Abstract
BackgroundTo meet the needs of foetal growth and development, marked changes in lipid profiles occur during pregnancy. Abnormal lipid metabolism is often accompanied by adverse pregnancy outcomes, which seriously affect maternal and infant health. Further understanding of the mechanism of lipid metabolism during pregnancy would be helpful to reduce the incidence of adverse pregnancy outcomes.MethodsPregnant mice were euthanized in the virgin (V) state, on day 5 of pregnancy (P5), on day 12 of pregnancy (P12), on day 19 of pregnancy (P19) and on lactation day 2 (L2). Body weight and energy expenditure were assessed to evaluate the general condition of the mice. Triglyceride (TG) levels, the cholesterol content in the liver, liver histopathology, serum lipid profiles, serum β-hydroxybutyrate levels, fibroblast growth factor-21 (FGF21) levels and the levels of relevant target genes were analysed.ResultsDuring early pregnancy, anabolism was found to play a major role in liver lipid deposition. In contrast, advanced pregnancy is an overall catabolic condition associated with both increased energy expenditure and reduced lipogenesis. Moreover, the accumulation of hepatic TG did not appear until P12, after the onset of endoplasmic reticulum (ER) stress on P5. Then, catabolism was enhanced, and FGF21 secretion was increased in the livers of female mice in late pregnancy. We further found that the expression of sec23a, which as the coat protein complex II (COPII) vesicle coat proteins regulates the secretion of FGF21, in the liver was decreased on P19.ConclusionWith the activation of ER stress and increased FGF21 secretion during pregnancy, the hepatic TG content changes, suggesting that ER stress and FGF21 may play an important role in balancing lipid homeostasis and meeting maternal and infant energy requirements in late pregnancy.
Highlights
To meet the needs of foetal growth and development, marked changes in lipid profiles occur during pregnancy
To further examine the potential alterations in lipid levels in the liver, we used a hepatic lipid content assay and found that the hepatic cholesterol content rose in the P19 group but decreased in the lactation day 2 (L2) group (Fig. 1d, e), which differs from observations in humans; these mice are not a good model of pregnancy in humans in which to study cholesterol metabolism
Throughout pregnancy, the expression of TG metabolism genes followed a distinct biphasic pattern To further study the lipid metabolism mechanism during pregnancy, microarray analysis was performed to identify changes in murine hepatic gene expression between the late pregnancy groups and V group; we found that the expression of a set of lipid synthesis-related genes, including stearoyl-CoA desaturase 1 (SCD1) and fatty acid synthase (FASN), was downregulated in the late pregnancy group
Summary
To meet the needs of foetal growth and development, marked changes in lipid profiles occur during pregnancy. Abnormal lipid metabolism is often accompanied by adverse pregnancy outcomes, which seriously affect maternal and infant health. In 1994, Sohlstrom A et al found that the liver fat content in rats on day 14 of gestation was increased by nearly 20% compared with that in virgin (V) controls [4]. Abnormal levels of lipids and their metabolites during pregnancy are related to adverse neonatal outcomes [5]. Changes in liver lipid metabolism are expected during pregnancy. A previous study reported that the lipid uptake and transport capacities of liver cells and triglyceride (TG) secretion levels are increased throughout reproduction [7]. The changes that occur in the levels of regulatory factors throughout the entire pregnancy period have not been reported
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