Maternal lipids predict Macrosomia risk

Author(s):  
Chong RAO ◽  
Fan PING
Keyword(s):  
2013 ◽  
Vol 163 (4) ◽  
pp. 983-988 ◽  
Author(s):  
Michael S. Kramer ◽  
Susan R. Kahn ◽  
Mourad Dahhou ◽  
James Otvos ◽  
Jacques Genest ◽  
...  

2013 ◽  
Vol 13 (1) ◽  
Author(s):  
Elaine M Fyfe ◽  
Karen S Rivers ◽  
John MD Thompson ◽  
Kamala PL Thiyagarajan ◽  
Katie M Groom ◽  
...  

2011 ◽  
Vol 28 (9) ◽  
pp. 1053-1059 ◽  
Author(s):  
U. M. Schaefer-Graf ◽  
K. Meitzner ◽  
H. Ortega-Senovilla ◽  
K. Graf ◽  
K. Vetter ◽  
...  

Author(s):  
Emilio Herrera ◽  
Gernot Desoye

AbstractMaternal lipids are strong determinants of fetal fat mass. Here we review the overall lipid metabolism in normal and gestational diabetes mellitus (GDM) pregnancies. During early pregnancy, the increase in maternal fat depots is facilitated by insulin, followed by increased adipose tissue breakdown and subsequent hypertriglyceridemia, mainly as a result of insulin resistance (IR) and estrogen effects. The response to diabetes is variable as a result of greater IR but decreased estrogen levels. The vast majority of fatty acids (FAs) in the maternal circulation are esterified and associated with lipoproteins. These are taken up by the placenta and hydrolyzed by lipases. The released FAs enter various metabolic routes and are released into fetal circulation. Although these determinants are modified in maternal GDM, the fetus does not seem to receive more FAs than in non-GDM pregnancies. Long-chain polyunsaturated FAs are essential for fetal development and are obtained from the mother. Mitochondrial FA oxidation occurs in fetal tissue and in placenta and contributes to energy production. Fetal fat accretion during the last weeks of gestation occurs very rapidly and is sustained not only by FAs crossing the placenta, but also by fetal lipogenesis. Fetal hyperinsulinemia in GDM mothers promotes excess accretion of adipose tissue, which gives rise to altered adipocytokine profiles. Fetal lipoproteins are low at birth, but the GDM effects are unclear. The increase in body fat in neonates of GDM women is a risk factor for obesity in early childhood and later life.


Placenta ◽  
2017 ◽  
Vol 51 ◽  
pp. 128-129
Author(s):  
C. Cantin ◽  
L. Carvajal ◽  
B. Fuenzalida ◽  
S. Contreras-Duarte ◽  
L. Sobrevia ◽  
...  

Author(s):  
F.B. Shorland ◽  
D.R. Body ◽  
J.P. Gass
Keyword(s):  

2020 ◽  
Vol 641 ◽  
pp. 123-134
Author(s):  
LN Zamora ◽  
NJ Delorme ◽  
M Byrne ◽  
MA Sewell

The eggs of echinoderms with lecithotrophic development provide structural and nutritional materials (lipids, proteins) to complete development without any external sources of nutrition. Previous studies have suggested that a relatively large proportion of the maternal lipid reserves remain after settlement to provision the early post-metamorphic juvenile. Here we examined lipid and protein utilization during lecithotrophic development of the asterinid starfish Stegnaster inflatus which has large (~400 µm diameter), negatively buoyant eggs. S. inflatus produces eggs with a large amount of lipid (mean ± SD: 2047 ± 315 ng egg-1), with 26% structural lipids and 74% energetic lipids dominated by diacylglycerol ether (DAGE; 66%). Similar amounts of protein were present in the egg (mean ± SD: 2143 ± 157 ng egg-1), with a lipid:protein ratio of 0.96. Approximately 80% of the egg protein is used prior to settlement. In contrast, 51.0% of the energetic lipids provided in the egg, and 40.3% of the DAGE remain for provisioning of the early juvenile. A review of lecithotrophic development in echinoderms reveals that asteroid, echinoid and ophiuroid species have an excess of 50% of the maternal lipids remaining in the settled post-larva. When considering maternal investment in offspring for lecithotrophic developers, we need to consider energetic use during the short dispersal period, as well as provisioning for post-metamorphic early juvenile life.


2012 ◽  
Vol 206 (1) ◽  
pp. S361-S362 ◽  
Author(s):  
Jeanette Chin ◽  
M. Sean Esplin ◽  
Michael Varner ◽  
Bob Silver
Keyword(s):  

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