Impairment of glucose metabolism in mice induced by dietary oxidized frying oil is different from that induced by conjugated linoleic acid.

Objective: We previously reported that a diet high in oxidized frying oil (OFO) is less adipogenic but induces glucose intolerance in rodents, a situation somewhat is similar to that in conjugated linoleic acid (CLA)-fed mice. The present study compared the lipid and glucose metabolism effects of dietary OFO and CLA to clarify how the OFO diet compromises glucose tolerance.

Methods: C57BL/6J mice were divided into four groups in which the CLA and CLA control (CC) groups received a low-fat diet supplemented with or without 1 g/100 g of CLA (1:1 mixture of cis-9, trans-11 and trans-10, cis-12), and the OFO and OFO control (CO) groups received a high-fat diet containing 20 g/100 g of OFO or fresh soybean oil, respectively.

Results: When compared with their respective controls (CLA versus CC and OFO versus CO), the OFO and CLA diets resulted in deprivation of adipose and downregulation of adipocyte marker genes, but a totally different response of lipid metabolism in the liver was observed, i.e., anabolism was enhanced by the CLA diet but catabolism was enhanced by the OFO diet. In contrast to the insulin resistance that occurred in CLA-fed mice, the glucose intolerance induced by the OFO diet was accompanied by decreases in insulin and C-peptide levels during an oral glucose tolerance test. Analysis of vitamin E and thiobarbituric acid-reactive substances in the liver showed the OFO diet, but not the CLA diet, compromised vitamin E status.

Conclusion: The impaired glucose metabolism resulting from OFO feeding is not related to CLA. In contrast to the hyperinsulinemia and insulin resistance induced by the CLA diet, the OFO diet-induced glucose intolerance is mediated by impairment of insulin secretion.