Maternal obesity disrupts biochemical trophoblast differentiation.

Placenta ◽  
2021 ◽  
Vol 112 ◽  
pp. e52
Author(s):  
Marta Hita Hernandez ◽  
Claire Priou ◽  
Esther Dos Santos ◽  
Paul Berveiller ◽  
François Vialard
2020 ◽  
Vol 134 (18) ◽  
pp. 2447-2451
Author(s):  
Anissa Viveiros ◽  
Gavin Y. Oudit

Abstract The global prevalence of obesity has been rising at an alarming rate, accompanied by an increase in both childhood and maternal obesity. The concept of metabolic programming is highly topical, and in this context, describes a predisposition of offspring of obese mothers to the development of obesity independent of environmental factors. Research published in this issue of Clinical Science conducted by Litzenburger and colleagues (Clin. Sci. (Lond.) (2020) 134, 921–939) have identified sex-dependent differences in metabolic programming and identify putative signaling pathways involved in the differential phenotype of adipose tissue between males and females. Delineating the distinction between metabolically healthy and unhealthy obesity is a topic of emerging interest, and the precise nature of adipocytes are key to pathogenesis, independent of adipose tissue volume.


2014 ◽  
Author(s):  
Theresia H Mina ◽  
Callam Davidson ◽  
Ashley Taylor ◽  
Jane E Norman ◽  
Rebecca M Reynolds

2020 ◽  
Vol 26 (10) ◽  
pp. 1119-1125
Author(s):  
Sara Bertrando ◽  
Pietro Vajro

: This review aims to focus the links existing between several aspects of the mother-child dyad in the intricate playground of obesity and Metabolic Syndrome (MetS), including its hepatic component, the Non- Alcoholic Fatty Liver Disease (NAFLD). In recent years human and animal model studies have shown that dietary interventions in mothers and offspring can be successful in reducing the risk of NAFLD development. Evidences also concern the new concept of a real intergenerational transmission of predisposition to metabolic disorders. Certain genes, such as SIRT1 and PNPLA3, and some epigenetic modifications, including micro RNAs function, seem to be responsible for fetal reprogramming in the setting of maternal obesity. These modifiers appear to be potential therapeutic targets to reduce the risk of future metabolic dysfunctions. : Controlling antepartum hyperglycemia, preventing gestational diabetes, and avoiding excessive weight gain during pregnancy can help reduce the relentless epidemic of childhood obesity and NAFLD. Also, the composition of the intestinal microbiota seems to be related to the development of metabolic disorders in the offspring. Several studies show that breastfed infants have a microbial signature different from formula-fed infants. Much interestingly, prolonged breastfeeding is beneficial not only for the newborn and his health in adult life, but also for the mothers’ health. Maternal benefits include reducing the risk of developing chronic diseases, such as diabetes mellitus, myocardial infarction and NAFLD as well. : In conclusion, all above mechanisms appear to intervene synergistically and may act as modifiable risk factors for infant and mother NAFLD.


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