Effect of Oxidized Frying Oil Consumption on Insulin Secretion by Pancreatic β-cells

• Main Authors: Ya-Fan Chiang, 蔣亞帆
• Other Authors: Pei-Min Chao
• Format: Others
• Language: zh-TW
• Published: 2009
• Online Access: http://ndltd.ncl.edu.tw/handle/99545142340967374493

碩士 === 中國醫藥大學 === 營養學系碩士班 === 97 === Being crisp and aromatic, fried foods are popular with consumers world-wide while the safety concerns about the ingestion of oxidized frying oil (OFO) are still raised. We had previously shown that OFO ingestion can influence lipid and glucose metabolism. Dietary OFO increases fatty acids oxidation in liver by activating peroxisome proliferator-activated receptor α. However, accompanied with TG reductions, glucose intolerance is observed in OFO-fed rodents. Since the serum levels of insulin and C-peptide in oral glucose tolerance test were both decreased in OFO-fed mice, we speculated the reduced ability to secrete insulin caused by dietary OFO is associated with oxidative damages and/or inflammatory responses of the pancreas. Accordingly, this study was aimed at investigating the underlying mechanisms of insulin secretion impairment associated with OFO consumption. To test the involvement of oxidative stress in pancreatic islets, Experiment I was conducted by dividing C57BL/6J mice into LF, HF and HO groups which received a basal diet containing 5 g/100 g fresh soybean oil or high fat diets containing 20 g/100 g of fresh soybean oil or OFO respectively. When glucose intolerance and hypoinsulinemia were observed in HO group (2 months of feeding), all mice were killed and their pancreatic islets were isolated. Results showed glucose stimulated insulin secretion (GSIS) of islets, both in the first phase and second phase, was significantly reduced in HO group compared with the other two groups (P<0.05),. The total insulin content in islets of HO group was not different from that of HF group, but was significantly lower than that of LF group (P<0.01). For oxidative indexes, livers vitamin E and TBARS in HO group were significantly lower (P<0.001) and higher (P<0.0001), respectively, than those of other groups. A higher oxidative stress was observed not only in livers, but also in pancreatic islets of HO group. Compared to HF or LF groups, the lipid hydroperoxide was increased, and the glutathione peroxidase-1 activity and total antioxidant capacity (HO vs. LF, P<0.05) was decreased in islets of HO groups. Moreover, the vitamin E levels in the pancreas of HO group were significantly lower than that of HF group (P<0.0001). For inflammatory indexes, there was no significant difference between HO and HF groups in islets of TNF-α levels. The immunoblotting showed, the protein levels of phosphorylated c-Jun NH2-terminal kinase (JNK) tended to be higher (p=0.06), and the protein levels of pancreatic duodenal homeobox-1 (PDX-1) significantly lowered in HO group compared with the other two groups (p=0.055). Using qRT-PCR, the mRNA levels of UCP2 in islets of HO and HF groups were significantly higher than those of LF group, while no difference in mRNA levels of PDX-1 downstream genes (preproinsulin-1 and 2、glucokinase and GLUT2) was observed between groups. In Experiment II, we tried to investigate whether the impairment of insulin secretion by pancreatic islets associated with dietary OFO consumption could be reversed by supplementation of vitamin E in vitro or in vivo. For the in vitro supplementation study, islets separated from LF, HF and HO groups were incubated with or without the addition of vitamin E (100 μM). The improvement of GSIS due to vitamin E supplementation was only observed in LF group, but not in HF and HO group. In in vivo supplementation study, mice were separated into HO, HF, HO+E and HF+E groups, with a dietary supplementation of 10-fold higher AIN-76 recommended vitamin E for the latter two groups. Results showed that the vitamin E supplementation not only corrected the vitamin E status in livers and pancreas of OFO-treated mice (P<0.0001), but also alleviated the reduction of serum levels of insulin, and GSIS caused by dietary OFO. In conclusion, this study provided evidences that dietary OFO-induced glucose intolerance and hypoinsulinemia was associated with oxidative damages of pancreatic islets, thus leading to GSIS impairment. Oral supplementation of vitamin E can partly overcome the OFO mediated GSIS impairment.