Persistent influence of maternal obesity on offspring health: Mechanisms from animal models and clinical studies

被引:34
|
作者
Wankhade, Umesh D. [1 ,2 ]
Thakali, Keshari M. [1 ,2 ]
Shankar, Kartik [1 ,2 ]
机构
[1] Univ Arkansas Med Sci, Arkansas Childrens Nutr Ctr, Little Rock, AR 72205 USA
[2] Univ Arkansas Med Sci, Dept Pediat, Little Rock, AR 72205 USA
关键词
Maternal obesity; Development programming; Epigenetics; Metabolism; GESTATIONAL WEIGHT-GAIN; HIGH-FAT DIET; BODY-MASS INDEX; ASSISTED REPRODUCTIVE TECHNOLOGY; INSULIN-RESISTANCE; ADIPOSE-TISSUE; DNA METHYLATION; GUT MICROBIOTA; METABOLIC SYNDROME; GENE-EXPRESSION;
D O I
10.1016/j.mce.2016.07.001
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The consequences of excessive maternal weight and adiposity at conception for the offspring are now well recognized. Maternal obesity increases the risk of overweight and obesity even in children born with appropriate-for-gestational age (AGA) birth weights. Studies in animal models have employed both caloric excess and manipulation of macronutrients (especially high-fat) to mimic hypercaloric intake present in obesity. Findings from these studies show transmission of susceptibility to obesity, metabolic dysfunction, alterations in glucose homeostasis, hepatic steatosis, skeletal muscle metabolism and neuroendocrine changes in the offspring. This review summarizes the essential literature in this area in both experimental and clinical domains and focuses on the translatable aspects of these experimental studies. Moreover this review highlights emerging mechanisms broadly explaining maternal obesity associated developmental programming. The roles of early developmental alterations and placental adaptations are also reviewed. Increasing evidence also points to changes in the epigenome and other emerging mechanisms such as alterations in the microbiome that may contribute to persistent changes in the offspring. Finally, we examine potential interventions that have been employed in clinical cohorts. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:7 / 19
页数:13
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