Maternal high fat feeding and gestational dietary restriction: Effects on offspring body weight, food intake and hypothalamic gene expression over three generations in mice

Giraudo, Silvia Q.; Della‐Fera, Mary Anne; Proctor, Lindsey; Wickwire, Kathie; Ambati, Suresh; Baile, Clifton A.

doi:10.1016/j.pbb.2010.04.017

Cited by 27 publications

(20 citation statements)

References 46 publications

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“…K-F YANG and others 111 used and the proportion of energy contributed by dietary fat, which are quite distinct from each other in these studies. Fat content of the experimental HF diet ranged from 34 to 60% of total energy, and most studies used saturated fat as the main source of fat in the diet (Giraudo et al 2010, Ainge et al 2011. In our study, the fat in the HF group provided 45% of the total calories and was mainly composed of lard, which is rich in saturated fatty acids fat.…”

Section: Discussionmentioning

confidence: 63%

Maternal high-fat diet programs Wnt genes through histone modification in the liver of neonatal rats

Yang

Cai²,

Xu³

et al. 2012

Journal of Molecular Endocrinology

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Maternal high-fat (HF) diets during gestation and lactation have been shown to contribute to metabolic disorders in offspring. Molecular and epigenetic mechanisms underlying this connection may be essential for the prevention and treatment of the fetal origins of metabolic diseases. The current study examined the impact of maternal HF diets on Wnt signaling and histone modification in offspring. Time-pregnant Sprague-Dawley rats were fed either control diet or HF diet during gestation and lactation and then the neonatal offspring of both groups were investigated. The neonatal offspring born to dams fed on HF diets exhibited increases in serum glucose and liver triglyceride levels. Maternal exposure to the HF diet also repressed the mRNA expression of Wnt1 and nuclear b-catenin protein in the liver of offspring. The altered Wnt1 gene expression may be due to the changes of acetylation of H4 at its promoter as well as acetylation of H4 and methylation of H3K9 at coding region. Maternal exposure to the HF diet induced suppression of the Wnt/b-catenin signaling pathway through histone modification, potentially increasing the risk of metabolic syndrome.

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Section: Discussionmentioning

confidence: 63%

Maternal high-fat diet programs Wnt genes through histone modification in the liver of neonatal rats

Yang

Cai²,

Xu³

et al. 2012

Journal of Molecular Endocrinology

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“…Many studies have found that ARC neuropeptides are not altered by maternal HFD or obesity in adult male mice and rats 5, 7, 80 , while other studies have shown that maternal HFD stimulates and/or suppresses Npy and Pomc expression 81–83 . Due to the role that these ARC neuropeptides have in hypothalamic control of energy homeostasis, we hypothesized that maternal HFD would augment Npy / Agrp and suppress Pomc / Cart .…”

Section: Discussionmentioning

confidence: 99%

“…These studies found lower birth weights in treated offspring compared to control offspring followed by a catch-up weight gain, adult obesity, and insulin resistance, especially on an obesogenic diet 3–5 . Other studies showed higher birth and adult weights in offspring of diet-induced obesity (DIO) dams compared to control offspring 6 .…”

Section: Introductionmentioning

confidence: 99%

Loss of ERα partially reverses the effects of maternal high-fat diet on energy homeostasis in female mice

Roepke

Yasrebi

Villalobos

et al. 2017

Sci Rep

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Maternal high-fat diet (HFD) alters hypothalamic developmental programming and disrupts offspring energy homeostasis in rodents. 17β-estradiol (E2) also influences hypothalamic programming through estrogen receptor (ER) α. Therefore, we hypothesized that females lacking ERα would be more susceptible to maternal HFD. To address this question, heterozygous ERα knockout (WT/KO) dams were fed a control breeder chow diet (25% fat) or a semi-purified HFD (45% fat) 4 weeks prior to mating with WT/KO males or heterozygous males with an ERα DNA-binding domain mutation knocked in (WT/KI) to produce WT, ERα KO, or ERα KIKO females lacking ERE-dependent ERα signaling. Maternal HFD increased body weight in WT and KIKO, in part, due to increased adiposity and daytime carbohydrate utilization in WT and KIKO, while increasing nighttime fat utilization in KO. Maternal HFD also increased plasma leptin, IL-6, and MCP-1 in WT and increased arcuate expression of Kiss1 and Esr1 (ERα) and liver expression of G6pc and Pepck in WT and KIKO. Contrary to our hypothesis, these data suggest that loss of ERα signaling blocks the influence of maternal HFD on energy homeostasis, inflammation, and hypothalamic and liver gene expression and that restoration of ERE-independent ERα signaling partially reestablishes susceptibility to maternal HFD.

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“…Weight loss in obese women prior to pregnancy has also demonstrated improved offspring metabolic phenotype (Kral et al, 2006; Smith et al, 2009). Further, during pregnancy, mild gestational food restriction or switching to control diet of dams on HFD is able to reverse the programming effects and even protect against HFD post-weaning (Gallou-Kabani et al, 2007; Giraudo et al, 2010). Therefore, weight-loss strategies or simple dietary changes to improve the metabolic milieu in mothers prior to pregnancy are likely to positively impact offspring phenotype.…”

Section: Future Directions and Possible Interventionsmentioning

confidence: 99%

Developmental Programming in Response to Maternal Overnutrition

Alfaradhi¹,

Ozanne²

2011

Front. Gene.

268

236

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Metabolic disorders have seen an increased prevalence in recent years in developed as well as developing countries. While it is clear lifestyle choices and habits have contributed to this epidemic, mounting evidence suggests the nutritional milieu during critical stages of development in early life can “program” individuals to develop the metabolic syndrome later in life. Extensive epidemiological data presents an association between maternal obesity and nutrition during pregnancy and offspring obesity, and a number of animal models have been established in order to uncover the underlying mechanisms contributing to the programming of physiological systems. It is hard to distinguish the causal factors due to the complex nature of the maternal–fetal relationship; however, in order to develop adequate prevention strategies it is vital to identify which maternal factor(s) – be it the diet, diet-induced obesity or weight gain – and at which time during early development instigate the programmed phenotype. Curtailing the onset of obesity at this early stage in life presents a promising avenue through which to stem the growing epidemic of obesity.

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Maternal high fat feeding and gestational dietary restriction: Effects on offspring body weight, food intake and hypothalamic gene expression over three generations in mice

Cited by 27 publications

References 46 publications

Maternal high-fat diet programs Wnt genes through histone modification in the liver of neonatal rats

Maternal high-fat diet programs Wnt genes through histone modification in the liver of neonatal rats

Loss of ERα partially reverses the effects of maternal high-fat diet on energy homeostasis in female mice

Developmental Programming in Response to Maternal Overnutrition

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