Fatty acids in normal and pathological pregnancies

Mauro, Amanda K.; Rengarajan, Aishwarya; Albright, Carly; Boeldt, Derek S.

doi:10.1016/j.mce.2021.111466

Cited by 12 publications

(8 citation statements)

References 143 publications

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“…Up to date, no studies have explored the potential fatty acid patters that associated with GDM odds through statistical method of dimension reduction like PCA. The results of the few studies that assessed the association of individual fatty acids with incident GDM showed some inconsistency with the present study's findings (9). Reasons for such variability include differences in gestational age at blood sample collection, biological specimen sampled, and the method of fatty acid measurement or expression.…”

Section: Discussioncontrasting

confidence: 98%

“…One case-control study nested in a cohort of US women suggested a beneficial role of odd-chain fatty acids, 22:5n-3 and 22:4n-6 in prevention of GDM, while 16:0, 18:3n-6, and 20:3n-6 at 10-14 weeks of pregnancy were associated with increased risk of GDM (10,11). In normal pregnancy, plasma phospholipids in maternal circulation would increase by nearly 50% as compared to non-pregnant circulation (9), and the composition of plasma fatty acids is expected to fluctuate throughout gestation, which may lead to the discrepancy in the association between individual fatty acids and GDM risk in different trimesters on pregnancy (15,17). Ortega-Senovilla et al found that in the serum of women with GDM, the concentrations of most fatty acids were lower than in control women, except for 20:4n-6 and 22:6n-3, which remained the same.…”

Section: Discussionmentioning

confidence: 99%

“…It should also be noted that the placenta plays an essential role in determining how fatty acids are transferred from maternal to embryonic circulation (49). Multiple studies have evaluated placental preference of fatty acid transport and found that the placenta places a higher preference on docosahexaenoic acid transport (9). However, GDM appears to influence the transfer of PUFAs from mother to fetus.…”

Section: Discussionmentioning

confidence: 99%

“…As the important composition of fat, fatty acids in tissues can reflect both the quantity and quality of dietary fat intake without being affected by recall bias and have been considered as reliable biomarkers in epidemiologic studies (8). However, up to date, limited studies have explored the difference of fatty acid profile between women with and without GDM (9). Some of them have suggested that certain fatty acids might be associated with the development of GDM, but the results were inconsistent and partly depends on the fatty acids involved (10)(11)(12)(13)(14)(15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

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Associations of Plasma Fatty Acid Patterns During Pregnancy With Gestational Diabetes Mellitus

Huang

Zhu

et al. 2022

Front. Nutr.

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BackgroundLimited studies have explored the difference of fatty acid profile between women with and without gestational diabetes mellitus (GDM), and the results were inconsistent. Individual fatty acids tend to be interrelated because of the shared food sources and metabolic pathways. Thus, whether fatty acid patters during pregnancy were related to GDM odds needs further exploration.ObjectiveTo identify plasma fatty acid patters during pregnancy and their associations with odds of GDM.MethodsA hospital-based case-control study including 217 GDM cases and 217 matched controls was carried out in urban Wuhan, China from August 2012 to April 2015. All the participants were enrolled at the time of GDM screening and provided fasting blood samples with informed consent. We measured plasma concentrations of fatty acids by gas chromatography–mass spectrometry, and derived potential fatty acid patterns (FAPs) through principal components analysis. Conditional logistic regression and restricted cubic spline model were used to evaluate the associations between individual fatty acids or FAPs and odds of GDM.ResultsTwenty individual fatty acids with relative concentrations ≥0.05% were included in the analyses. Compared with control group, GDM group had significantly higher concentrations of total fatty acids, 24:1n-9, and relatively lower levels of 14:0, 15:0, 17:0, 18:0, 24:0, 16:1n-7, 20:1n-9,18:3n-6, 20:2n-6, 18:3n-3, 20:3n-3, 22:5n-3. Two novel patterns of fatty acids were identified to be associated with lower odds of GDM: (1) relatively higher odd-chain fatty acids, 14:0, 18:0, 18:3n-3, 20:2n-6, 20:3n-6 and lower 24:1n-9 and 18:2n-6 [adjusted odds ratio (OR) (95% confidence interval) (CI) for quartiles 4 vs. 1: 0.42 (0.23–0.76), P-trend = 0.002], (2) relatively higher n-3 polyunsaturated fatty acids, 24:0, 18:3n-6 and lower 16:0 and 20:4n-6 [adjusted OR (95% CI) for quartiles 4 vs. 1: 0.48 (0.26–0.90), P-trend = 0.018].ConclusionOur findings suggested that two novel FAPs were inversely associated with GDM odds. The combination of circulating fatty acids could be a more significant marker of GDM development than individual fatty acids or their subgroups.

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Section: Discussioncontrasting

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Associations of Plasma Fatty Acid Patterns During Pregnancy With Gestational Diabetes Mellitus

Huang

Zhu

et al. 2022

Front. Nutr.

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“…This may explain the findings in preeclampsia of accumulation of TUFAs in third-trimester placentas ( Wada et al, 2017 ); significantly increased highly polyunsaturated cholesterol esters, triacylglycerols, and phosphatidylcholines; increased total phospholipids ( Brown et al, 2016 ); and increased sphingomyelin ( Del Gaudio et al, 2020 ). When compared to controls, preeclampsia maternal serum has increased PUFAs ( Al et al, 1995 ; Anand et al, 2016 ; Irwinda et al, 2021 ) with an elevated omega 6:3 ratio ( Williams et al, 1995 ) and increased oxidation of several lipids ( He et al, 2021 ; Mauro et al, 2022 ), while lipids are relatively normal in fetal blood ( van der Schouw et al, 1991 ). The finding of increased de novo synthesis of ceramides in the placenta, increased maternal serum ceramides, and reduced lysosomal breakdown prompted one research group to typify preeclampsia as a sphingolipid storage disease ( Melland-Smith et al, 2015 ).…”

Section: Lipidomics Of Preeclampsiamentioning

confidence: 99%

A theoretical model of dietary lipid variance as the origin of primary ciliary dysfunction in preeclampsia

Hart

2023

Front. Mol. Biosci.

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Serving as the cell’s key interface in communicating with the outside world, primary cilia have emerged as an area of multidisciplinary research interest over the last 2 decades. Although the term “ciliopathy” was first used to describe abnormal cilia caused by gene mutations, recent studies focus on abnormalities of cilia that are found in diseases without clear genetic antecedents, such as obesity, diabetes, cancer, and cardiovascular disease. Preeclampsia, a hypertensive disease of pregnancy, is intensely studied as a model for cardiovascular disease partially due to many shared pathophysiologic elements, but also because changes that develop over decades in cardiovascular disease arise in days with preeclampsia yet resolve rapidly after delivery, thus providing a time-lapse view of the development of cardiovascular pathology. As with genetic primary ciliopathies, preeclampsia affects multiple organ systems. While aspirin delays the onset of preeclampsia, there is no cure other than delivery. The primary etiology of preeclampsia is unknown; however, recent reviews emphasize the fundamental role of abnormal placentation. During normal embryonic development, trophoblastic cells, which arise from the outer layer of the 4-day-old blastocyst, invade the maternal endometrium and establish extensive placental vascular connections between mother and fetus. In primary cilia of trophoblasts, Hedgehog and Wnt/catenin signaling operate upstream of vascular endothelial growth factor to advance placental angiogenesis in a process that is promoted by accessible membrane cholesterol. In preeclampsia, impaired proangiogenic signaling combined with an increase in apoptotic signaling results in shallow invasion and inadequate placental function. Recent studies show primary cilia in preeclampsia to be fewer in number and shortened with functional signaling abnormalities. Presented here is a model that integrates preeclampsia lipidomics and physiology with the molecular mechanisms of liquid–liquid phase separation in model membrane studies and the known changes in human dietary lipids over the last century to explain how changes in dietary lipids might reduce accessible membrane cholesterol and give rise to shortened cilia and defects in angiogenic signaling, which underlie placental dysfunction of preeclampsia. This model offers a possible mechanism for non-genetic dysfunction in cilia and proposes a proof-of-concept study to treat preeclampsia with dietary lipids.

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Vitronectin promotes insulin resistance in trophoblast cells by activating JNK in gestational diabetes mellitus

Ju,

Shen,

Guo

et al. 2024

Cell Biology International

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Gestational diabetes mellitus (GDM) is a common disorder in the clinic, which may lead to severe detrimental outcomes both for mothers and infants. However, the underlying mechanisms for GDM are still not clear. In the present study, we performed label‐free proteomics using placentas from GDM patients and normal controls. Vitronectin caused our attention among differentially expressed proteins due to its potential role in the pathological progression of GDM. Vitronectin was increased in the placentas of GDM patients, which was confirmed by Western blot analysis. Vitronectin represses insulin signal transduction in trophoblast cells, whereas the knockdown of vitronectin further potentiates insulin‐evoked events. Neutralization of CD51/61 abolishes the repressed insulin signal transduction in vitronectin‐treated trophoblast cells. Moreover, vitronectin activates JNK in a CD51/61‐depedent manner. Inhibition of JNK rescues impaired insulin signal transduction induced by vitronectin. Overall, our data indicate that vitronectin binds CD51/61 in trophoblast cells to activate JNK, and thus induces insulin resistance. In this regard, increased expression of vitronectin is likely a risk factor for the pathological progression of GDM. Moreover, blockade of vitronectin production or its receptors (CD51/61) may have therapeutic potential for dealing with GDM.

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Fatty acids in normal and pathological pregnancies

Cited by 12 publications

References 143 publications

Associations of Plasma Fatty Acid Patterns During Pregnancy With Gestational Diabetes Mellitus

Associations of Plasma Fatty Acid Patterns During Pregnancy With Gestational Diabetes Mellitus

A theoretical model of dietary lipid variance as the origin of primary ciliary dysfunction in preeclampsia

Vitronectin promotes insulin resistance in trophoblast cells by activating JNK in gestational diabetes mellitus

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