Obesity is a chronic multifactorial disease and is currently a public health problem. Maternal obesity during pregnancy is more dangerous as it impairs the health of the mother and future generations. Obesity leads to several metabolic disorders. Since white adipose tissue is an endocrine tissue, obesity often leads to disordered secretion of inflammatory, glycemic, lipid and renin–angiotensin system (RAS) components. The RAS represents a link between obesity and its metabolic consequences. Therefore, our goal was to evaluate the possible changes caused by a high-fat diet in RAS-related receptor expression in the uterus and placenta of pregnant mice and determine the underlying effects of these changes in the fetuses’ body composition. Breeding groups were formed after obesity induction by high-fat (HF) diet. Dams and fetuses were euthanized on the 19th day of the gestational period. The HF diet effectively induced obesity, glucose intolerance and insulin resistance in mice. Fetuses born from HF dams showed increased body weight and adiposity. Both results were accompanied by increased AT₁R expression in placenta and uterus together with increased angiotensin-converting enzyme expression in the uterus and a decreased expression of MAS1 in placenta of HF dams. These results suggest a link between RAS, maternal obesity induced by HF diet and the fetuses’ body adiposity. This new path now can be more thoroughly explored.

肥胖是一种慢性多因素疾病，目前是公共健康问题。怀孕期间的孕妇肥胖更危险，因为它会损害母亲和子孙后代的健康。肥胖会导致几种代谢异常。由于白色脂肪组织是内分泌组织，因此肥胖通常会导致炎症，血糖，脂质和肾素-血管紧张素系统（RAS）成分的分泌紊乱。RAS代表肥胖与其代谢后果之间的联系。因此，我们的目标是评估高脂饮食引起的妊娠小鼠子宫和胎盘RAS相关受体表达的可能变化，并确定这些变化对胎儿身体成分的潜在影响。通过高脂饮食诱导肥胖后，形成繁殖群体。在妊娠期的第19天，对大坝和胎儿实施安乐死。HF饮食有效地诱发了小鼠的肥胖，葡萄糖耐受不良和胰岛素抵抗。HF大坝出生的胎儿体重和肥胖增加。两种结果均伴有AT升高HF大坝的胎盘和子宫中的₁ R表达以及子宫中血管紧张素转换酶的表达增加和MAS1的表达降低。这些结果表明，RAS，HF饮食诱发的孕妇肥胖与胎儿的身体肥胖之间存在联系。现在可以更彻底地探索这一新路径。