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Maternal high fat diet is associated with decreased plasma n-3 fatty acids and fetal hepatic apoptosis in nonhuman primates.

Grant WF, Gillingham MB, Batra AK, Fewkes NM, Comstock SM, Takahashi D, Braun TP, Grove KL, Friedman JE, Marks DL - PLoS ONE (2011)

Bottom Line: To begin to understand the contributions of maternal obesity and over-nutrition to human development and the early origins of obesity, we utilized a non-human primate model to investigate the effects of maternal high-fat feeding and obesity on breast milk, maternal and fetal plasma fatty acid composition and fetal hepatic development.Furthermore, the HFD fetal plasma n-6:n-3 ratio was elevated and was significantly correlated to the maternal plasma n-6:n-3 ratio and maternal hyperinsulinemia.This study links chronic maternal consumption of a HFD with fetal hepatic apoptosis and suggests that a potentially pathological maternal fatty acid milieu is replicated in the developing fetal circulation in the nonhuman primate.

View Article: PubMed Central - PubMed

Affiliation: Neuroscience Graduate Program, Oregon Health & Science University, Portland, Oregon, United States of America.

ABSTRACT
To begin to understand the contributions of maternal obesity and over-nutrition to human development and the early origins of obesity, we utilized a non-human primate model to investigate the effects of maternal high-fat feeding and obesity on breast milk, maternal and fetal plasma fatty acid composition and fetal hepatic development. While the high-fat diet (HFD) contained equivalent levels of n-3 fatty acids (FA's) and higher levels of n-6 FA's than the control diet (CTR), we found significant decreases in docosahexaenoic acid (DHA) and total n-3 FA's in HFD maternal and fetal plasma. Furthermore, the HFD fetal plasma n-6:n-3 ratio was elevated and was significantly correlated to the maternal plasma n-6:n-3 ratio and maternal hyperinsulinemia. Hepatic apoptosis was also increased in the HFD fetal liver. Switching HFD females to a CTR diet during a subsequent pregnancy normalized fetal DHA, n-3 FA's and fetal hepatic apoptosis to CTR levels. Breast milk from HFD dams contained lower levels of eicosopentanoic acid (EPA) and DHA and lower levels of total protein than CTR breast milk. This study links chronic maternal consumption of a HFD with fetal hepatic apoptosis and suggests that a potentially pathological maternal fatty acid milieu is replicated in the developing fetal circulation in the nonhuman primate.

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Related in: MedlinePlus

Offspring body composition.DEXA analysis of macaque offspring at post-natal day 30 (P30) and post-natal day 90 (P90) from CTR (white bars) and HFD (black bars) diet groups. A. Total weight of macaque offspring at P30 and P90. B. Normalized fat mass of macaque offspring between CTR and HFD diet groups at P30 and P90 (*P<.05 versus CTR, Student's t-test). C. Normalized lean body mass (LBM) of macaque offspring between CTR and HFD diet groups at P30 and P90 (*P<.05 versus CTR, Student's t-test). D. Normalized bone mineral content (BMC) of macaque offspring between CTR and HFD diet groups at P30 and P90. All data is expressed as mean ± standard error (P30 CTR; n = 15, P30 HFD; n = 17, P90 CTR; n = 13, P90 HFD; n = 19).
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pone-0017261-g005: Offspring body composition.DEXA analysis of macaque offspring at post-natal day 30 (P30) and post-natal day 90 (P90) from CTR (white bars) and HFD (black bars) diet groups. A. Total weight of macaque offspring at P30 and P90. B. Normalized fat mass of macaque offspring between CTR and HFD diet groups at P30 and P90 (*P<.05 versus CTR, Student's t-test). C. Normalized lean body mass (LBM) of macaque offspring between CTR and HFD diet groups at P30 and P90 (*P<.05 versus CTR, Student's t-test). D. Normalized bone mineral content (BMC) of macaque offspring between CTR and HFD diet groups at P30 and P90. All data is expressed as mean ± standard error (P30 CTR; n = 15, P30 HFD; n = 17, P90 CTR; n = 13, P90 HFD; n = 19).

Mentions: Given the proinflammatory environment our cohort of HFD animals were exposed to in-utero, combined with increased apoptosis in the fetal liver and the significant changes in breast milk composition, we examined the offspring from CTR and HFD dams to determine if phenotype differences were apparent in the postnatal period. Previous work with this model demonstrated that the offspring of HFD dams had similar bodyweights at postnatal day 30 (P30) and post-natal day 90 (P90) as CTR offspring, and higher levels of body-fat at P90 [47]. The current results again showed that body weights were similar between the CTR and HFD offspring at the P30 and P90 time points (Figure 5A) and that the HFD offspring had higher body fat at P90 than CTR offspring, as determined by DEXA scanning (Figure 5B). In addition, HFD offspring had significantly lower lean body mass than CTR offspring at P90 (figure 5C). We measured bone mineral content as well and found no differences at either P30 or P90 offspring between the two diet groups (Figure 5D). Thus, while total body weights are similar at P90 between CTR and HFD offspring, the HFD offspring have higher body fat and lower lean body mass than CTR offspring.


Maternal high fat diet is associated with decreased plasma n-3 fatty acids and fetal hepatic apoptosis in nonhuman primates.

Grant WF, Gillingham MB, Batra AK, Fewkes NM, Comstock SM, Takahashi D, Braun TP, Grove KL, Friedman JE, Marks DL - PLoS ONE (2011)

Offspring body composition.DEXA analysis of macaque offspring at post-natal day 30 (P30) and post-natal day 90 (P90) from CTR (white bars) and HFD (black bars) diet groups. A. Total weight of macaque offspring at P30 and P90. B. Normalized fat mass of macaque offspring between CTR and HFD diet groups at P30 and P90 (*P<.05 versus CTR, Student's t-test). C. Normalized lean body mass (LBM) of macaque offspring between CTR and HFD diet groups at P30 and P90 (*P<.05 versus CTR, Student's t-test). D. Normalized bone mineral content (BMC) of macaque offspring between CTR and HFD diet groups at P30 and P90. All data is expressed as mean ± standard error (P30 CTR; n = 15, P30 HFD; n = 17, P90 CTR; n = 13, P90 HFD; n = 19).
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3045408&req=5

pone-0017261-g005: Offspring body composition.DEXA analysis of macaque offspring at post-natal day 30 (P30) and post-natal day 90 (P90) from CTR (white bars) and HFD (black bars) diet groups. A. Total weight of macaque offspring at P30 and P90. B. Normalized fat mass of macaque offspring between CTR and HFD diet groups at P30 and P90 (*P<.05 versus CTR, Student's t-test). C. Normalized lean body mass (LBM) of macaque offspring between CTR and HFD diet groups at P30 and P90 (*P<.05 versus CTR, Student's t-test). D. Normalized bone mineral content (BMC) of macaque offspring between CTR and HFD diet groups at P30 and P90. All data is expressed as mean ± standard error (P30 CTR; n = 15, P30 HFD; n = 17, P90 CTR; n = 13, P90 HFD; n = 19).
Mentions: Given the proinflammatory environment our cohort of HFD animals were exposed to in-utero, combined with increased apoptosis in the fetal liver and the significant changes in breast milk composition, we examined the offspring from CTR and HFD dams to determine if phenotype differences were apparent in the postnatal period. Previous work with this model demonstrated that the offspring of HFD dams had similar bodyweights at postnatal day 30 (P30) and post-natal day 90 (P90) as CTR offspring, and higher levels of body-fat at P90 [47]. The current results again showed that body weights were similar between the CTR and HFD offspring at the P30 and P90 time points (Figure 5A) and that the HFD offspring had higher body fat at P90 than CTR offspring, as determined by DEXA scanning (Figure 5B). In addition, HFD offspring had significantly lower lean body mass than CTR offspring at P90 (figure 5C). We measured bone mineral content as well and found no differences at either P30 or P90 offspring between the two diet groups (Figure 5D). Thus, while total body weights are similar at P90 between CTR and HFD offspring, the HFD offspring have higher body fat and lower lean body mass than CTR offspring.

Bottom Line: To begin to understand the contributions of maternal obesity and over-nutrition to human development and the early origins of obesity, we utilized a non-human primate model to investigate the effects of maternal high-fat feeding and obesity on breast milk, maternal and fetal plasma fatty acid composition and fetal hepatic development.Furthermore, the HFD fetal plasma n-6:n-3 ratio was elevated and was significantly correlated to the maternal plasma n-6:n-3 ratio and maternal hyperinsulinemia.This study links chronic maternal consumption of a HFD with fetal hepatic apoptosis and suggests that a potentially pathological maternal fatty acid milieu is replicated in the developing fetal circulation in the nonhuman primate.

View Article: PubMed Central - PubMed

Affiliation: Neuroscience Graduate Program, Oregon Health & Science University, Portland, Oregon, United States of America.

ABSTRACT
To begin to understand the contributions of maternal obesity and over-nutrition to human development and the early origins of obesity, we utilized a non-human primate model to investigate the effects of maternal high-fat feeding and obesity on breast milk, maternal and fetal plasma fatty acid composition and fetal hepatic development. While the high-fat diet (HFD) contained equivalent levels of n-3 fatty acids (FA's) and higher levels of n-6 FA's than the control diet (CTR), we found significant decreases in docosahexaenoic acid (DHA) and total n-3 FA's in HFD maternal and fetal plasma. Furthermore, the HFD fetal plasma n-6:n-3 ratio was elevated and was significantly correlated to the maternal plasma n-6:n-3 ratio and maternal hyperinsulinemia. Hepatic apoptosis was also increased in the HFD fetal liver. Switching HFD females to a CTR diet during a subsequent pregnancy normalized fetal DHA, n-3 FA's and fetal hepatic apoptosis to CTR levels. Breast milk from HFD dams contained lower levels of eicosopentanoic acid (EPA) and DHA and lower levels of total protein than CTR breast milk. This study links chronic maternal consumption of a HFD with fetal hepatic apoptosis and suggests that a potentially pathological maternal fatty acid milieu is replicated in the developing fetal circulation in the nonhuman primate.

Show MeSH
Related in: MedlinePlus