Embryonic programming of heart disease in response to obesity during pregnancy

Ahmed, Aisha; Delgado-Olguı́n, Paul

doi:10.1016/j.bbadis.2019.01.028

Cited by 9 publications

(8 citation statements)

References 130 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…57 Cardiomyocyte immature metabolism (mainly fuelled by the glycolytic pathway) leads to foetal cardiac hypertrophy (different from the adult hypertrophy-related increase in contractile elements) and may persist throughout life. 11 Maternal diabetes stimulates foetal cardiomyocyte proliferation while inhibiting its maturation through the pentose phosphate pathway. 58 This leads to heart hypertrophy due to a high number of cardiomyocytes with lower contractile capability and the enrichment of apoptotic cells induced by increased mitochondrial production of reactive oxygen species (ROS).…”

Section: Maternal Glucose Metabolism and Influence On Foetal Organs Growthmentioning

confidence: 99%

“…Foetal programming alterations often lead to a homeostatic state that presents lower metabolic plasticity and lower adaptability to postnatal insults, predisposing to early development of chronic disease (eg metabolic, cardiovascular and endocrine disease). [9][10][11] Specific stimuli, mostly of maternal origin, may affect foetal gene expression, which may lead to foetal programming at any stage of development. Some alterations induce temporary adaptations, while others can persist throughout adult life or even generations.…”

Section: Introductionmentioning

confidence: 99%

“…Maternal malnutrition results in fewer cardiomyocyte number and inadequate maturation already observed in early stages 57 . Cardiomyocyte immature metabolism (mainly fuelled by the glycolytic pathway) leads to foetal cardiac hypertrophy (different from the adult hypertrophy‐related increase in contractile elements) and may persist throughout life 11 . Maternal diabetes stimulates foetal cardiomyocyte proliferation while inhibiting its maturation through the pentose phosphate pathway 58 .…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Metabolic Disease Programming: From Mitochondria to Epigenetics, Glucocorticoid Signalling and Beyond

Grilo

Tocantins

Diniz

et al. 2021

Eur J Clin Investigation

View full text Add to dashboard Cite

Embryonic and foetal development are critical periods of development in which several environmental cues determine health and disease in adulthood. Maternal conditions and an unfavourable intrauterine environment impact foetal development and may programme the offspring for increased predisposition to metabolic diseases and other chronic pathologic conditions throughout adult life. Previously, non-communicable chronic diseases were only associated with genetics and lifestyle. Now the origins of non-communicable chronic diseases are associated with earlylife adaptations that produce long-term dysfunction. Early-life environment sets the long-term health and disease risk and can span through multiple generations. Recent research in developmental programming aims at identifying the molecular mechanisms responsible for developmental programming outcomes that impact cellular physiology and trigger adulthood disease. The identification of new therapeutic targets can improve offspring's health management and prevent or overcome adverse consequences of foetal programming. This review summarizes recent biomedical discoveries in the Developmental Origins of Health and Disease (DOHaD) hypothesis and highlight possible developmental programming mechanisms, including prenatal structural defects, metabolic (mitochondrial dysfunction, oxidative stress, protein modification), epigenetic and glucocorticoid signalling-related mechanisms suggesting molecular clues for the causes and consequences of programming of increased susceptibility of offspring to metabolic disease after birth. Identifying mechanisms involved in DOHaD can contribute to early interventions in pregnancy or 2 of 21 | GRILO et aL.

show abstract

Section: Maternal Glucose Metabolism and Influence On Foetal Organs Growthmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Metabolic Disease Programming: From Mitochondria to Epigenetics, Glucocorticoid Signalling and Beyond

Grilo

Tocantins

Diniz

et al. 2021

Eur J Clin Investigation

View full text Add to dashboard Cite

show abstract

“…Pregestational obesity not only promotes the development of maternal gestational diabetes and fetal overgrowth; it has extensive consequences on the metabolic and endocrine development of the growing fetus as well. During embryonic development (the first 8 weeks after conception), environmental factors, such as changes in nutrient transport to the embryo mediated by an unfavorable maternal endocrine environment, might lead to obesogenic fetal programming with subsequent fetal overgrowth and long-term health consequences for the offspring, such as childhood obesity or cardiovascular diseases in later life [ 31 ]. Thereby, placental nutrient transport (due to altered placental gene expression) might be either modified by an altered adipokine secretion, as suggested by some authors [ 32 , 33 ], or by the chronic hyperinsulinemic environment associated with insulin resistance in mothers with obesity, as observed in this study.…”

Section: Discussionmentioning

confidence: 99%

Glucometabolic Alterations in Pregnant Women with Overweight or Obesity but without Gestational Diabetes Mellitus: An Observational Study

Linder,

Eppel,

Kotzaeridi

et al. 2023

Obes Facts

View full text Add to dashboard Cite

Introduction: Maternal overweight is a risk factor for Gestational Diabetes Mellitus (GDM). However, emerging evidence suggests that an increased maternal body mass index (BMI) promotes the development of perinatal complications even in women who do not develop GDM. This study aims to assess physiological glucometabolic changes associated with increased BMI. Methods: 21 women with overweight and 21 normal weight controls received a metabolic assessment at 13 weeks of gestation, including a 60 min frequently sampled intravenous glucose tolerance test. A further investigation was performed between 24 and 28 weeks in women who remained normal glucose tolerant. Results: At baseline, mothers with overweight showed impaired insulin action, whereby the calculated insulin sensitivity index (CSI) was lower as compared to normal weight controls (3.5 vs. 6.7 10-4 min-1 [microU/ml]-1, p=0.025). After excluding women who developed GDM, mothers with overweight showed higher average glucose during the oral glucose tolerance test (OGTT) at third trimester. Moreover, early pregnancy insulin resistance and secretion were associated with increased placental weight in normal glucose tolerant women. Conclusion: Mothers with overweight or obesity show an unfavourable metabolic environment already at the early stage of pregnancy, possibly associated with perinatal complications in women who remain normal glucose tolerant.

show abstract

“…To date, a plethora of experiments have focused mainly on the under and over-nutrition of mothers (e.g., a low protein diet [23], high fat diet [24], caloric restrictions [25], and obesity [26]). Recent studies have shown that bioactive compounds introduced into the maternal diet may significantly influence the composition and/or functioning of certain tissues and organs [27][28][29].…”

Section: Introductionmentioning

confidence: 99%

Maternal and Early Postnatal Diet Supplemented with Conjugated Linoleic Acid Isomers Affect Lipid Profile in Hearts of Offspring Rats with Mammary Tumors

Białek

Czauderna

2020

Animals

View full text Add to dashboard Cite

Linking the early life environment with later health status is known as “developmental programming”. This study aimed to assess whether the introduction of conjugated linoleic acids (CLAs) into the maternal diet affects the content fatty acids (FAs), conjugated FAs (CFAs), cholesterol, oxysterols, malondialdehyde (MDA) and tocopherols in the hearts of their female offspring treated with 7,12-dimethylbenz[a]anthracene and if offspring supplementation enhanced the effect of maternal supplementation. FA, cholesterol and oxysterol contents were determined by gas chromatography-mass spectrometry, while contents of CFAs and MDA were determined by high-performance liquid chromatography (HPLC) with photodiode detection. The supplementation of mothers with CLAs significantly decreased the amount of atherogenic saturated FAs and enhanced the level of eicosapentaenoic FA in the hearts of offspring. Continuous progeny supplementation decreased the content of arachidonic acid in hearts. Supplementation of the maternal diet with CLAs and its continuation during the postnatal period increased the ratio of hypo to hypercholesterolemic FAs. Significantly fewer oxysterols were detected in the hearts of progeny of dams fed with CLAs as compared to the offspring of mothers receiving safflower oil. Both fetal and postnatal CLA intake significantly reduced 7β-hydroxycholesterol accumulation. It can be concluded that CLA supplementation during the fetal and postnatal period may be an effective method of maintaining the cardiac health status of newborns.

show abstract

Embryonic programming of heart disease in response to obesity during pregnancy

Cited by 9 publications

References 130 publications

Metabolic Disease Programming: From Mitochondria to Epigenetics, Glucocorticoid Signalling and Beyond

Metabolic Disease Programming: From Mitochondria to Epigenetics, Glucocorticoid Signalling and Beyond

Glucometabolic Alterations in Pregnant Women with Overweight or Obesity but without Gestational Diabetes Mellitus: An Observational Study

Maternal and Early Postnatal Diet Supplemented with Conjugated Linoleic Acid Isomers Affect Lipid Profile in Hearts of Offspring Rats with Mammary Tumors

Contact Info

Product

Resources

About