Maternal Macronutrient Consumption and the Developmental Origins of Metabolic Disease in the Offspring

被引:53
|
作者
Kereliuk, Stephanie M. [1 ,2 ]
Brawerman, Gabriel M. [1 ,2 ]
Dolinsky, Vernon W. [1 ,2 ]
机构
[1] Univ Manitoba, Dept Pharmacol & Therapeut, Winnipeg, MB R3E 3P4, Canada
[2] Univ Manitoba, Childrens Hosp Res Inst Manitoba, Diabet Res Envisioned & Accomplished Manitoba DRE, Winnipeg, MB R3E 3P4, Canada
关键词
developmental programming; metabolic disease; cardiovascular disease; high-fat diet; sucrose; HIGH-FAT DIET; GESTATIONAL DIABETES-MELLITUS; SYSTOLIC BLOOD-PRESSURE; IN-UTERO EXPOSURE; INSULIN-RESISTANCE; ADIPOSE-TISSUE; PROTEIN RESTRICTION; OXIDATIVE STRESS; GENE-EXPRESSION; PREGNANT RATS;
D O I
10.3390/ijms18071451
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Recent research aimed at understanding the rise in obesity and cardiometabolic disease in children suggests that suboptimal maternal nutrition conditions organ systems and physiological responses in the offspring contributing to disease development. Understanding the mechanisms by which the macronutrient composition of the maternal diet during pregnancy or lactation affects health outcomes in the offspring may lead to new maternal nutrition recommendations, disease prevention strategies and therapies that reduce the increasing incidence of cardiometabolic disease in children. Recent mechanistic animal model research has identified how excess fats and sugars in the maternal diet alter offspring glucose tolerance, insulin signaling and metabolism. Maternal nutrition appears to influence epigenetic alterations in the offspring and the programming of gene expression in key metabolic pathways. This review is focused on experimental studies in animal models that have investigated mechanisms of how maternal consumption of macronutrients affects cardiometabolic disease development in the offspring. Future research using "-omic" technologies is essential to elucidate the mechanisms of how altered maternal macronutrient consumption influences the development of disease in the offspring.
引用
收藏
页数:27
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