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研究母鼠高脂饮食导致子代大鼠产生胰岛素抵抗(IR)的机制,包括母体高脂饮食摄入造成子代大鼠发育编程异常和成年后的代谢疾病,以及对子代大鼠骨骼肌和脂肪组织发育相关基因的影响。将雌性SD大鼠随机分为2组,NC组喂以标准饲料,高脂组喂以高脂饲料,整个过程监控动物体质量、生化指标、口服糖耐量(OGTT)并计算胰岛素敏感指数(ISI)。与正常雄鼠交配后,繁殖子鼠按性别和母鼠来源分为4组:正常雌性组、正常雄性组、高脂雌性组和高脂雄性组。子代大鼠断奶后喂以标准饲料18周,同样监控体质量、生化指标、OGTT和ISI。处死动物后,获取股四头肌并观察其细胞核和线粒体形态。另外检测子代大鼠在胚胎和胎儿阶段的脂肪和肌肉发育的基因表达情况。结果表明:高脂母鼠及其子鼠显示出明显的IR症状,而母鼠高脂饮食摄入使子鼠在胚胎胎儿阶段的脂肪和肌肉发育的基因表达受到严重干扰。研究结果说明,高脂的宫内环境可能通过影响脂肪和肌肉发育导致子鼠产生IR。
To study the mechanism of insulin resistance (IR) induced by high-fat diets in offspring of mothers, including abnormal developmental programming in adult offspring and metabolic disorders in adult rats caused by high fat diet, and on skeletal muscle And adipose tissue development-related genes. The female SD rats were randomly divided into two groups. The rats in NC group were fed with standard diet and the high-fat diet group were fed with high-fat diet. The body weight, biochemical indexes and oral glucose tolerance (OGTT) were monitored during the whole process and insulin sensitivity index ). After mating with normal males, the offspring mice were divided into 4 groups according to sex and maternal origin: normal female group, normal male group, high fat female group and high fat male group. Offspring rats were fed a standard diet for 18 weeks after weaning, with similar monitoring of body weight, biochemical parameters, OGTT and ISI. After the animals were sacrificed, the quadriceps femoris was harvested and its nucleus and mitochondrial morphology were observed. In addition, the gene expression profiles of fat and muscle development in offspring and fetus were detected. The results showed that hyperlipidemic rats and their offspring showed obvious IR symptoms, while the high fat diet in maternal rats severely interfered with the gene expression of fat and muscle during embryonic fetal stage. The results suggest that high-fat intrauterine environment may cause IR in the offspring by affecting fat and muscle development.