Maternal Lipids and Fetal Overgrowth: Making Fat from Fat

Barbour, Linda A.; Hernandez, Teri L.

doi:10.1016/j.clinthera.2018.08.007

Cited by 90 publications

(83 citation statements)

References 80 publications

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“…Although much of the focus on fetal growth has been through a glucocentric lens, there is increasing recognition that it is not only maternal glucose that contributes to fetal fat accretion and that triglycerides (TGs) and FFAs also play a significant role ( 35 – 39 ). Another unexpected twist in our earlier CGM data ( 29 ), during which women with obesity on a controlled diet demonstrated higher 24-h glycemic profiles, was that a single fasting TG measured once at ∼14–16 weeks in pregnancy correlated more strongly with NB %fat by skinfolds than any of the glycemic profiles by CGM.…”

Section: The Underappreciated Role Of Maternal Lipids As a Contributomentioning

confidence: 99%

“…1 ). Lipid metabolism in pregnancy is also highly variable, partly related to the estrogen-induced influence of VLDL production in pregnancy and CM-TG in the diet, superimposed on the degree of maternal adipose tissue IR ( 31 , 39 ). The degree to which TGs and FFAs may contribute to fetal fat accretion has yet to be fully elucidated, but observations that maternal glucose does not solely explain fetal overgrowth support its future investigation as a therapeutic target.…”

Section: Targeting Who What and When To Prevent Adverse Pregnancy Omentioning

confidence: 99%

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Metabolic Culprits in Obese Pregnancies and Gestational Diabetes Mellitus: Big Babies, Big Twists, Big Picture

Barbour

2019

Diabetes Care

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Pregnancy has been equated to a "stress test" in which placental hormones and growth factors expose a mother's predisposition toward metabolic disease, unleashing her previously occult insulin resistance (IR), mild b-cell dysfunction, and glucose and lipid surplus due to the formidable forces of pregnancy-induced IR. Although pregnancy-induced IR is intended to assure adequate nutrition to the fetus and placenta, in mothers with obesity, metabolic syndrome, or those who develop gestational diabetes mellitus, this overnutrition to the fetus carries a lifetime risk for increased metabolic disease. Norbert Freinkel, nearly 40 years ago, coined this excess intrauterine nutrient exposure and subsequent offspring developmental risk "fuel-mediated teratogenesis," not limited to only excess maternal glucose. Our attempts to better elucidate the causes and mechanisms behind this double-edged IR of pregnancy, to metabolically characterize the intrauterine environment that results in changes in newborn body composition and later childhood obesity risk, and to examine potential therapeutic approaches that might target maternal metabolism are the focus of this article. Rapidly advancing technologies in genomics, proteomics, and metabolomics offer us innovative approaches to interrogate these metabolic processes in the mother, her microbiome, the placenta, and her offspring that contribute to a phenotype at risk for future metabolic disease. If we are successful in our efforts, the researcher, endocrinologist, obstetrician, and health care provider fortunate enough to care for pregnant women have the unique opportunity to positively impact health outcomes not only in the short term but in the long run, not just in one life but in twodand possibly, for the next generation.

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Section: The Underappreciated Role Of Maternal Lipids As a Contributomentioning

confidence: 99%

Section: Targeting Who What and When To Prevent Adverse Pregnancy Omentioning

confidence: 99%

Metabolic Culprits in Obese Pregnancies and Gestational Diabetes Mellitus: Big Babies, Big Twists, Big Picture

Barbour

2019

Diabetes Care

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“…Moreover, offspring who were overgrown during fetal development (macrosomia) as a result of maternal obesity had impaired glucose tolerance, elevated fasting insulin level, as well as increased adiposity and metabolic diseases (Stanford et al . ; Barbour & Hernandez, ). Thus, maintaining proper vasculogenesis and placental function in obese mothers is a critical step for preventing metabolic dysfunction in their offspring (Bairagi et al .…”

Section: Introductionmentioning

confidence: 97%

Exercise prevents the adverse effects of maternal obesity on placental vascularization and fetal growth

Son

Liu

Tian

et al. 2019

The Journal of Physiology

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Key pointsr Maternal exercise improves the metabolic health of maternal mice challenged with a high-fat diet.r Exercise intervention of obese mothers prevents fetal overgrowth. r Exercise intervention reverses impaired placental vascularization in obese mice. r Maternal exercise activates placental AMP-activated protein kinase, which was inhibited as a result of maternal obesity.Abstract More than one-third of pregnant women in the USA are obese and maternal obesity (MO) negatively affects fetal development, which predisposes offspring to metabolic diseases. The placenta mediates nutrient delivery to fetuses and its function is impaired as a result of MO. Exercise ameliorates metabolic dysfunction resulting from obesity, although its effect on placental function of obese mothers has not been explored. In the present study, C57BL/6J female mice were randomly assigned into two groups fed either a control or a high-fat diet (HFD) and then the mice on each diet were further divided into two subgroups with/without exercise. In HFD-induced obese mice, daily treadmill exercise during pregnancy reduced body weight gain, lowered serum glucose and lipid concentration, and improved insulin sensitivity of maternal mice. Importantly, maternal exercise prevented fetal overgrowth (macrosomia) induced by MO. To further examine the preventive effects of exercise on fetal overgrowth, placental vascularization and nutrient transporters were analysed. Vascular density and the expression of vasculogenic factors were reduced as a result of MO but were recovered by maternal exercise. On the other hand, the contents of nutrient transporters were not substantially altered by MO or exercise, suggesting that the protective effects of exercise in MO-induced fetal overgrowth were primarily a result of the alteration of placental vascularization and improved maternal metabolism. Furthermore, exercise enhanced downstream insulin signalling and activated AMP-activated protein kinase in HFD placenta. In sum, maternal exercise prevented fetal overgrowth induced by MO, which was Jun Seok Son received MS Degree in Kinesiology from Seoul National University. Currently, Jun Seok is a PhD student in the . His research interests focus on the impacts of maternal obesity, exercise, nutrition and other physiological conditions on fetal development and offspring health, especially the epigenetic mechanisms linking nutrients/metabolites to progenitor cell differentiation into myocytes/adipocytes. Ultimately, he aims to translate his work into clinical practice with respect to improving health outcomes for mothers and children affected by obesity.

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“…Foetal development is in uenced by neonatal and maternal metabolism [34,35] , and in the present study, we analysed the effects of neonatal carnitine levels and amino acids on neonatal growth parameters. We found that cord blood glycine levels were correlated with GDM a .…”

Section: Discussionmentioning

confidence: 99%

Mid-late pregnancy maternal glycolipids in gestational diabetes mellitus (GDM) fluctuated in glycosylated hemoglobin levels of 5.5%-6.4% associated with umbilical cord blood of amino acid and carnitine profiles: a nested case-cohort observational study

Long¹,

Chen²,

Yang³

et al. 2020

Preprint

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Background To explore the relationship between maternal-neonatal clinical data and the changes of cord blood amino acid and carnitine levels between pregnant women with gestational diabetes mellitus (GDM) when glycosylated hemoglobin levels of 5.5%-6.4% excluded diabetic medicine as GDMa group and the control group. Methods In all, 312 qualified participants were recruited with permission from the ethical department of the Fifth Affiliated Hospital of Sun Yat-Sen University and divided into two groups (GDMa and non-GDM) after adjusting for maternal age and body mass index (BMI) between the 1 June 2017 and 30 April 2020. All maternal-neonatal data were collected and analysed at the centre. Results Interestingly, glycine in cord blood was not only significantly different between groups(594.19 vs 407.45, P < 0.001), but also associated among those pregnant women in GDM when glycosylated hemoglobin levels of 5.5%-6.4% through the standard of diet control and exercise (b = 0.449, P = 0.010). Meanwhile, neonatal hypoglycemia had the positive association with GDM monitoring glycosylated hemoglobin levels of 5.5%-6.4% (P = 0.031, OR 5.77 95%CI[1.18, 28.36]), but none of correlations with umbilical cord blood of amino acids and carnitines. Conclusions The study identifies some differences and relationships in maternal-neonatal data only when GDMa group, glycosylated hemoglobin levels of 5.5%-6.4% without diabetic medicine, compared with the control group which adjusted by age and BMI. Particularly, umbilical cord blood of glycine levels is related to the diabetic status of glycosylated hemoglobin 5.5%-6.4% in GDM during pregnancy and could be potential diabetic mechanism by maternal-fetal interface.

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Maternal Lipids and Fetal Overgrowth: Making Fat from Fat

Cited by 90 publications

References 80 publications

Metabolic Culprits in Obese Pregnancies and Gestational Diabetes Mellitus: Big Babies, Big Twists, Big Picture

Metabolic Culprits in Obese Pregnancies and Gestational Diabetes Mellitus: Big Babies, Big Twists, Big Picture

Exercise prevents the adverse effects of maternal obesity on placental vascularization and fetal growth

Mid-late pregnancy maternal glycolipids in gestational diabetes mellitus (GDM) fluctuated in glycosylated hemoglobin levels of 5.5%-6.4% associated with umbilical cord blood of amino acid and carnitine profiles: a nested case-cohort observational study

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