Hastie R, Lappas M
Obstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and Gynaecology, University of Melbourne, Mercy Hospital for Women, Heidelberg, Victoria, Australia; Mercy Perinatal Research Centre, Mercy Hospital for Women, Heidelberg, Victoria, Australia.
Obstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and Gynaecology, University of Melbourne, Mercy Hospital for Women, Heidelberg, Victoria, Australia; Mercy Perinatal Research Centre, Mercy Hospital for Women, Heidelberg, Victoria, Australia.
Placenta. 2014 Sep;35(9):673-83. doi: 10.1016/j.placenta.2014.06.368. Epub 2014 Jun 26.
Mitochondria dysfunction has been extensively implicated in the progression of these metabolic disorders, their role in placental tissue of diabetic and/or obese pregnant women is yet to be investigated. The aim of this study was to determine the effect of pre-existing type 1 and type 2 diabetes mellitus (DM), and pre-existing maternal obesity on placental mitochondrial function as assessed by mitochondrial content, electron transport chain (ETC) complex activities and oxidative stress.
Human placenta was obtained at the time of term Caesarean section from (i) non-obese (n = 19) and obese (n = 23) normal glucose tolerant (NGT) pregnant women; (ii) women with type 1 DM (n = 14) and BMI-matched NGT women (n = 14); and (iii) women with type 2 DM (n = 11) and BMI-matched NGT women (n = 11). The following endpoints were assessed: placental mitochondrial content by citrate synthase activity and mitochondrial DNA (mtDNA content); mitochondrial respiratory chain activity (complexes I, II, II & III, III and IV), and mitochondrial ROS (as assessed by mitochondrial hydrogen peroxide (H2O2) levels).
When compared to placenta from NGT non-obese women, there was significantly lower mitochondrial DNA (mtDNA) content and electron transport chain complex I activity, and significantly higher mitochondrial H2O2 levels in placenta from NGT obese women (P < 0.05). Placental tissue from type 1 DM women showed significant reductions in ETC complex I, II & III, and III activity and increased H2O2 levels when compared to BMI-matched NGT women (P < 0.05). Type 2 DM women only exhibited significantly reduced ETC complex II & III activity when compared to BMI-matched NGT women (P < 0.05).
Women with pre-existing obesity or diabetes have decreased placental mitochondrial respiratory chain enzyme activities which may have detrimental consequences on placental function and therefore fetal growth and development.
线粒体功能障碍与这些代谢紊乱的进展密切相关，但其在糖尿病和/或肥胖孕妇胎盘组织中的作用尚待研究。本研究的目的是通过线粒体含量、电子传递链（ETC）复合物活性和氧化应激来确定孕前1型和2型糖尿病（DM）以及孕前母体肥胖对胎盘线粒体功能的影响。
在足月剖宫产时获取人胎盘，来自以下三组：（i）非肥胖（n = 19）和肥胖（n = 23）的糖耐量正常（NGT）孕妇；（ii）1型糖尿病女性（n = 14）和体重指数匹配的NGT女性（n = 14）；（iii）2型糖尿病女性（n = 11）和体重指数匹配的NGT女性（n = 11）。评估以下终点指标：通过柠檬酸合酶活性和线粒体DNA（mtDNA含量）评估胎盘线粒体含量；线粒体呼吸链活性（复合物I、II、II与III、III和IV）以及线粒体ROS（通过线粒体过氧化氢（H2O2）水平评估）。
与NGT非肥胖女性的胎盘相比，NGT肥胖女性的胎盘线粒体DNA（mtDNA）含量和电子传递链复合物I活性显著降低，线粒体H2O2水平显著升高（P < 0.05）。与体重指数匹配的NGT女性相比，1型糖尿病女性的胎盘组织中ETC复合物I、II与III以及III活性显著降低，H2O2水平升高（P < 0.05）。与体重指数匹配的NGT女性相比，2型糖尿病女性仅表现出ETC复合物II与III活性显著降低（P < 0.05）。
孕前肥胖或糖尿病女性的胎盘线粒体呼吸链酶活性降低，这可能对胎盘功能产生不利影响，进而影响胎儿的生长发育。
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