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15 - Interventional strategies to improve outcome in obese pregnancies: insulin resistance and gestational diabetes

from Section 4 - Interventions

Published online by Cambridge University Press:  05 August 2012

By
Scott M. Nelson  and
Lucilla Poston
Edited by
Matthew W. Gillman  and
Lucilla Poston
Matthew W. Gillman
Affiliation:
Harvard Medical School
Lucilla Poston
Affiliation:
King's College London
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Summary

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].

Keywords

gestational diabetesglucose homeostasisinsulin sensitivityprotein metabolismtype 2 diabetespregnancylipid metabolismmaternal obesity
Type
Chapter
Information
Maternal Obesity , pp. 179 - 198
Publisher: Cambridge University Press
Print publication year: 2012

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