship with these postprandial abnormalities, whereas HOMA, which discriminated between the groups, partly explained (r(2 ) = 23%, P < 0.01) the significant increase in non-chylomicron TG. CONCLUSIONS: Android obese patients with a fasting TG in the normal range a nd not different from the Fasting TG of lean controls had an abnormal postp randial lipemia response, indicated by a significantly greater TG in the no nchylomicron subfraction than in controls. These alterations may be partly due to postprandial changes in endogenous lipoproteins as a consequence of insulin resistance.