White Melanie R, Yates Dustin T
Stress Physiology Laboratory, Department of Animal Science, University of Nebraska-Lincoln, Lincoln, NE, United States.
Front Physiol. 2023 Sep 1;14:1250134. doi: 10.3389/fphys.2023.1250134. eCollection 2023.
Intrauterine growth restriction (IUGR) arises when maternal stressors coincide with peak placental development, leading to placental insufficiency. When the expanding nutrient demands of the growing fetus subsequently exceed the capacity of the stunted placenta, fetal hypoxemia and hypoglycemia result. Poor fetal nutrient status stimulates greater release of inflammatory cytokines and catecholamines, which in turn lead to thrifty growth and metabolic programming that benefits fetal survival but is maladaptive after birth. Specifically, some IUGR fetal tissues develop enriched expression of inflammatory cytokine receptors and other signaling cascade components, which increases inflammatory sensitivity even when circulating inflammatory cytokines are no longer elevated after birth. Recent evidence indicates that greater inflammatory tone contributes to deficits in skeletal muscle growth and metabolism that are characteristic of IUGR offspring. These deficits underlie the metabolic dysfunction that markedly increases risk for metabolic diseases in IUGR-born individuals. The same programming mechanisms yield reduced metabolic efficiency, poor body composition, and inferior carcass quality in IUGR-born livestock. The ω-3 polyunsaturated fatty acids (PUFA) are diet-derived nutraceuticals with anti-inflammatory effects that have been used to improve conditions of chronic systemic inflammation, including intrauterine stress. In this review, we highlight the role of sustained systemic inflammation in the development of IUGR pathologies. We then discuss the potential for ω-3 PUFA supplementation to improve inflammation-mediated growth and metabolic deficits in IUGR offspring, along with potential barriers that must be considered when developing a supplementation strategy.
当母体应激源与胎盘发育高峰期同时出现时，就会发生宫内生长受限（IUGR），从而导致胎盘功能不全。当生长中的胎儿不断增加的营养需求随后超过发育不良的胎盘的能力时，就会导致胎儿低氧血症和低血糖。胎儿营养状况不佳会刺激炎症细胞因子和儿茶酚胺的更多释放，进而导致节俭生长和代谢编程，这对胎儿存活有益，但出生后会产生不良影响。具体而言，一些IUGR胎儿组织会出现炎症细胞因子受体和其他信号级联成分的表达增加，即使出生后循环炎症细胞因子不再升高，这也会增加炎症敏感性。最近的证据表明，更强的炎症状态会导致IUGR后代特有的骨骼肌生长和代谢缺陷。这些缺陷是代谢功能障碍的基础，显著增加了IUGR出生个体患代谢疾病的风险。相同的编程机制会导致IUGR出生的家畜代谢效率降低、身体组成不佳和胴体质量较差。ω-3多不饱和脂肪酸（PUFA）是具有抗炎作用的饮食来源的营养保健品，已被用于改善慢性全身炎症状况，包括宫内应激。在本综述中，我们强调了持续全身炎症在IUGR病理发展中的作用。然后，我们讨论了补充ω-3 PUFA改善IUGR后代炎症介导的生长和代谢缺陷的潜力，以及制定补充策略时必须考虑的潜在障碍。
