妊娠期胰岛素抵抗发生机制研究进展

Research Progress on the Mechanism of Insulin Resistance in Pregnancy

由于妊娠期雌、孕激素水平上升,母体对葡萄糖利用率增加,为维持正常的糖代谢水平,胰岛素需求量增加。同时随着妊娠过程的推进,母体胰岛素作用的靶器官对外源性或内源性胰岛素作用的敏感性降低,这种现象被称为妊娠期胰岛素抵抗(IR)。妊娠期往往伴有生理性的IR,但对于患有妊娠期糖尿病、妊娠期高血压疾病、多囊卵巢综合征等并发症的孕妇,IR程度可能更加显著。妊娠期IR是多种因素共同作用的结果,其机制尚未完全阐明。妊娠期IR已被证实与多种妊娠并发症及不良妊娠结局相关,影响母儿预后,因此对妊娠期妇女IR的监测及干预具有积极意义。对有高危因素的孕妇应开展早期干预、制定个性化治疗方案,降低妊娠期并发症发病率,从而降低不良妊娠结局的发生率。本研究就妊娠期IR与孕前体重、细胞因子、炎症、孕前内分泌系统疾病、胎盘、激素、肠道微生物、遗传、生活习惯等因素相关性的最新研究进展进行综述,进一步明确妊娠期IR的原因,以期为实施早期干预妊娠期IR提供参考。

Because of the increase of estrogen and progestogen levels during pregnancy,maternal glucose utilization increases,and the insulin requirements increase in order to maintain the normal glucose metabolism level.At the same time,with the progression of pregnancy,the target organ of maternal insulin action becomes less sensitive to exogenous or endogenous insulin action,which is called insulin resistance(IR)in pregnancy.Pregnancy is often accompanied by physiological IR,but for pregnant women with complications such as gestational diabetes mellitus,hypertensive disorder complicating pregnancy,polycystic ovary syndrome,the degree of IR may be more significant.Therefore,it may be inferred that IR during pregnancy is the result of multiple factors,and its mechanism has not been fully elucidated.It has been proved that IR in pregnancy is associated with many pregnancy complications and adverse pregnancy out-comes,and affects maternal and fetal prognosis.Early intervention and individualized treatment for pregnant women with high risk fac-tors can reduce the incidence of pregnancy complications and adverse pregnancy outcomes.This article reviews the recent research prog-ress on the relationship between IR during pregnancy and pre-pregnancy weight,cytokines,inflammation,pre-pregnancy endocrine sys-tem,placenta,hormones,intestinal microbiology,heredity and living habits,to further clarify the causes of insulin resistance during pregnancy,in order to provide reference for early intervention of pregnancy induced insulin resistance.