A high oxidised frying oil content diet is less adipogenic, but induces glucose intolerance in rodents

Oxidised frying oil (OFO) and fish oil have been shown to be peroxisome proliferator-activated receptor (PPAR)a activators and their ingestion results in pleotropic peroxisome proliferator responses in rats. To examine the effect of dietary OFO on adiposity, four groups of weanling Sprague-Dawley rats were fed isoenergetically with, respectively, a low fat basal diet containing 5 g/ 100 g of fresh soybean oil (LSB) or a high fat diet containing 20 g/100 g of fresh soybean oil (HSB), OFO (HO) or fish oil (HF). The tissue mass, cell size and lipid/DNA ratio in the retroperitoneal fat pad and serum leptin levels were lowest in the HO group (P< 0 center dot 05), indicating that dietary OFO has a greater anti-adipogenic action than dietary fish oil. However, a tendency to hyperglycaemia was observed in the HO group (P=0 center dot 0528). To examine the effect of dietary OFO on glucose tolerance, three groups of rats and three groups of mice were fed, respectively, the LSB, HSB or HO diet, and an oral glucose tolerance test was performed. After oral glucose load, the area under the curve for blood glucose (AUC(glu)) over 2 h was significantly higher, and that for serum insulin (AUC(ins)) over 90 min was significantly lower, in the HO group than in the other two groups (P< 0 center dot 05). These results demonstrate that, in rats and mice, a high OFO diet is less adipogenic, but induces glucose intolerance.