早期营养过剩所致母鼠肥胖对子代小鼠代谢特征的影响

Effects of chronic postnatal overnutrition-induced maternal obesity on metabolic features in offspring

目的探讨母鼠肥胖及高脂饮食对子代小鼠代谢特征的影响。方法将正常体质量ICR母鼠(对照组,即CTR组)及采用早期营养过剩方法建立的肥胖母鼠(早期营养过剩组,即CPO组)分别与同龄正常雄性ICR小鼠交配。将两组雄性子代断乳后随机分为高脂饲料组(CTR-H组和CPO-H组)和标准饲料组(CTR-S组和CPO-S组),分别饲喂高脂饲料或标准饲料至5月龄。哺乳结束(21 d)测定母鼠体质量、肝/体质量和腹部脂肪/体质量。不同饲料喂养10周后,对子代小鼠进行葡萄糖耐量试验,5月龄时测定空腹血糖及血清胰岛素水平,计算胰岛素抵抗指数(IRI)。苏木精-伊红(HE)染色后观察子代小鼠腹部脂肪组织细胞形态,比较脂肪细胞面积。结果 CPO组母鼠体质量、肝/体质量及腹部脂肪/体质量均显著高于CTR组(P<0.05)。不同饲料喂养10周后,CPO组子代小鼠存在糖耐量受损情况,CPO-H组糖耐量损伤更严重。CTR-H组和CPO-H组小鼠空腹血糖水平和IRI分别高于CTR-S组和CPO-S组(P<0.01);CPO-H组小鼠血清胰岛素水平高于其他组(P<0.01)。CTR-H组和CPO-H组小鼠腹部脂肪细胞面积分别大于CTR-S组和CPO-S组(P<0.01),CPO-S组大于CTR-S组(P<0.01),CPO-H组大于CTR-H组(P<0.01)。结论母鼠肥胖能够增加子代小鼠肥胖和发生代谢紊乱的风险,在高脂饲料喂养时更为显著。

Objective To investigate the effects of maternal obesity and high-fat diet on the metabolic features in offspring mice. Methods Female ICR mice with normal body weight （control group, or CTR group） and obese mice induced by chronic postnatal overnutrition （postnatal overnutrition group, or CPO group） were selected to mate with normal male ICR mice of the same age. Male litters in both groups were randomly divided into high-fat diet group （CTR-H group and CPO-H group） and standard chow diet group （CTR-S group and CPO-S group） at the end of breast feeding, and were managed with with high-fat diet and standard chow diet respectively till 5 months of age. The body weight, liver/body weight and abdominal fat/body weight of female mice were measured after breast feeding （21 d）. Ten weeks after feeding with different diet, glucose intolerance test of offspring mice was performed, fasting blood glucose and serum insulin were examined, and insulin resistant index （IRI） was calculated. The histological features of abdominal tissues of offspring mice were observed with HE staining, and the areas of adipocytes were compared. Results The body weight, liver/body weight and abdominal fat/body weight of maternal mice in CPO group were significantly higher than those in CTR group （P〈0.05）. Ten weeks after feeding with different diet, there was impaired glucose tolerance in the offspring mice from CPO group, and that was more severe in CPO-H group. The fasting blood glucose and IRI in CTR-H group and CPO-H group were higher than those in CTR-S group and CPO-S group respectively （P〈0.01）. The serum insulin in CPO-H group was higher than those in the other groups （P〈0.01）. The areas of abdominal adipocytes in CTR-H group and CPO-H group were larger than those in CTR-S group and CPO-S group respectively （P〈0.01）, the area of abdominal adipocytes in CPO-S group was larger than that in CTR-S group （P〈0.01）, and the area of abdominal adipocytes in CPO-H group was larger than that in CTR-H group （P〈0.01）. Conclusion Maternal obesity may contribute to the development of obesity and metabolic dysfunctions in their offspring, and the impact may be exacerbated by high-fat diet feeding.