Overnight, the pregnant woman changes from a postprandial state characterized by elevated and sustained glucose levels to a fasting state characterized by decreased plasma glucose and some amino acids. Plasma concentrations of free fatty acids, triglycerides, and cholesterol are also higher in the fasting state. his pregnancy-induced switch in fuels from glucose to lipids has been called accelerated starvation. Certainly, when fasting is prolonged in the pregnant woman, these alterations are exaggerated and ketonemia rapidly appears.
he concentrations of lipids, lipoproteins, and apolipoproteins in plasma rise appreciably during pregnancy (Appendix, p. 1259). Increased insulin resistance and estrogen stimulation during pregnancy are responsible for the maternal hyperlipidemia. Augmented lipid synthesis and food intake contribute to maternal fat accumulation during the first two trimesters (Herrera, 2014). In the third trimester, however, fat storage declines or ceases. his is a consequence of enhanced lipolytic activity, and decreased lipoprotein lipase activity reduces circulating triglyceride uptake into adipose tissue. his transition to a catabolic state favors maternal use oflipids as an energy source and spares glucose and amino acids for the fetus.
Maternal hyperlipidemia is one of the most consistent and striking changes of lipid metabolism during late pregnancy. Triacylglycerol and cholesterol levels in very-low-density lipoproteins (VLDLs), low-density lipoproteins (LDLs), and highdensity lipoproteins (HDLs) are increased during the third trimester compared with those in nonpregnant women. During the third trimester, the average level of total serum cholesterol is 267 ± 30 mg/dL, ofLDL-C is 136 ± 33 mg/dL, ofHDL-C is 81 ± 17 mg/dL, and of triglycerides is 245 ± 73 mg/dL (Lippi, 2007). After delivery, the concentrations of these lipids, lipoproteins, and apolipoproteins decline. Breastfeeding drops maternal triglyceride levels but increases those of HDL-C. The efects of breastfeeding on total cholesterol and LDL-C levels are unclear (Gunderson, 2014).
Hyperlipidemia is theoretically a concern because it is associated with endothelial dysfunction. From studies, however, endothelium-dependent vasodilation responses actually improve across pregnancy (Saarelainen, 2006). Ihis is partly because increased HDL-C concentrations likely inhibit LDL oxidation and thus protect the endothelium. hese indings suggest that the increased cardiovascular disease risk in multiparas may be related to factors other than maternal hypercholesterolemia.
This peptide hormone is primarily secreted by adipose tissue in nonpregnant humans. It plays a key role in body fat and energy expenditure regulation and in reproduction. For example, leptin is important for implantation, cell proliferation, and angiogenesis (Vazquez, 2015). Leptin deiciency is associated with anovulation and infertility, whereas certain leptin mutations cause extreme obesity (Tsai, 2015).
Among normal-weight pregnant women, serum leptin levels rise and peak during the second trimester and plateau until term in concentrations two to four times higher than those in nonpregnant women. Among obese women, leptin levels correlate with adiposity (Ozias, 2015; Tsai, 2015). In all cases, leptin levels fall after delivery, relecting the significant amounts produced by the placenta (Vazquez, 2015).