from Section 4 - Interventions
Published online by Cambridge University Press: 05 August 2012
Introduction
In this chapter we address the metabolic sequelae of maternal obesity, and by detailing effects on glucose, lipid, and protein metabolism, parallels with type 2 diabetes are highlighted. These similarities and the success of lifestyle intervention strategies for the prevention of type 2 diabetes may provide a road map for the development of strategies to modify maternal hyperglycemia – a key determinant of pregnancy complications.
Maternal metabolism
Lipid metabolism
Lipid metabolism undergoes major adjustment during pregnancy as although there is no change in either basal carbohydrate oxidation or non-oxidizable carbohydrate metabolism there is a significant 50% to 80% increase in basal fat oxidation during pregnancy and also in response to glucose [1]. There is also a marked hyperlipidemia in pregnancy [2–4]. Specifically very low-density lipoprotein (VLDL) triglyceride concentrations increase three-fold from 14 weeks gestation to term [5], with concomitant decreases in hepatic lipase activity [2]. This increase in plasma triglyceride concentration results may drive in the appearance of small, dense low-density lipoprotein (LDL) particles, particularly in late pregnancy [6]. Plasma cholesterol levels rise to a lesser degree due to an early decrease in LDL followed by a modest continuous rise in high-density lipoprotein (HDL) (particularly the HDL-2 subfraction) by over 40% after 14 weeks gestation [5]. HDL cholesterol exhibits a triphasic profile, rising to a peak at 25 weeks, and then declining to 32 weeks with maintenance at this level until term [7]. These changes in lipoprotein concentrations are associated with the progressive increases in estradiol, progesterone, and human placental lactogen [7], and estrogens are known to enhance VLDL production and decrease hepatic lipase activity and may play a key role in the accumulation of triglycerides in lipoproteins of higher density than VLDL [8].
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