Center for Advanced Orthopedic Studies, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
Bone. 2012 Feb;50(2):444-51. doi: 10.1016/j.bone.2011.06.019. Epub 2011 Jun 24.
Early life nutrition has substantial influences on postnatal health, with both under- and overnutrition linked with permanent metabolic changes that alter reproductive and immune function and significantly increase metabolic disease risk in offspring. Since perinatal nutrition depends in part on maternal metabolic condition, maternal diet during gestation and lactation is a risk factor for adult metabolic disease. Such developmental responses may be adaptive, but might also result from constraints on, or pathological changes to, normal physiology. The rising prevalence of both obesity and osteoporosis, and the identification of links among bone, fat, brain, and gut, suggest that obesity and osteoporosis may be related, and moreover that their roots may lie in early life. Here we focus on evidence for how maternal diet during gestation and lactation affects metabolism and skeletal acquisition in humans and in animal models. We consider the effects of overall caloric restriction, and macronutrient imbalances including high fat, high sucrose, and low protein, compared to normal diet. We then discuss potential mechanisms underlying the skeletal responses, including perinatal developmental programming via disruption of the perinatal leptin surge and/or epigenetic changes, to highlight unanswered questions and identify the most critical areas for future research.
早期营养对产后健康有重要影响，营养不足和过剩都与永久性代谢变化有关，这些变化会改变生殖和免疫功能，并显著增加后代患代谢疾病的风险。由于围产期营养部分取决于母体的代谢状况，因此母体在妊娠和哺乳期的饮食是成年代谢疾病的一个风险因素。这种发育反应可能是适应性的，但也可能是由于对正常生理的限制或病理性改变造成的。肥胖症和骨质疏松症的发病率不断上升，以及骨骼、脂肪、大脑和肠道之间联系的确定，表明肥胖症和骨质疏松症可能有关联，而且它们的根源可能在于生命早期。在这里，我们重点关注母体在妊娠和哺乳期的饮食如何影响人类和动物模型的代谢和骨骼获取的证据。我们考虑了总热量限制以及宏量营养素失衡（包括高脂肪、高蔗糖和低蛋白）与正常饮食相比的影响。然后，我们讨论了骨骼反应的潜在机制，包括通过破坏围产期瘦素激增和/或表观遗传变化进行围产期发育编程，以突出未解决的问题并确定未来研究的最关键领域。
