Critical periods of increased fetal vulnerability to a maternal high fat diet

Maria del Mar Plata, Lyda Williams, Yoshinori Seki, Kirsten Hartil, Harpreet Kaur, Chia Lei Lin, Ariana Fiallo, Alan S. Glenn, Ellen B. Katz, Mamta Fuloria, Maureen J. Charron, Patricia M. Vuguin

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Background: Fetal adaptations to high fat (HF) diet in utero (IU) that may predispose to Metabolic Syndrome (MetS) in adulthood include changes in fetal hepatic gene expression. Studies were performed to determine whether maternal exposure to HF diet at different stages during pregnancy had different effects on the fetus, including hepatic gene expression. Methods: Female wild type mice were fed either a HF or breeding chow (C) for 2 wks prior to mating. The experimental groups were composed of embryonic day (e) 18.5 fetuses obtained from WT female mice that were fed HF (HF, 35.5% fat) or breeding chow (C, 9.5% fat) for 2 wk before mating until e9.5 of pregnancy (periconception-midpregnancy). At e9.5 dams were switched to the opposite diet (C-HF or HF-C). Results: Exposure to HF diet throughout pregnancy reduced maternal weight gain compared to C diet (p < 0.02 HF vs. C). HF-C dams had significantly decreased adiponectin levels and litter size when compared to C-HF (p < 0.02 HF-C vs C-HF). Independent of the timing of exposure to HF, fetal weight and length were significantly decreased when compared to C diet (HF, C-HF and HF-C vs. C p < 0.02). HF diet during the second half of pregnancy increased expression of genes in the fetal liver associated with fetal growth (C-HF vs C p < 0.001), glucose production (C-HF vs C p < 0.04), oxidative stress and inflammation (C-HF vs C p < 0.01) compared to C diet. Conclusions: This model defines that there are critical periods during gestation in which the fetus is actively shaped by the environment. Early exposure to a HF diet determines litter size while exposure to HF during the second half of pregnancy leads to dysregulation of expression of key genes responsible for fetal growth, hepatic glucose production and oxidative stress. These findings underscore the importance of future studies designed to clarify how these critical periods may influence future risk of developing MetS later in life.

Original languageEnglish (US)
Article number80
JournalReproductive Biology and Endocrinology
Volume12
Issue number1
DOIs
StatePublished - 2014

Fingerprint

High Fat Diet
Fats
Mothers
Gene Expression
Litter Size
Fetus
Liver
Fetal Development
Breeding
Oxidative Stress
Diet
Maternal Exposure
Glucose
Fetal Weight
Adiponectin

ASJC Scopus subject areas

  • Developmental Biology
  • Endocrinology
  • Reproductive Medicine

Cite this

del Mar Plata, M., Williams, L., Seki, Y., Hartil, K., Kaur, H., Lin, C. L., ... Vuguin, P. M. (2014). Critical periods of increased fetal vulnerability to a maternal high fat diet. Reproductive Biology and Endocrinology, 12(1), [80]. https://doi.org/10.1186/1477-7827-12-80

Critical periods of increased fetal vulnerability to a maternal high fat diet. / del Mar Plata, Maria; Williams, Lyda; Seki, Yoshinori; Hartil, Kirsten; Kaur, Harpreet; Lin, Chia Lei; Fiallo, Ariana; Glenn, Alan S.; Katz, Ellen B.; Fuloria, Mamta; Charron, Maureen J.; Vuguin, Patricia M.

In: Reproductive Biology and Endocrinology, Vol. 12, No. 1, 80, 2014.

Research output: Contribution to journalArticle

del Mar Plata, M, Williams, L, Seki, Y, Hartil, K, Kaur, H, Lin, CL, Fiallo, A, Glenn, AS, Katz, EB, Fuloria, M, Charron, MJ & Vuguin, PM 2014, 'Critical periods of increased fetal vulnerability to a maternal high fat diet', Reproductive Biology and Endocrinology, vol. 12, no. 1, 80. https://doi.org/10.1186/1477-7827-12-80
del Mar Plata, Maria ; Williams, Lyda ; Seki, Yoshinori ; Hartil, Kirsten ; Kaur, Harpreet ; Lin, Chia Lei ; Fiallo, Ariana ; Glenn, Alan S. ; Katz, Ellen B. ; Fuloria, Mamta ; Charron, Maureen J. ; Vuguin, Patricia M. / Critical periods of increased fetal vulnerability to a maternal high fat diet. In: Reproductive Biology and Endocrinology. 2014 ; Vol. 12, No. 1.
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abstract = "Background: Fetal adaptations to high fat (HF) diet in utero (IU) that may predispose to Metabolic Syndrome (MetS) in adulthood include changes in fetal hepatic gene expression. Studies were performed to determine whether maternal exposure to HF diet at different stages during pregnancy had different effects on the fetus, including hepatic gene expression. Methods: Female wild type mice were fed either a HF or breeding chow (C) for 2 wks prior to mating. The experimental groups were composed of embryonic day (e) 18.5 fetuses obtained from WT female mice that were fed HF (HF, 35.5{\%} fat) or breeding chow (C, 9.5{\%} fat) for 2 wk before mating until e9.5 of pregnancy (periconception-midpregnancy). At e9.5 dams were switched to the opposite diet (C-HF or HF-C). Results: Exposure to HF diet throughout pregnancy reduced maternal weight gain compared to C diet (p < 0.02 HF vs. C). HF-C dams had significantly decreased adiponectin levels and litter size when compared to C-HF (p < 0.02 HF-C vs C-HF). Independent of the timing of exposure to HF, fetal weight and length were significantly decreased when compared to C diet (HF, C-HF and HF-C vs. C p < 0.02). HF diet during the second half of pregnancy increased expression of genes in the fetal liver associated with fetal growth (C-HF vs C p < 0.001), glucose production (C-HF vs C p < 0.04), oxidative stress and inflammation (C-HF vs C p < 0.01) compared to C diet. Conclusions: This model defines that there are critical periods during gestation in which the fetus is actively shaped by the environment. Early exposure to a HF diet determines litter size while exposure to HF during the second half of pregnancy leads to dysregulation of expression of key genes responsible for fetal growth, hepatic glucose production and oxidative stress. These findings underscore the importance of future studies designed to clarify how these critical periods may influence future risk of developing MetS later in life.",
author = "{del Mar Plata}, Maria and Lyda Williams and Yoshinori Seki and Kirsten Hartil and Harpreet Kaur and Lin, {Chia Lei} and Ariana Fiallo and Glenn, {Alan S.} and Katz, {Ellen B.} and Mamta Fuloria and Charron, {Maureen J.} and Vuguin, {Patricia M.}",
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AU - del Mar Plata, Maria

AU - Williams, Lyda

AU - Seki, Yoshinori

AU - Hartil, Kirsten

AU - Kaur, Harpreet

AU - Lin, Chia Lei

AU - Fiallo, Ariana

AU - Glenn, Alan S.

AU - Katz, Ellen B.

AU - Fuloria, Mamta

AU - Charron, Maureen J.

AU - Vuguin, Patricia M.

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N2 - Background: Fetal adaptations to high fat (HF) diet in utero (IU) that may predispose to Metabolic Syndrome (MetS) in adulthood include changes in fetal hepatic gene expression. Studies were performed to determine whether maternal exposure to HF diet at different stages during pregnancy had different effects on the fetus, including hepatic gene expression. Methods: Female wild type mice were fed either a HF or breeding chow (C) for 2 wks prior to mating. The experimental groups were composed of embryonic day (e) 18.5 fetuses obtained from WT female mice that were fed HF (HF, 35.5% fat) or breeding chow (C, 9.5% fat) for 2 wk before mating until e9.5 of pregnancy (periconception-midpregnancy). At e9.5 dams were switched to the opposite diet (C-HF or HF-C). Results: Exposure to HF diet throughout pregnancy reduced maternal weight gain compared to C diet (p < 0.02 HF vs. C). HF-C dams had significantly decreased adiponectin levels and litter size when compared to C-HF (p < 0.02 HF-C vs C-HF). Independent of the timing of exposure to HF, fetal weight and length were significantly decreased when compared to C diet (HF, C-HF and HF-C vs. C p < 0.02). HF diet during the second half of pregnancy increased expression of genes in the fetal liver associated with fetal growth (C-HF vs C p < 0.001), glucose production (C-HF vs C p < 0.04), oxidative stress and inflammation (C-HF vs C p < 0.01) compared to C diet. Conclusions: This model defines that there are critical periods during gestation in which the fetus is actively shaped by the environment. Early exposure to a HF diet determines litter size while exposure to HF during the second half of pregnancy leads to dysregulation of expression of key genes responsible for fetal growth, hepatic glucose production and oxidative stress. These findings underscore the importance of future studies designed to clarify how these critical periods may influence future risk of developing MetS later in life.

AB - Background: Fetal adaptations to high fat (HF) diet in utero (IU) that may predispose to Metabolic Syndrome (MetS) in adulthood include changes in fetal hepatic gene expression. Studies were performed to determine whether maternal exposure to HF diet at different stages during pregnancy had different effects on the fetus, including hepatic gene expression. Methods: Female wild type mice were fed either a HF or breeding chow (C) for 2 wks prior to mating. The experimental groups were composed of embryonic day (e) 18.5 fetuses obtained from WT female mice that were fed HF (HF, 35.5% fat) or breeding chow (C, 9.5% fat) for 2 wk before mating until e9.5 of pregnancy (periconception-midpregnancy). At e9.5 dams were switched to the opposite diet (C-HF or HF-C). Results: Exposure to HF diet throughout pregnancy reduced maternal weight gain compared to C diet (p < 0.02 HF vs. C). HF-C dams had significantly decreased adiponectin levels and litter size when compared to C-HF (p < 0.02 HF-C vs C-HF). Independent of the timing of exposure to HF, fetal weight and length were significantly decreased when compared to C diet (HF, C-HF and HF-C vs. C p < 0.02). HF diet during the second half of pregnancy increased expression of genes in the fetal liver associated with fetal growth (C-HF vs C p < 0.001), glucose production (C-HF vs C p < 0.04), oxidative stress and inflammation (C-HF vs C p < 0.01) compared to C diet. Conclusions: This model defines that there are critical periods during gestation in which the fetus is actively shaped by the environment. Early exposure to a HF diet determines litter size while exposure to HF during the second half of pregnancy leads to dysregulation of expression of key genes responsible for fetal growth, hepatic glucose production and oxidative stress. These findings underscore the importance of future studies designed to clarify how these critical periods may influence future risk of developing MetS later in life.

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