Long‐term effects of high lipid and high energy diet on serum lipid, brain fatty acid composition, and memory and learning ability in mice

Yu, Huanling; Bi, Yanxia; Ma, Weiwei; He, Lingling; Yuan, Linhong; Feng, Jiaxuan; Xiao, Rong

doi:10.1016/j.ijdevneu.2009.12.001

Cited by 74 publications

(46 citation statements)

References 36 publications

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“…9 ). acid content correlated with maternal serum LDL-C levels ( 11 ). In this present study, in the absence of maternal obesity induced by HLE diet, the adult male offspring also showed higher serum cholesterol and lower nonfasting serum insulin levels.…”

Section: Discussionsupporting

confidence: 63%

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Adaptive responses by mouse fetus to a maternal HLE diet by downregulating SREBP1: a microarray- and bio-analytic-based study

Miao

Gao

et al. 2013

Journal of Lipid Research

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health problems as the ones observed in epidemiological studies ( 4,5 ). So, maternal high-fat diet is an important predisposing factor to the onset and development of obesity, insulin resistance, and cardiovascular diseases in offspring ( 6 ). Indeed, a high-fat diet during gestation has been shown to lead to a lack of increase in insulin release and ATP content in response to glucose stimulation in islets from 3-month-old male and female offspring ( 5 ).However, the mechanisms linking high-fat nutrition in early life with later health problems remain unclear. Preliminary work has been performed on several candidate mechanisms, including: 1 ) white adipose tissue glucocorticoid sensitivity ( 7 ); 2 ) gene modifi cation status, such as DNA methylation (epigenetic mechanism) ( 4 ); 3 ) oxidative stress in dams, which might be transferred to the pups during gestation, later promoting disease development in the offspring ( 8 ); and 4 ) a maternal high-fat diet by itself, which triggers lipotoxicity in the fetal livers and later affects the offspring's health status ( 9 ). Indeed, the metabolic alterations usually observed during pregnancy combined with increased dietary fat intake, increase the triglycerides available to be hydrolyzed for transfer to the offspring, inducing an adaptive toxic response in the offspring's liver; this lipotoxicity leads to macrophage infi ltration into the liver, and to increased cytokine secretion. This infl ammatory state activates the pathways involved in oxidative stress and in gluconeogenesis ( 9 ). These conditions may predispose the offspring to alterations in their lipid metabolism in adult life.An understanding of how maternal nutrients infl uence offspring's development of adult diseases may be gained using proteomic methodologies and microarray analyses.Abstract Maternal diet has long been recognized as a signifi cant factor affecting offspring development and health, but the target genes affected by a maternal high-lipid diet are currently unknown. In this study, the gene expression profi le of neonatal mouse liver was analyzed using gene chips to identify genes with signifi cant up-or downregulated expression levels due to maternal high-fat diet during gestation. Real-time PCR and Western blotting were used to measure key genes selected using microarray. Serum lipid, glucose, and insulin levels in adult offspring from dams fed with chow or a high-lipid diet were measured using commercial kits. Results indicate that the expression of genes involved in cholesterol and fatty acid synthesis were signifi cantly inhibited, while the expression of genes involved in glycolysis were signifi cantly decreased by maternal high-lipid diet during gestation. SREBP1 might be the key gene regulating genes involved in fatty acid, glucose, and cholesterol metabolism in response to a maternal high-fat diet. Maternal nutrient intake during gestation has long been recognized as a signifi cant factor affecting the incidence of features of the adult metabolic syndrome in offspring. Indeed, human ...

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Section: Discussionsupporting

confidence: 63%

“…After 1 week, 15 male and 15 female mice were transferred to one cage and fed the control diet [chow diet (CD)] or a high-lipid high-energy (HLE) diet (composed of 84% CD, 15.8% lard fat, and 0.2% cholesterol). These diets were used in one of our previous studies ( 11 ). Two days later, pregnant female mice were individually housed in cages.…”

Section: Methodsmentioning

confidence: 99%

Adaptive responses by mouse fetus to a maternal HLE diet by downregulating SREBP1: a microarray- and bio-analytic-based study

Miao

Gao

et al. 2013

Journal of Lipid Research

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“…The traditional Mediterranean-style diet has fewer meats and carbohydrates and more plant-based foods and monounsaturated fat than a typical American diet. Following the traditional Mediterranean-style diet may lower incidence and prevalence of learning and memory functions [40,41] . In this regard, correlational studies have confirmed that polyphenols contribute to the prevention and treatment of learning and memory impairment [42,43].…”

Section: Discussionmentioning

confidence: 99%

Effects of Walnut Polyphenol on Learning and Memory Functions in Hypercholesterolemia Mice

Shi¹,

Chen²,

Zhao³

et al. 2014

JFNR

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Evidence suggests that dietary walnuts are able to induce improvements in memory and learning functions. In addition, polyphenols have been shown to modulate critical neuronal signalling pathways involved in processes of learning and memory. The aim of our present work was to study the effect of polyphenol extracts from walnut testa (42%) on learning and memory functions in hypercholesterolemia mice based on obesity, hypercholesterolemia and oxidative stress. At the beginning of the experiment, mice were divided into 3 groups, one of them served as normol control group (NCG), the second as hypercholesterolemia control group (HCG), the last as walnut polyphenol-treated group (WTG). After 8 weeks of treatment, we investigated the performance of C57BL/6J mice in Morris water maze test. The results showed that the escape latency was significant increase in HCG, when compared to NCG and WTG. In addition, the number of crossings was significant decrease in HCG, when compared to NCG and WTG (-47.35% and -43.35%, respectively, P < 0.01). The swimming distance was longer in HCG than NCG and WTG [F (2,96) = 44.45, P < 0.001]. However, there was no significant difference in swimming speed among NCG, HCG and WTG [F (2, 96) = 0.167, P > 0.05]. On the other hand, walnut polyphenol (WP) significantly decreased serum total triglycerides, cholesterol and malondialdehyde (MDA) level (-36.31%, -31.48% and -21.51%, respectively, P < 0.01) and increased superoxide dismutase (SOD) activity (+48.39%, P < 0.01). Administration of WP significantly decreased MDA level (-36.86%, P < 0.01) and increased SOD activity (+17.08%, P < 0.01) in brain tissues. In conclusion, walnut polyphenol was able to improve learning and memory functions.

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“…When 16-month-old rats were fed diets high in fat and cholesterol they made more errors in a test of working memory especially when memory loads were high, and they also showed altered hippocampal morphology (60). Similar studies of mice showed that high-fat diets worsen performance in learning and memory tests (49,181). There is some evidence that the effects of obesity on neuroplasticity and cognitive function differ in males and females.…”

Section: Animal Studiesmentioning

confidence: 98%

Impaired Adaptive Cellular Responses to Oxidative Stress and the Pathogenesis of Alzheimer's Disease

Texel

Mattson

2011

Antioxidants & Redox Signaling

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As is generally true with other age-related diseases, Alzheimer's disease (AD) involves oxidative damage to cellular components in the affected tissue, in this case the brain. The causes and consequences of oxidative stress in neurons in AD are not fully understood, but considerable evidence points to important roles for accumulation of amyloid b-peptide upstream of oxidative stress and perturbed cellular Ca 2+ homeostasis and energy metabolism downstream of oxidative stress. The identification of mutations in the b-amyloid precursor protein and presenilin-1 as causes of some cases of early onset inherited AD, and the development of cell culture and animal models based on these mutations has greatly enhanced our understanding of the AD process, and has greatly expanded opportunities for preclinical testing of potential therapeutic interventions. In this regard, and of particular interest to us, is the elucidation of adaptive cellular stress response pathways (ACSRP) that can counteract multiple steps in the AD neurodegenerative cascades, thereby limiting oxidative damage and preserving cognitive function. ACSRP can be activated by factors ranging from exercise and dietary energy restriction, to drugs and phytochemicals. In this article we provide an overview of oxidative stress and AD, with a focus on ACSRP and their potential for preventing and treating AD. Antioxid. Redox Signal. 14, 1519-1534.

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Long‐term effects of high lipid and high energy diet on serum lipid, brain fatty acid composition, and memory and learning ability in mice

Abstract: A long-term high lard diet increased offspring serum TC and LDL-C levels and affected the brain's fatty acid composition, and memory and learning ability. The polyunsaturated fatty acid content of the brain may be correlated with serum cholesterol levels.

Cited by 74 publications

References 36 publications

Adaptive responses by mouse fetus to a maternal HLE diet by downregulating SREBP1: a microarray- and bio-analytic-based study

Adaptive responses by mouse fetus to a maternal HLE diet by downregulating SREBP1: a microarray- and bio-analytic-based study

Effects of Walnut Polyphenol on Learning and Memory Functions in Hypercholesterolemia Mice

Impaired Adaptive Cellular Responses to Oxidative Stress and the Pathogenesis of Alzheimer's Disease

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