| Objective With the improvement of living standards,change the way of life,worldwide,the incidence of abnormal glucose tolerance during pregnancy has soared,abnormal glucose tolerance during pregnancy for the mother and child will produce adverse effects,to explore the different feeding mode impact on children’s abnormal glucose tolerance during pregnancy and its mechanism of action,is conducted in this study.In this study,a model of abnormal glucose tolerance in pregnant mice was established by feeding high-fat diets during pregnancy.By observing the glucose and lipid metabolism in offspring mice and the protein expression in the liver AMPK/ACC signaling pathway,the effects of different dietary patterns on glucose and lipid accumulation in offspring mice and related mechanisms were explored.Methods7-week old C57BL/6J mice were selected for the experiment,and were fed adaptively for one week.After 10 days of feeding,mice in the model group fed with high-fat diet and the control group fed with normal diet were caged at 2:1 for male and female.After successful conception,the mice were fed normal diet and given an oral glucose tolerance test(OGTT)at D20: before the experiment,the mice were fasted for 16 hours and weighed and recorded.Trace blood was collected from the tail vein of the mice to detect the fasting blood glucose value.Then the blood glucose value at each time point0,30,60 and 120 min after the infusion of glucose was detected and recorded accordingto the weight of the mice and the standard of 10μl/g.The abnormal value was selected as the model group.The successful model group was divided into model control group,model high-fat group,model high-fiber group and model caloric restriction group.A conventional control group was also included.The first five weeks of normal feed,the sixth week of intervention,each group was fed with a different feed,feeding to the 12 th week of subdivision.The body weight of the mice was recorded,and the eyeball blood,liver,fat,kidney,spleen and pancreas were collected.Western Blot was used to detect fat transport-related proteins(AMPKα1,ACC,p-ACC,p-AMPKα1)in mouse liver.MRNA expression of AMPK 1 and ACC in liver fat was detected by q RT-PCR.Results(1)Relevant indicators for model construction: The blood glucose level of female rats in the model group during pregnancy was significantly higher than that of the control group(P <0.05);OGTT experiments on the 20 th day of pregnancy showed that the blood glucose of the model group was 0,30,60,and 120 minutes.The values??increased first and then decreased gradually,but the blood glucose level of the female mice in the model group was higher than that of the control group(P <0.05).The area under the AUC curve was as follows: model group> control group(P <0.05);serum insulin levels and The insulin resistance index model group was significantly higher than the control group(P <0.05).The above results prove that the glucose tolerance model during pregnancy has been successfully constructed.(2)Offspring mouse body weight and blood glucose indicators: The body weight of the mice showed a difference at the seventh week,and the model high-fat group was higher than the conventional control group(P <0.05);the model was higher at eight,nine,ten,and eleven weeks.The fat group was significantly higher than the conventional control group and the model calorie-restricted group(P <0.05).At the twelfth week,the mice in the model calorie-restricted group had the lowest weight,and the model high-fat grouphad the highest weight.There were differences between them(P <0.05).In the model high-fat group,the blood glucose value of the mice increased rapidly in the early stage,then gradually flattened,and was significantly higher than the other four groups(P<0.05).The blood glucose values of the mice in the model calorie-restricted group and the model cellulose group showed a slight downward trend.At 12 weeks,the blood glucose levels of the two groups were lower than those of the conventional control group(P <0.05).(3)Four related indexes of blood lipids in offspring mice: the levels of TCH,TG,LDL-C in the high-fat group of the model increased,and HDL-C decreased,which was statistically different from the conventional control(P <0.05);model calorie limit The levels of TCH,TG,and LDL-C in the group decreased,while the levels of HDL-C increased.Compared with the conventional control,the difference was statistically significant.There were no significant differences between the four indicators of blood lipids in the model high-fiber group and the conventional control group(P> 0.05).(4)Offspring mouse organ indicators: the weight of liver,fat and spleen of the model high-fat group was significantly higher than that of the conventional control group(P<0.05),and the weight of the kidney and pancreas was not significantly different from that of the conventional control(P> 0.05);The liver weight of mice in the model calorie-restricted group was lower than that in the conventional control group(P <0.05),and the weights of fat,kidney,spleen,and pancreas were not significantly different from those in the conventional control(P> 0.05);Routine control group(P <0.05).(5)AMPK-ACC pathway-related indicators: AMPKα1,p-AMPKα1,and ACC expressed protein concentrations in liver tissue of model high-fat mice were decreased,compared with the conventional control group(P <0.05);In comparison,AMPKα1 and p-AMPKα1 protein expressions were up-regulated in the liver tissues of the model caloric-restricted group and the model high-fibre group(P <0.05).Compared with the model high-fat group,the model calorie-restricted group significantly increased thep-ACC protein concentration in liver tissues,and the difference was statistically significant(P <0.05).Conclusion Dietary intervention can change the glycolipid metabolism of the offspring with abnormal glucose tolerance during pregnancy.The high-fat diet reduced the protein concentrations of AMPKα1 and p-AMPKα1 in the liver,resulting in decreased fat and carbohydrate metabolism and lipid accumulation.Caloric restricted diet and high-fiber diet enhanced the protein concentrations of AMPKα1 and p-AMPKα1to a certain extent.The metabolic cycle of fats and carbohydrates through AMPK/ACC pathway effectively improved lipid accumulation. |
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