Maternal Lipid Metabolism during Normal Pregnancy and Its Implications to Fetal Development
Abstract
Whereas accumulation of fat depots occurs during the first two-thirds of gestation, increased adipose tissue lipolysis and hyperlipidemia develops in the last trimester. Insulin resistance and increased estrogens in late pregnancy contribute to these changes. Lipoprotein receptors and fatty acid binding proteins in the placenta allow the transfer of long-chain polyunsaturated fatty acids to the fetus. Enhanced oxidative stress in pregnancy may be related to maternal hyperlipidemia. Maternal plasma nonesterified fatty acids and cholesterol correlate with those in the fetus, and maternal adipocytokines have been associated with fetal growth. However, positive correlations between maternal nonesterified fatty acids or triacylglycerols and neonatal body weight or fat mass have only been found in gestational diabetics. Under the limited capacity of the fetus to modify the structure of essential polyunsaturated fatty acids, their long-chain derivatives have to be transferred from the mother through the placenta in appropriate amounts to warrant the normal fetal development.
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Placental growth factor reduces insulin receptor expression and signaling and decreases insulin-stimulated GLUT4 translocation to the plasma membrane of skeletal muscle cells.
“Placental growth factor reduces insulin receptor expression and its signaling as well as decreases insulin-stimulated translocation of GLUT4 protein to the plasmatic membrane of skeletal muscle cells.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [22]
In early pregnancy, placental hormones increase food intake and promote energy storage, whereas in late pregnancy these reserves are mobilized to support the developing fetus.
“In the early stages of pregnancy, the hormones produced by the placenta increase food intake and promote energy storage, whereas in late pregnancy these reserves are mobilized to support the developing fetus [21,22].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [22]
Progesterone contributes to insulin resistance by decreasing insulin's ability to inhibit hepatic gluconeogenesis and reducing insulin-stimulated glucose uptake by skeletal muscle.
“Additionally, progesterone plays a role in insulin resistance development, which decreases insulin’s ability to inhibit gluconeogenesis by the liver and reduces insulin-stimulated glucose uptake by skeletal muscle.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [22]
In early pregnancy, prolactin and human placental lactogen lead to pancreatic beta-cell mass expansion and decreased apoptosis, increasing insulin production.
“In early pregnancy, prolactin and human placental lactogen lead to pancreatic β-cell mass expansion and decreased apoptosis and, as a result, there is an increase in insulin production [19,22].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [22]
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Palomba, S., Falbo, A., Chiossi, G., Muscogiuri, G., Fornaciari, E., Orio, F., Tolino, A., Colao, A., La Sala, G. B., & Zullo, F. (2014) · Steroids · doi:10.1016/j.steroids.2014.06.005 · Cited by 69 · see citing works
Impact of Gestational Diabetes Mellitus on Fetal Growth and Nutritional Status in Newborns
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- Authors
- Herrera, E., & Ortega-Senovilla, H.
- Affiliations
- Universidad CEU, San Pablo, Madrid, Spain
- Venue
- Clinical Lipidology
- Publisher
- Informa UK Limited
- Published
- 2010-12-01
- Volume
- 5
- Issue
- 6
- Pages
- 899-911
- ISSN
- 1758-4299 (ISSN-L)
- 1758-4302
- OpenAlex
- W2160996825
- Cited by
- 114
- References
- 5
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 7 · 2023: 11 · 2022: 12 · 2021: 17 · 2020: 14 · 2019: 9 · 2018: 9 · 2017: 2 · 2016: 5 · 2015: 7 · 2014: 3 · 2013: 2 · 2012: 4
- FWCI
- 1.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical Lipidology (publishedVersion)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Keywords
- maternal lipid metabolism, pregnancy, fetal development, adipose tissue lipolysis, hyperlipidemia, insulin resistance, estrogen, placenta, long-chain polyunsaturated fatty acids, placental transfer, oxidative stress, free fatty acids, cholesterol, adipokines, fetal growth, gestational diabetes mellitus, neonatal body weight
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