Adriëtte Oostvogels

4 101 Maternal lipids and offspring’s lipids & glucose Introduction There is increasing evidence that the origin of the development of many diseases in offspring can be found in intrauterine conditions related to maternal metabolism. 1 Maternal lipid profile is one of the metabolic compounds known to influence foetal developmental processes, such as foetal growth. 2 Lipid metabolism changes in pregnancy: an accumulation of lipids in maternal tissue in the first and second trimester is followed by increased lipolysis in the last trimester resulting in maternal hyperlipidaemia. 2 This alteration is necessary to improve the availability of essential metabolites for foetal growth and development. 2 Maternal lifestyle, like a fat-rich diet, lack of physical activity and high maternal prepregnancy body mass index (pBMI), can influence the lipid profile, 3-5 resulting in hyperlipidaemia during pregnancy. Although placental transfer of lipid components is limited compared to glucose and amino acid transfer, 2 several cohort studies reported a positive association between maternal serum triglycerides (TG) levels in the first, 6 middle, 7 and last 8 trimester of gestation and neonatal birth weight. High birth weight increases the risk of childhood overweight, 9 and children with overweight and obesity are more likely to have an adverse lipid profile and glucose levels, possibly due to reduced insulin sensitivity. 10 Earlier research within our cohort showed that maternal free fatty acids (FFA), total cholesterol (TC) and apolipoprotein B (ApoB) during early pregnancy were associated with offspring’s body fat percentage and the risk for overweight at age 5-6 years. 11 Because high body fat percentage and overweight can lead to an adverse lipid profile and altered glycaemic control, 10 it suggests that maternal lipids are indirectly associated with offspring’s lipid profile and glycaemic control in childhood (Figure 1). Maternal lipids in pregnancy may also program offspring’s lipid metabolism directly in utero, as van der Graaf et al. showed that offspring with familial hypercholesterolemia from the maternal side had significantly higher cholesterol, low density lipoprotein (LDL) and ApoB levels than offspring with familial hypercholesterolemia from the paternal side. 12 Although animal studies did not examine associations with maternal lipid levels, a direct positive association was found between high-fat intake during pregnancy and offspring’s postnatal TC levels. 13 A review of animal studies reported conflicting results concerning high-fat intake during pregnancy and glycaemic control. 14 In addition, the association between maternal high-fat diet and offspring glycaemic control appears to be sex specific, although studies contradict each other as to which sex is more sensitive. 15