Martin-Gronert M S, Ozanne S E
Department of Clinical Biochemistry, Addenbrooke's Hospital, University of Cambridge, Cambridge, UK.
J Intern Med. 2007 May;261(5):437-52. doi: 10.1111/j.1365-2796.2007.01800.x.
It is widely accepted that an association exists between the intrauterine environment in which a fetus grows and develops and the subsequent development of type 2 diabetes. Any disturbance in maternal ability to provide nutrients and oxygen to the fetus can lead to fetal intrauterine growth restriction (IUGR). Here we will review IUGR in rodent models, in which maternal metabolism has been experimentally manipulated to investigate the molecular basis of the relationship between IUGR and development of type 2 diabetes in later life, and the identification of the molecular derangements in specific metabolically - sensitive organs/tissues.
胎儿生长发育所处的子宫内环境与2型糖尿病的后续发展之间存在关联,这一观点已被广泛接受。母体向胎儿提供营养和氧气的能力出现任何紊乱,都可能导致胎儿宫内生长受限(IUGR)。在此,我们将回顾啮齿动物模型中的宫内生长受限情况,在这些模型中,母体代谢已通过实验手段进行调控,以研究宫内生长受限与晚年2型糖尿病发展之间关系的分子基础,以及特定代谢敏感器官/组织中分子紊乱的识别。