Effect of prenatal exposure to LPS combined with pre- and post-natal high-fat diet on hippocampus in rat offspring

Huang, Chih-Hsien; Du, Jingxia; Deng, Wen; Xiao, Cheng; Zhang, Shou-Yan; Zhao, Shujuan; Tao, Mengjia; Chen, G.-Z.; Hao, Xueqin

doi:10.1016/j.neuroscience.2014.12.002

Cited by 17 publications

(15 citation statements)

References 21 publications

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“…Elevated levels of proinflammatory cytokines in the brain are directly linked with impaired hippocampal-dependent memory [48, 49] and the offspring hippocampus is particularly susceptible to maternal inflammation [50]. Perinatal and juvenile exposure to a chow diet supplemented with saturated fat, cholesterol, and sugar, produced elevations in expression of the cytokines TNF-alpha and IL-6, with concurrent morphological changes in the hippocampal CA-1 region [51]. Similar to effects observed following prenatal LPS injections which promote acute inflammation [52], hippocampal pyramidal cells were smaller in pups born from dams fed the fat, cholesterol, and sugar-enriched diet [51].…”

Section: Neurobiological Mechanismsmentioning

confidence: 99%

“…Perinatal and juvenile exposure to a chow diet supplemented with saturated fat, cholesterol, and sugar, produced elevations in expression of the cytokines TNF-alpha and IL-6, with concurrent morphological changes in the hippocampal CA-1 region [51]. Similar to effects observed following prenatal LPS injections which promote acute inflammation [52], hippocampal pyramidal cells were smaller in pups born from dams fed the fat, cholesterol, and sugar-enriched diet [51]. Maternal saturated fat consumption is also associated with increased expression of the proinflammatory cytokine, IL-1β at P20 and during adulthood, as well as increased microglia expression in the CA1, CA3 and dentate gyrus of the hippocampus [25].…”

Section: Neurobiological Mechanismsmentioning

confidence: 99%

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Early life exposure to obesogenic diets and learning and memory dysfunction

Noble

Kanoski

2016

Current Opinion in Behavioral Sciences

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Obesogenic dietary factors, such as simple sugars and saturated fatty acids, have been linked to memory impairments and hippocampal dysfunction. Recent evidence suggests that the brain may be particularly vulnerable to the effects of obesogenic diets during early life periods of rapid growth, maturation, and brain development. Investigations utilizing rodent models indicate that early life exposure to “high fat diets” (40-65% kcal derived from fat) or simple sugars (sucrose or high fructose corn syrup) can impair hippocampus-dependent learning and memory processes. In some cases, these deficits occur independent of obesity and metabolic derangement and can persist into adulthood despite dietary intervention. Various neurobiological mechanisms have been identified that may link early life consumption of obesogenic dietary factors with hippocampal dysfunction, including increased neuroinflammation and reduced neurotrophin mediated regulation of neurogenesis and synaptic plasticity. Age, duration of exposure, and dietary composition are key variables contributing to the interaction between early life diet and cognitive dysfunction, however, more research is needed to unravel the precise critical windows of development and causal dietary factors.

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Section: Neurobiological Mechanismsmentioning

confidence: 99%

Section: Neurobiological Mechanismsmentioning

confidence: 99%

Early life exposure to obesogenic diets and learning and memory dysfunction

Noble

Kanoski

2016

Current Opinion in Behavioral Sciences

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“…Lipopolysaccharide (LPS), a component of the outer membrane of Gram-negative bacteria, is frequently used to induce inflammation in mice, and injection around gestational day (GD) 7-9 of pregnancy (where the day after mating is day 0) increases the rate of fetal resorption [ 14 , 15 , 16 , 17 , 18 , 19 , 20 ] and reduces fetal weight [ 14 , 19 ]. Few studies have combined HFD and LPS during pregnancy [ 21 , 22 ], but these examined adult offspring phenotypes rather than pregnancy outcomes and did not begin the HFD prior to pregnancy to induce maternal obesity. We predicted that maternal obesity induced by a HFD would exacerbate the response to a low dose of LPS, leading to synergistic effects on fetal growth and survival.…”

Section: Introductionmentioning

confidence: 99%

Maternal Obesity Does Not Exacerbate the Effects of LPS Injection on Pregnancy Outcomes in Mice

Virginkar

Christians

2020

Biology

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Obesity increases the risk of a number of pregnancy complications, potentially due to chronic inflammation. We predicted that an obesogenic high-fat diet (HFD) in mice would create an inflammatory environment that would exacerbate the effects of lipopolysaccharide (LPS), an inflammatory insult, administered during pregnancy. Females were placed on a HFD or a low-fat diet (LFD) prior to mating, injected with 2 µg LPS or control on gestational day 7 and collected on day 14. Treatment with LPS increased the odds that a female thought to be pregnant at injection had no conceptuses at day 14 (p = 0.024), suggesting that injection with LPS was more likely to induce complete abortion. However, there was no effect of diet on the odds of having no conceptuses at day 14 and no interaction between diet and LPS injection. Diet and LPS injection had no effect on the number of viable fetuses in females still pregnant at day 14. For fetal weight, there was a significant interaction between diet and treatment (p = 0.017), whereby LPS reduced fetal weight in HFD females but not in LFD females. However, LPS treatment of HFD females reduced fetal weight to that observed in control-injected LFD females. Although LPS increased the odds of abortion, there was little evidence that a HFD exacerbated the effects of LPS.

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“…Recent perspectives papers and reviews have advanced a strong rationale for considering the combined effects of diet and stress in pregnancy with respect to fetal programming of offspring health outcomes, including brain development, immunity, and obesity risk [ 43 , 44 , 45 , 46 ]. This is based on a combination of evidence from non-pregnant populations and animal models of pregnancy, wherein an interactive effect of diet and stress has been found to affect metabolic [ 47 , 48 , 49 ] and inflammatory [ 50 , 51 , 52 ] pathways. While a handful of human pregnancy studies have reported associations between maternal psychosocial state and diet/nutritional status [ 53 , 54 , 55 , 56 , 57 , 58 , 59 ], there are, to the best of our knowledge, no published studies that have investigated the interactive effects of maternal diet and stress on the inflammatory milieu during pregnancy.…”

Section: Introductionmentioning

confidence: 99%

Maternal Stress Potentiates the Effect of an Inflammatory Diet in Pregnancy on Maternal Concentrations of Tumor Necrosis Factor Alpha

et al. 2018

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Maternal inflammation during pregnancy is known to adversely impact fetal development, birth outcomes, and offspring physical and mental health. Diet and stress have been identified as important determinants of inflammation, yet their combined effects have not been examined in the context of pregnancy. The aim of this study was to examine the relationship between maternal diet with inflammatory potential and psychological stress, and to determine their interaction effect on concentrations of tumor necrosis factor (TNF)-α across pregnancy. We conducted a prospective longitudinal study of n = 202 women with three assessments during pregnancy, which included: ecological momentary assessment (EMA) of maternal stress using the perceived stress scale (PSS) short version; 24-h dietary recalls from which the dietary inflammatory index (DII) was computed; and serum measurements of TNF-α. Across pregnancy, higher perceived stress was associated with consumption of a more pro-inflammatory diet (r = 0.137; p < 0.05). In a linear regression model adjusted for covariates, DII was positively associated with TNF-α (B = 0.093, p = 0.010). The effect of the pro-inflammatory diet on concentrations of TNF-α was more pronounced in women reporting higher levels of stress (B = 0.134, p = 0.018 for DII*PSS interaction). These results highlight the need to consider nutrition and stress concurrently in the context of inflammation during pregnancy.

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Effect of prenatal exposure to LPS combined with pre- and post-natal high-fat diet on hippocampus in rat offspring

Cited by 17 publications

References 21 publications

Early life exposure to obesogenic diets and learning and memory dysfunction

Early life exposure to obesogenic diets and learning and memory dysfunction

Maternal Obesity Does Not Exacerbate the Effects of LPS Injection on Pregnancy Outcomes in Mice

Maternal Stress Potentiates the Effect of an Inflammatory Diet in Pregnancy on Maternal Concentrations of Tumor Necrosis Factor Alpha

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