Effect Of High Fat Dietand Oxidated Protein On Small Mice Gut Flora And Redox State

Over taking of fat can cause imbalance of gut flora and oxidated stree then cause（metabolic syndrome. MS）. If the exces fat in the diet and oxidated animal protein will inducegrowth of bacteria producing oxygen free radical （ROS） in colon and inhibite sensitivecommensal bacteria （such as lactobacilli and Bacillusbifidus）, which might cause colonic OSand onset of MS is not being studied systematically.In1^stexpriment, mice were adminstrated with high fat diet （HFD） or that added with oneof four antioxidants with low bioavailability. The results show that high fat diet inducedmalondialdehyde （MDA） formation and inhibited total antioxidation capacity （T-AOC） inmice colon, decreased lacbacilli and induced growth of Escherichia coli and enterococcus.Lipoic acid and resveratrol （RES） significantly prevent colonic ROS and disturbance of flora.All antioxidants, especifically for RES, inhibited MDA. Correlation analysis showed that bothE. coli and enterococcus were positivly correlated with colonic ROS and MDA. Colonlactobacilli were positivly correlated with colonic T-AOC. These results suggested that highfat induced OS and flora disturbance in colon, with was prvented by antioxidants dependingon the type.In2^ndexpriment, HFD treated mice was divided into three group group according weightincluding obesity （OB）, sub-obesity （sub-OB） and obesity-resistant （OB-Re） mic, wich wastreated with HFD containing0.03%of0.06%Res. The results showed that lactobacilli inobesity mice was signaificantly lower than that in the other two gourps （P<0.05）. T-AOC wasalso low in its colon lumen. HFD with0.06%Res significantly increase lumen T-AOC in OB,sub-OB and OB-Re mice by256%,147%and335%. There was a negative correlationbetween colon lactobacilli and ROS, between lactobacilli and E. coli or enterococcus, and itwas positivly correlated with lumen T-AOC. Enterococcus was positivly correlated with colonROS. Results suggest that decrease of colon lumen T-AOC and lactobacilli might be relaed toonset of OB. Re would in colon lumen and effect differently on bacteria and inhibited obesity.In3^rdexpriment, H₂O₂/Cu²⁺, HClO and MDA were used to modify casein to mimicoxidation of animal protein during storage and process. All these treatment, especially forHClO, increased carbonyl （P <0.05）. HClO oxidated casein had low digestibility, tyrosineand cysteine （P <0.05）, which decreased colon lactobacilli in mice. The survived lactobacillishowed high antioxidant ability. E. coli and enterococcus was increased accompany withdecrease of T-AOC in both colon lumen and mucosa. Digestibility of modified protein wasnegativly and positivly correlated with lactobacilli and with E. coli and enterococcus,respectively. T-AOC of colon lumen was negativly and positivly correlated with enterococcusand lactobacilli, respectively. These results suggest that excess animal protein induced growthof bacteria produing ROS, such as E. coli and enterococcus, in colon and inhited growth ofOS sensitive lactobacilli, which caused ROS in mucosa. Finally, in vivo fermental researchwas done and the result was consistant with the one in vitro.In conclusion,1) HFD caused colonic ROS by induced growth of ROS producingbacteria and inhibiton of ROS sensitive lactobacilli that dcrease lumen T-AOC.2) Resveratrol reached colon lumen and regulated redox state both in lumen and mucosa and prevent floradisturbance.3) Oxidated animal protein with low digestibility induce flora disturbance whichcaused ROS in colon.