Department of Obstetrics and Gynecology, The Lundquist Institute at Harbor-UCLA Medical Center, Torrance, California, USA; and David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California, USA.
Nutr Rev. 2020 Dec 1;78(Suppl 2):25-31. doi: 10.1093/nutrit/nuaa121.
In the United States and Mexico, the obesity epidemic represents a significant public health problem. Although obesity is often attributed to a Western-style, high-fat diet and decreased activity, there is now compelling evidence that this, in part, occurs because of the developmental programming effects resulting from exposure to maternal overnutrition. Human and animal studies demonstrate that maternal obesity and high-fat diet result in an increased risk for childhood and adult obesity. The potential programming effects of obesity have been partly attributed to hyperphagia, which occurs as a result of increased appetite with reduced satiety neuropeptides or neurons. However, depending on maternal nutritional status during the nursing period, the programmed hyperphagia and obesity can be exacerbated or prevented in offspring born to obese mothers. The underlying mechanism of this phenomenon likely involves the plasticity of the appetite regulatory center and thus presents an opportunity to modulate feeding and satiety regulation and break the obesity cycle.
在美国和墨西哥，肥胖症是一个严重的公共卫生问题。虽然肥胖通常归因于西式高脂肪饮食和活动量减少，但现在有确凿的证据表明，部分原因是由于母体营养过剩导致的发育编程效应。人体和动物研究表明，母体肥胖和高脂肪饮食会增加儿童和成人肥胖的风险。肥胖的潜在编程效应部分归因于过度摄食，这是由于食欲增加而饱食感神经肽或神经元减少所致。然而，根据哺乳期母体的营养状况，肥胖母亲所生后代的编程性过度摄食和肥胖可以被加剧或预防。这种现象的潜在机制可能涉及食欲调节中心的可塑性，因此为调节进食和饱腹感调节提供了机会，并打破肥胖循环。
