Post-weaning diet determines metabolic risk in mice exposed to overnutrition in early life
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Post-weaning diet determines metabolic risk in mice exposed to overnutrition in early life Vicky King1, Jane E Norman1, Jonathan R Seckl2 and Amanda J Drake2*
Abstract Background: Maternal overnutrition during pregnancy is associated with an increased risk of obesity and cardiometabolic disease in the offspring; a phenomenon attributed to ‘developmental programming’. The post-weaning development of obesity may associate with exacerbation of the programmed metabolic phenotype. In mice, we have previously shown that exposure to maternal overnutrition causes increased weight gain in offspring before weaning, but exerts no persistent effects on weight or glucose tolerance in adulthood. In order to determine whether post-weaning exposure to a cafeteria diet might lead to an exacerbation of programmed effects, offspring born and raised by mothers on control (CON) or cafeteria (DIO) diets were transferred onto either CON or DIO diets at weaning. Findings: Post-weaning DIO caused the development of obesity, with hyperglycaemia and hyperinsulinaemia in males; and obesity with hyperinsulinaemia in females and with increased cholesterol levels in both sexes. Exposure to maternal overnutrition during pregnancy and lactation caused only subtle additional effects on offspring phenotype. Conclusions: These results suggest that post-weaning exposure to a high-fat high-sugar diet has a more profound effect on offspring weight gain and glucose tolerance than exposure to maternal overnutrition. These data emphasise the importance of optimising early life nutrition in offspring of both obese and lean mothers. Keywords: Maternal overnutrition, Obesity, Developmental programming
Findings Human and animal studies have shown that the environment in early life can increase the risk of later metabolic disease [1]. There is increasing interest in the role of maternal obesity in the ‘programming’ of offspring disease risk [2] and recent studies have shown that maternal obesity and gestational weight gain are independently associated with offspring cardiometabolic risk and with all-cause mortality [3,4]. This is of substantial importance given the increasing prevalence of obesity worldwide, including amongst women of childbearing age [5]. In order to understand the mechanisms by which exposure to maternal obesity leads to programming of offspring phenotype, animal models have been developed, many of which recapitulate the findings in human studies,
showing effects on offspring adiposity, glucose-insulin homeostasis, blood pressure and appetite [6-8]. Using a mouse model, we recently reported remarkably few effects of maternal overnutrition on body weight and metabolism in the directly exposed (F1) offspring [9]. Despite this, there were effects on birthweight and metabolism in a second generation, suggesting that there were persistent effects in F1 offspring leading to the transmission of effects [9]. Since in humans, postnatal obesity appears to be an important determinant of metabolic disease [10], and po
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