Regulation of maternal–fetal metabolic communication

Bowman, Caitlyn E.; Arany, Zoltàn; Wolfgang, Michael J.

doi:10.1007/s00018-020-03674-w

Cited by 55 publications

(34 citation statements)

References 271 publications

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“…They found that the rate of fatty acid delivery to the fetal compartment was modulated by the incorporation of fatty acids into placental lipid pools ( 19 ). FAO reduction can shift the flux of fatty acids away from oxidation toward lipid pools ( 30 ), which suggests that FAO capacity can affect fatty acid delivery to the fetus ( 29 , 56 ). There are studies showed that FAO capacity was reduced in trophoblast cells isolated from obese women ( 29 ), and acylcarnitine concentration and CPT1 and/or CPT2 expression were lower in the placenta ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

Maternal High-Fat Diet Impairs Placental Fatty Acid β-Oxidation and Metabolic Homeostasis in the Offspring

Zhang

Wang

et al. 2022

Front. Nutr.

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Maternal overnutrition can affect fetal growth and development, thus increasing susceptibility to obesity and diabetes in later life of the offspring. Placenta is the central organ connecting the developing fetus with the maternal environment. It is indicated placental fatty acid metabolism plays an essential role in affecting the outcome of the pregnancy and fetus. However, the role of placental fatty acid β-oxidation (FAO) in maternal overnutrition affecting glucose metabolism in the offspring remains unclear. In this study, C57BL/6J female mice were fed with normal chow or high-fat diet before and during pregnancy and lactation. The placenta and fetal liver were collected at gestation day 18.5, and the offspring's liver was collected at weaning. FAO-related genes and AMP-activated protein kinase (AMPK) signaling pathway were examined both in the placenta and in the human JEG-3 trophoblast cells. FAO-related genes were further examined in the liver of the fetuses and in the offspring at weaning. We found that dams fed with high-fat diet showed higher fasting blood glucose, impaired glucose tolerance at gestation day 14.5 and higher serum total cholesterol (T-CHO) at gestation day 18.5. The placental weight and lipid deposition were significantly increased in maternal high-fat diet group. At weaning, the offspring mice of high-fat diet group exhibited higher body weight, impaired glucose tolerance, insulin resistance and increased serum T-CHO, compared with control group. We further found that maternal high-fat diet downregulated mRNA and protein expressions of carnitine palmitoyltransferase 2 (CPT2), a key enzyme in FAO, by suppressing the AMPK/Sirt1/PGC1α signaling pathway in the placenta. In JEG-3 cells, protein expressions of CPT2 and CPT1b were both downregulated by suppressing the AMPK/Sirt1/PGC1α signaling pathway under glucolipotoxic condition, but were later restored by the AMPK agonist 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR). However, there was no difference in CPT2 and CPT1 gene expression in the liver of fetuses and offspring at weaning age. In conclusion, maternal high-fat diet can impair gene expression involved in FAO in the placenta by downregulating the AMPK signaling pathway, and can cause glucose and lipid dysfunction of offspring at weaning, indicating that placental FAO may play a crucial role in regulating maternal overnutrition and metabolic health in the offspring.

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Section: Discussionmentioning

confidence: 99%

Maternal High-Fat Diet Impairs Placental Fatty Acid β-Oxidation and Metabolic Homeostasis in the Offspring

Zhang

Wang

et al. 2022

Front. Nutr.

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“…The extensive microvilli on the surface of STBs substantially increase the surface area to contact maternal blood, efficiently ensure the maternal-fetal exchange of membrane-permeable molecules, particles, and polar molecules, during which a variety of transmembrane transporters are involved. 48 The most important glucose transporter (GLUT) in the placenta is GLUT. GLUT1 is expressed in the basal membrane of STBs throughout pregnancy, while high expression of GLUT3 is found in CTBs at the first trimester, but not at full-term.…”

Section: Maternal-fetal Nutrient Transportation Through the Placentamentioning

confidence: 99%

Placental Development and Pregnancy-Associated Diseases

Yue

et al. 2021

Maternal-Fetal Medicine

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Serving as the interface between the fetal and maternal environments during gestation, the placenta plays critical roles in the protection of the developing fetus and the maintenance of maternal health. The placenta is primarily derived from the embryonic trophectoderm which differentiates into various subtypes of trophoblast cells through villous and extravillous pathways. The interactions among trophoblasts and multiple decidual cells and immune cells at the maternal-fetal interface fundamentally form the functional units of the placenta, which are responsible for blood perfusion and maternal-fetal material exchange, immune tolerance, and the regulation of pregnancy adaptation. Defects in placental development and functional maintenance are in tight association with adverse pregnancy outcomes such as preeclampsia. In this article, we review recent advances on human trophoblast cell differentiation and the construction of placental functional units and discuss the placental and maternal factors that may contribute to the occurrence of preeclampsia.

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“…In the early stage of pregnancy, under normal conditions, the glucose and fatty acid uptake is facilitated by adipose tissue, producing an increase in fat reserves. However, as pregnancy progresses, there is a change in the metabolism characterized by insulin resistance and a decrease in glucose metabolism [ 12 ]. In pregnant women with normal weight, the RQ is not significantly modified, although they show lower values in conditions of overweight and obesity [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of Low Protein-High Carbohydrate Diet during Early and Late Pregnancy on Respiratory Quotient and Visceral Adiposity

Navarro-Meza

Dı́az-Muñoz

García-Solano

et al. 2022

Oxidative Medicine and Cellular Longevity

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Background. Low Protein-High Carbohydrate (LPHC) diet during pregnancy is considered a nutritional and health problem related to the development of maternal metabolic alterations, such as fatty liver and obesity in the perinatal and postnatal period. It is known that increase in visceral adiposity tissue (VAT) modulates maternal metabolic rate, with the respiratory quotient (RQ) being a parameter related to that variable; however, it is unknown whether LPHC intake during pregnancy affects the VAT and the RQ. In this study, we examine if consumption of LPHC during pregnancy modifies the VAT and RQ in early and late periods of pregnancy. Methods. This is a longitudinal and cross-sectional study with Wistar rats during gestation (G) (3, 8, 15, and 20) and nonpregnant rats. Rats were fed with a control diet with 63/18% carbohydrate/protein and an experimental diet with 79/6% carbohydrate/protein. We studied water and food consumption and metabolic parameters such as RQ and energy expenditure (EE), calculated by indirect calorimetry. In the cross-sectional study, we determined visceral fat, as well as the concentration of free fatty acids, insulin, glucose, and lipid profile in serum. Results. Nonpregnant rats with LPHC intake decreased significantly in VAT (86%) and the RQ (18%); in pregnant rats in early (8G) and late pregnancy (15G) in LPHC diet, both parameters (VAT and RQ) (25%-92%) increased during light time. When comparing time points during pregnancy in the control and LPHC groups, the RQ increased in 15G during daytime compared to 8G during the night period (17 and 5%, respectively). In late pregnancy, LPHC intake and triacylglyceride levels increased and cholesterol and glucose decreased (45 and 26%, respectively), in comparison to nonpregnant rats. Conclusions. LPHC intake in nonpregnant rats decreases the RQ and VAT. Interestingly, the opposite occurs in early pregnancy: the RQ and VAT increased, and this correlates with free fatty acid (FFA) levels. The increase in RQ and VAT during light time in early pregnancy increased mobilization of carbohydrate and protein metabolism. These results suggest that LPHC intake during pregnancy increases the glucose metabolism as a compensatory mechanism for energy needs in the fetus and the mother in early pregnancy.

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Regulation of maternal–fetal metabolic communication

Cited by 55 publications

References 271 publications

Maternal High-Fat Diet Impairs Placental Fatty Acid β-Oxidation and Metabolic Homeostasis in the Offspring

Maternal High-Fat Diet Impairs Placental Fatty Acid β-Oxidation and Metabolic Homeostasis in the Offspring

Placental Development and Pregnancy-Associated Diseases

Effects of Low Protein-High Carbohydrate Diet during Early and Late Pregnancy on Respiratory Quotient and Visceral Adiposity

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