Abstract
Protein imbalance during pregnancy affects women in underdeveloped and developing countries and is associated with compromised offspring growth and an increased risk of metabolic diseases in later life. We studied in a porcine model the glucose and urea metabolism, and circulatory hormone and metabolite profile of offspring exposed during gestation, to maternal isoenergetic low–high (LP-HC), high–low (HP-LC) or adequate (AP) protein–carbohydrate ratio diets. At birth, LP-HC were lighter and the plasma acetylcarnitine to free carnitine ratios at 1 day of life was lower compared to AP offspring. Plasma urea concentrations were lower in 1 day old LP-HC offspring than HP-LC. In the juvenile period, increased insulin concentrations were observed in LP-HC and HP-LC offspring compared to AP, as was body weight from HP-LC compared to LP-HC. Plasma triglyceride concentrations were lower in 80 than 1 day old HP-LC offspring, and glucagon concentrations lower in 80 than 1 day old AP and HP-LC offspring. Plasma urea and the ratio of glucagon to insulin were lower in all 80 than 1 day old offspring. Aminoacyl-tRNA, arginine and phenylalanine, tyrosine and tryptophan metabolism, histidine and beta-alanine metabolism differed between 1 and 80 day old AP and HP-LC offspring. Maternal protein imbalance throughout pregnancy did not result in significant consequences in offspring metabolism compared to AP, indicating enormous plasticity by the placenta and developing offspring.
Highlights
The Developmental Origins of Health and Disease hypothesis proposes that exposure of the developing fetus to a hostile uterine environment during critical phases of growth and development can significantly impact the offspring’s short- and long-term health [1,2].Inadequate nutrition during pregnancy, both in composition and amount, is a significant stressor on the developing embryo/fetus as the mother is the sole source of nutrients
Results showed that the average piglet body weight, female and male offspring body weight and average live born piglet body weight were lower from LP-HC compared to AP gilts (Supplementary Table S3)
In the population of experimental piglets used in this study (AP, n = 53; LP-HC, n = 49; HP-LC, n = 58), LP-HC offspring were significantly lighter than AP (p = 0.04) at day 1 of life, and HP-LC (p = 0.02) were significantly lighter than AP offspring at 80 days of life (Table 1)
Summary
The Developmental Origins of Health and Disease hypothesis proposes that exposure of the developing fetus to a hostile uterine environment during critical phases of growth and development can significantly impact the offspring’s short- and long-term health [1,2].Inadequate nutrition during pregnancy, both in composition and amount, is a significant stressor on the developing embryo/fetus as the mother is the sole source of nutrients. Studies have shown that exposure to maternal protein undernutrition during fetal development can affect the structural and functional features of offspring and lead to an increased propensity for chronic disease [2]. The majority of animal studies examining the effect maternal protein imbalance on offspring development, have been performed in rodents, which, at birth, are developmentally less mature than human infants [10]. In many of these rodent studies the effect of maternal diet composition on offspring development and health, semi-synthetic diets were used [11,12,13]. Exposure has been conducted during both gestation and lactation [13,14,15,16], complicating analysis of how in utero exposure is linked to the onset of metabolic diseases later in life
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