Abstract
Worldwide, the number of people with diabetes has quadrupled since 1980 reaching 422 million in 2014 (World Health Organization). This distressing rise in diabetes also affects pregnant women and thus, in regard to early programming of adult diseases, creates a vicious cycle of metabolic dysfunction passed from one generation to another. Metabolic diseases are complex and caused by the interplay between genetic and environmental factors. High-glucose exposure during in utero development, as observed with gestational diabetes mellitus (GDM), is an established risk factor for metabolic diseases. Despite intense efforts to better understand this phenomenon of early memory little is known about the molecular mechanisms associating early exposure to long-term diseases risk. However, evidence promotes glucose associated oxidative stress as one of the molecular mechanisms able to influence susceptibility to metabolic diseases. Thus, we decided here to further explore the relationship between early glucose exposure and cellular stress in the context of early development, and focus on the concept of glycemic memory, its consequences, and sexual dimorphic and epigenetic aspects.
Highlights
The late 1980s marked a fundamental period in epidemiology with the observation by Barker and colleagues of a positive correlation between infant mortality rates and mortality from ischemic heart disease, bronchitis and stomach cancer in adulthood [1]
With the studies following Barker’s 1986 publication, low birth weight became a symbol of poor fetal growth due to inadequate intrauterine conditions associated with increased risk for metabolic and age-related diseases
large for gestational age neonates (LGA) neonatal birth can be considered a surrogate marker of poor glycemic control during pregnancy, as it is the LGA/gestational diabetes mellitus (GDM) combined condition that translates to increased risk of metabolic syndrome that is not seen when fetal growth is averaged in a diabetic intrauterine environment [73]
Summary
The late 1980s marked a fundamental period in epidemiology with the observation by Barker and colleagues of a positive correlation between infant mortality rates and mortality from ischemic heart disease, bronchitis and stomach cancer in adulthood [1]. This has been described as a U-shaped association of birth weight and adult disease risk [2] This first observation was confirmed by numerous studies in the general population [3,4] leading to the conclusion that both extremes of fetal growth have a measurable influence on long-term health creating a vicious cycle of metabolic dysfunction passed from one generation to another. Our group has demonstrated that the long-term consequences of early exposure could be mediated through high glucose related impaired response to oxidative damage [7] in mesenchymal stem cell These observations suggest that oxidative stress influences and is influenced by cellular metabolic status. We propose to further review this relationship between glucose exposure and cellular stress in the context of age-related and metabolic disease early programming
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