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Type: Journal article
Title: Characterisation of the maternal response to chronic phase shifts during gestation in the rat: implications for fetal metabolic programming
Author: Varcoe, T.
Boden, M.
Voultsios, A.
Salkeld, M.
Rattanatray, L.
Kennaway, D.
Citation: PLoS One, 2013; 8(1):1-13
Publisher: Public Library of Science
Issue Date: 2013
ISSN: 1932-6203
Statement of
Tamara J. Varcoe, Michael J. Boden, Athena Voultsios, Mark D. Salkeld, Leewen Rattanatray, David J. Kennaway
Abstract: Disrupting maternal circadian rhythms through exposure to chronic phase shifts of the photoperiod has lifelong consequences for the metabolic homeostasis of the fetus, such that offspring develop increased adiposity, hyperinsulinaemia and poor glucose and insulin tolerance. In an attempt to determine the mechanisms by which these poor metabolic outcomes arise, we investigated the impact of chronic phase shifts (CPS) on maternal and fetal hormonal, metabolic and circadian rhythms. We assessed weight gain and food consumption of dams exposed to either CPS or control lighting conditions throughout gestation. At day 20, dams were assessed for plasma hormone and metabolite concentrations and glucose and insulin tolerance. Additionally, the expression of a range of circadian and metabolic genes was assessed in maternal, placental and fetal tissue. Control and CPS dams consumed the same amount of food, yet CPS dams gained 70% less weight during the first week of gestation. At day 20, CPS dams had reduced retroperitoneal fat pad weight (−15%), and time-of-day dependent decreases in liver weight, whereas fetal and placental weight was not affected. Melatonin secretion was not altered, yet the timing of corticosterone, leptin, glucose, insulin, free fatty acids, triglycerides and cholesterol concentrations were profoundly disrupted. The expression of gluconeogenic and circadian clock genes in maternal and fetal liver became either arrhythmic or were in antiphase to the controls. These results demonstrate that disruptions of the photoperiod can severely disrupt normal circadian profiles of plasma hormones and metabolites, as well as gene expression in maternal and fetal tissues. Disruptions in the timing of food consumption and the downstream metabolic processes required to utilise that food, may lead to reduced efficiency of growth such that maternal weight gain is reduced during early embryonic development. It is these perturbations that may contribute to the programming of poor metabolic homeostasis in the offspring.
Keywords: Liver; Fetus; Placenta; Animals; Rats; Rats, Wistar; Hormones; Insulin; Glucose Tolerance Test; Mothers; Gene Expression Regulation, Developmental; Circadian Rhythm; Pregnancy; Eating; Photoperiod; Female; Male; Circadian Clocks
Rights: © 2013 Varcoe et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
RMID: 0020124869
DOI: 10.1371/journal.pone.0053800
Grant ID:
Appears in Collections:Obstetrics and Gynaecology publications

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