Adam-Raileanu Anca, Miron Ingrith, Lupu Ancuta, Bozomitu Laura, Sasaran Maria Oana, Russu Ruxandra, Rosu Solange Tamara, Nedelcu Alin Horatiu, Salaru Delia Lidia, Baciu Ginel, Mihai Cristina Maria, Chisnoiu Tatiana, Beser Omer Faruk, Lupu Vasile Valeriu
Pediatrics, Faculty of Medicine, "Grigore T. Popa" University of Medicine and Pharmacy, 700115 Iasi, Romania.
Pediatrics, Faculty of Medicine, "George Emil Palade" University of Medicine, Pharmacy, Science and Technology, 540142 Targu Mures, Romania.
Nutrients. 2025 Jan 31;17(3):555. doi: 10.3390/nu17030555.
The developmental origins of adult disease theory support the concept that undernourished fetuses are at risk of developing metabolic syndrome due to the energy-saving 'Thrifty Phenotype'. This metabolic plasticity represents an evolutionary adaptation that allows individuals to resist the intense pressure caused by cyclically recurring periods of nutritional deprivation. A comprehensive review was conducted following an extensive literature search in the PubMed/Medline and EMBASE databases concerning reports on fetal/intrauterine growth restriction and its metabolic-related long-term outcomes. We only included articles written in English that were published before 1 July 2024. There are several underlying mechanisms and metabolic and endocrine adjustments shaped by the perinatal environment, and they all contribute to progression towards adult disease. From in utero malnutrition or other insults during the fetal period to fetal programing and postnatal catch-up growth, it is difficult to identify the exact moment when this adaptative phenomenon meant to assure fetal survival and to set children on their own physiological growth curves lose its beneficial effect, establishing the trajectory to obesity, insulin resistance, and other hallmarks of metabolic syndrome. With clinical correspondence to an altered body mass, composition, and eating behaviors, it is evident that the metabolic complications linked to FGR are intricate and arise from disturbances in several pathways and organs, but the underlying processes responsible for the long-term consequences are just starting to be understood. The lack of continuity in perinatal-to-pediatric FGR research sets the challenge of exploring new directions in future scientific opportunities. These will hopefully represent a cornerstone in the management of FGR-related metabolic disorders in children, preventing these disorders from evolving into adult disease.
成人疾病发育起源理论支持这样一种观点,即营养不良的胎儿由于节能的“节俭表型”而有患代谢综合征的风险。这种代谢可塑性代表了一种进化适应,使个体能够抵御周期性反复出现的营养剥夺所带来的巨大压力。在PubMed/Medline和EMBASE数据库中进行了广泛的文献检索,以查找有关胎儿/宫内生长受限及其代谢相关长期后果的报告,随后进行了全面综述。我们仅纳入了2024年7月1日前发表的英文文章。围产期环境塑造了多种潜在机制以及代谢和内分泌调节,它们都促使疾病向成人期发展。从子宫内营养不良或胎儿期的其他损伤到胎儿编程和出生后追赶生长,很难确定这种旨在确保胎儿存活并使儿童走上自身生理生长曲线的适应性现象在何时失去其有益作用,从而确立肥胖、胰岛素抵抗和代谢综合征其他特征的发展轨迹。从临床上看,体重、身体成分和饮食行为发生了变化,与胎儿生长受限相关的代谢并发症显然错综复杂,是由多个途径和器官的紊乱引起的,但导致长期后果的潜在过程才刚刚开始被理解。围产期至儿科胎儿生长受限研究缺乏连续性,这为未来探索新的科学方向带来了挑战。这些有望成为儿童胎儿生长受限相关代谢紊乱管理的基石,防止这些紊乱发展为成人疾病。