氧化炸油對營養代謝之干擾：單一代與兩代研究

Impacts of Dietary Oxidized Frying Oil on Nutrient Metabolism: Single- and Two-Generation Studies

油炸是常見的烹調方式，氧化炸油（oxidized frying oil;OFO）隨著食物吸附而食入人體，其安全性廣受大眾注意。本回顧簡介油炸過程油脂化學反應與成分變化—包括營養素改變及有物生成、攝食OFO飲食對營養代謝之干擾，及其對子代之影響。當動物給予等量OFO或新鮮油相比，常見肝脂、血脂與體脂降低，這是因為OFO中氧化脂肪酸活化peroxisome proliferator-activated receptor轉錄因子，促進脂質走向異化代謝；但攝食OFO鼠會發展為葡萄糖不耐及胰島素分泌不足，這與過氧化壓力損傷胰臟細胞有關；此外OFO飲食藉由誘發肝臟細胞色素P450解酵素，可能促進維生素E與A的異化分解。近年我們研究懷孕期間給予OFO飲食對於子代成年後的肥胖敏感性，結果雄性子代有不易胖特質，可能與促進脂質異化與生熱有關。若是將OFO中極性化合物（polar compounds;PC）分離出，餵予懷孕母鼠，則觀察到畸胎，推測是PC透過xenobioticreceptors，干擾維生素A酸代謝。有關OFO或PC引起的促進脂肪酸與維生素Ａ異化分解、畸胎及抑制胚胎或新生兒生長，非補充抗氧化劑能夠克服。

Deep-fried foods are very popular, but the safety of oxidized frying oil（OFO）, which is ingested with fried food, is always a concern. This review summarizes the chemical reactions and changes in levels of nutrients and toxicants in the oil during deep-fat frying, the interference with nutrient metabolism after ingestion of an OFO-containing diet, and the impacts on offspring of mothers who received an OFO diet. When rodents fed diets with equal amounts of OFO or fresh oil were compared, lower plasma and liver lipid concentration and less adiposity were consistently observed in the OFO-fed group. This can be attributed to peroxisome proliferator-activated receptor（PPAR）, which is activated by the oxidized fatty acids in the OFO, thus increasing lipid catabolism. However, glucose intolerance and insulin deficiency were observed in rodents fed the OFO diet. This was demonstrated to be caused by oxidative stress-associated -cell dysfunction. OFO-induced cytochrome P450-detoxifying enzymes are believed to be involved in the increased catabolism of vitamins E and A. Recently, we studied whether maternal ingestion of OFO during pregnancy influenced the susceptibility to diet-induced obesity in the adult offspring. The resistance to diet-induced obesity was seen in male offspring, which was ascribed to the increased lipid catabolism and heat thermogenesis. In addition, polar compounds（PCs）isolated from the OFO were found to be teratogenic. This phenomenon might be associated with a disturbance of retinoic acid（RA）metabolism via modulation of xenobiotic receptor activity by OFO or PCs. The detrimental effects related to OFO or PC ingestion, including disturbance of RA metabolism, teratogenesis, and retardation of fetal growth, could not be overcome by antioxidant supplementation.