出生体重与孕龄:非传染性疾病人群健康的早期生命管理策略

Salmi Issa Al, H. Suad
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引用次数: 4

摘要

在过去的几十年里,非传染性疾病在全球范围内呈上升趋势。发展中国家承受着更严重的非传染性疾病负担。同样,低出生体重在世界各地都在增加,其中大多数常见于发展中国家,但在发达国家,医疗保健的进步成功地提高了极低出生体重婴儿的存活率。近年来,人们对胎儿的早期发育以及妊娠期的生长对后期疾病发展的影响产生了极大的兴趣,尤其是所谓的“关键期”。肾脏生长的“关键期”是从妊娠第九周开始的快速生长期,这是由细胞快速分裂决定的。子宫内不同器官系统的生长可能不均衡,因为不同的组织在不同的时间有不同的生长关键期。LBW反映了对子宫发育的不利影响,导致了这种早期疾病编程现象。控制我们命运的不仅是基因的存在与否,还有基因表达可能因早期营养环境等因素而永久改变的方式。许多流行病学研究结果表明,成人生活中的疾病风险是由以前遇到的环境决定的。出生时体积小、细胞数量少可能导致各种NCD问题。产后环境因素进一步加剧了对身体器官的代谢需求,导致各种器官功能因代谢率的增加而不堪重负。因此,这导致了对各种结构的需求增加,例如肾单位的超滤,随之而来的是器官功能障碍。因此,制定早期策略健康计划对于检测LBW和/或早产患者早期可能出现的主要风险因素非常重要。引言糖尿病、高血压和肾病等非传染性慢性病在全球许多人群中迅速增加。贫困和社会经济劣势,以及生活方式和饮食的变化是重要的促成因素[1,2]。节俭假说提出,2型糖尿病(T2DM)和代谢综合征的许多组成部分是由于胎儿生长发育良好的宫内环境引起的。大量研究证实,与低出生体重(LBW)相关,糖尿病或糖耐量受损的风险增加[3]。尽管批评者很多,节俭表型调节了遗传因素在T2DM病因中的重要作用,并得出结论“毫无疑问,早期生活中的环境营养因素在T2DM和代谢综合征的其他组成部分中起着主要的致病作用。Barker等人指出,T2DM和高血压在子宫内发育不良的生长过程中有着共同的起源,X综合征应称为“小婴儿”综合征[4]。有人提出,LBW与包括成年糖尿病发展在内的各种代谢综合征成分之间的关联反映了子宫内内分泌胰腺细胞、肾细胞和其他组织生长减少的长期影响,这可能是母亲营养不良的结果。ReSeARcH ARtItem
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Birthweight and Gestational Age: Early Life Management Strategy to Population Health for Non-Communicable Diseases
Non-communicable diseases (NCD) are rising throughout the globe over the last few decades. Developing countries bear the worse burden of these NCD. Similarly, low birthweight is increasing around the world where most of this prevalence commonly seen in the developing countries but as well in the well-developed countries where advancement of health care managed to increase the survival of the very low birthweight babies. In recent years, there has been great interest in the early development of the foetus and the impact of growth during the gestational period on the development of diseases in later life, and in particular that termed a ‘critical period’. The ‘critical period’ of growth of the kidney is the rapid growth period that starts from the ninth week of gestation onwards, which is determined by rapid cell division. Disproportionate growth of different organ systems in utero can occur because different tissues have different critical periods of growth at different times. LBW, which reflects adverse effects on development in the uterus, contributes to this phenomenon of disease programming in early life. It is not only the presence or absence of genes that control our destiny, but the way in which gene expression may be permanently changed by, for example, the nutritional environment in early life. Many epidemiological findings suggest that the risk of disease in adult life is programmed, and/or imprinted by the environment encountered before. The role of small size at birth with low number of cells may contribute to various NCD problem. Post-natal environmental factors further compound such a metabolic demand on body organs that lead to various organ function being overwhelmed with increase in metabolic rate. Hence this leads to increase demand upon various structures, such as nephron with hyperfiltration, organ dysfunction ensues. Hence, an early strategy health program is of great importance to be instituted to detect major risk factors which may arise early in life in those with LBW and or prematurity. Introduction Non-communicable Chronic diseases, such as diabetes, high blood pressure and kidney disease, are increasing rapidly in many populations globally. Poverty and socio-economic disadvantage, together with lifestyle and dietary changes are significant contributing factors [1,2]. Thrifty hypothesis proposes that type 2 diabetes mellitus (T2DM) and numerous components of metabolic syndrome consequence from derisory intrauterine environments for best fetal growth. Numerous studies have confirmed an increased risk of diabetes or impaired glucose tolerance in relation to low birthweight (LBW) [3]. In spite of number of critics, thrifty phenotype has modulated an important role for genetic factors in the aetiology of T2DM and concluded that “environmental, undoubtedly nutritional factors operating in early life play a chief causative part in T2DM and other components of metabolic syndrome. Barker, et al. stated that T2DM and high blood pressure have a shared origin during growth in sub-optimal development in utero, and that syndrome X ought to be called “the small-baby” syndrome [4]. It is proposed that the association between LBW and various metabolic syndrome components including diabetes development in adulthood reflects the long-term effects of decreased growth of the endocrine pancreas cells, kidney cells and other tissues in utero, which may be a consequence of maternal undernutrition. ReSeARcH ARtIcle
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