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Citation
Tags
HERO ID
7241062
Reference Type
Journal Article
Title
Effect of Maternal Obesity on Placental Lipid Metabolism
Author(s)
Calabuig-Navarro, V; Haghiac, M; Minium, J; Glazebrook, P; Ranasinghe, GC; Hoppel, C; Hauguel de-Mouzon, S; Catalano, P; O'Tierney-Ginn, P; ,
Year
2017
Is Peer Reviewed?
Yes
Journal
Endocrinology
ISSN:
0013-7227
EISSN:
1945-7170
Volume
158
Issue
8
Page Numbers
2543-2555
Language
English
PMID
28541534
DOI
10.1210/en.2017-00152
Web of Science Id
WOS:000406757000013
Abstract
Obese women, on average, give birth to babies with high fat mass. Placental lipid metabolism alters fetal lipid delivery, potentially moderating neonatal adiposity, yet how it is affected by maternal obesity is poorly understood. We hypothesized that fatty acid (FA) accumulation (esterification) is higher and FA β-oxidation (FAO) is lower in placentas from obese, compared with lean women. We assessed acylcarnitine profiles (lipid oxidation intermediates) in mother-baby-placenta triads, in addition to lipid content, and messenger RNA (mRNA)/protein expression of key regulators of FA metabolism pathways in placentas of lean and obese women with normal glucose tolerance recruited at scheduled term Cesarean delivery. In isolated trophoblasts, we measured [3H]-palmitate metabolism. Placentas of obese women had 17.5% (95% confidence interval: 6.1, 28.7%) more lipid than placentas of lean women, and higher mRNA and protein expression of FA esterification regulators (e.g., peroxisome proliferator-activated receptor γ, acetyl-CoA carboxylase, steroyl-CoA desaturase 1, and diacylglycerol O-acyltransferase-1). [3H]-palmitate esterification rates were increased in trophoblasts from obese compared with lean women. Placentas of obese women had fewer mitochondria and a lower concentration of acylcarnitines, suggesting a decrease in mitochondrial FAO capacity. Conversely, peroxisomal FAO was greater in placentas of obese women. Altogether, these changes in placental lipid metabolism may serve to limit the amount of maternal lipid transferred to the fetus, restraining excess fetal adiposity in this population of glucose-tolerant women.
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