Accumulation of endoplasmic reticulum stress and lipogenesis in the liver through generational effects of high fat diets

Li, Jiong; Huang, Jin; Li, Jian-Shuang; Chen, Hong; Huang, Kun; Zheng, Ling

doi:10.1016/j.jhep.2011.10.018

Cited by 146 publications

(122 citation statements)

References 48 publications

Supporting

Mentioning

110

Contrasting

Unclassified

Order By: Relevance

“…SREBPs can be upregulated upon ER stress ( 32 ). Most recently, researchers observed that ER stress in the liver would accumulate through generational effects in mice from dams fed with high-fat diets ( 33 ). In our study, we observed a decreased SREBP1 expression in neonates from dams fed with HLE diet during gestation, and this decrease persisted in adults.…”

Section: Discussionsupporting

confidence: 67%

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

View full text Add to dashboard Cite

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 ...

show abstract

Section: Discussionsupporting

confidence: 67%

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

View full text Add to dashboard Cite

show abstract

“…could not be discerned from the study. Another example of transgenerational wash-in is found in the epigenetic inheritance of obesity in mice fed high-fat diets for three successive generations (Li et al, 2012). Obesity occurred earlier in development and was more severe across generations as follows, F 2 >F 1 >F 0 , suggesting a phenotypic wash-in or, as the authors put it, a 'transgenerational accumulation of epigenetic modifications'.…”

Section: Transgenerational 'Wash-in'mentioning

confidence: 99%

Dynamics of epigenetic phenomena: intergenerational and intragenerational phenotype ‘washout’

Burggren

2015

Journal of Experimental Biology

107

View full text Add to dashboard Cite

Epigenetic studies of both intragenerational and transgenerational epigenetic phenotypic modifications have proliferated in the last few decades. However, the strong reductionist focus on mechanism that prevails in many epigenetic studies to date has diverted attention away what might be called the 'dynamics' of epigenetics and its role in comparative biology. Epigenetic dynamics describes how both transgenerational and intragenerational epigenetic phenotypic modifications change in non-linear patterns over time. Importantly, a dynamic perspective suggests that epigenetic phenomena should not be regarded as 'digital' (on-off), in which a modified trait necessarily suddenly disappears between one generation and the next. Rather, dynamic epigenetic phenomena may be better depicted by graded, time-related changes that can potentially involve the 'washout' of modified phenotype both within and across generations. Conceivably, an epigenetic effect might also 'wash-in' over multiple generations, and there may be unexplored additive effects resulting from the pressures of environmental stressors that wax, wane and then wax again across multiple generations. Recognition of epigenetic dynamics is also highly dependent on the threshold for detection of the phenotypic modification of interest, especially when phenotypes wash out or wash in. Thus, studies of transgenerational epigenetic effects (and intragenerational effects, for that matter) that search for persistence of the phenomenon are best conducted with highly sensitive, precise quantitative methods. All of the scenarios in this review representing epigenetic dynamics are possible and some even likely. Focused investigations that concentrate on the time course will reveal much about both the impact and mechanisms of epigenetic phenomena.

show abstract

“…Although the sexual cycle takes longer to complete (∼6 d) than the asexual cycle (∼2 d), the observed period is much longer than expected if the changes were due to a direct plastic response. In addition to simple plastic responses, in some systems, exposure to an environmental cue must occur over multiple generations to trigger a plastic response (36). We tested for this possibility by propagating rotifers for 40 d as clonal lines in each of the eight environments used in exp2 (i.e., approximately the time period over which we observed evolutionary responses in exp2).…”

Section: Significancementioning

confidence: 99%

Higher rates of sex evolve during adaptation to more complex environments

Luijckx

Gasim

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

A leading hypothesis for the evolutionary maintenance of sexual reproduction proposes that sex is advantageous because it facilitates adaptation. Changes in the environment stimulate adaptation but not all changes are equivalent; a change may occur along one or multiple environmental dimensions. In two evolution experiments with the facultatively sexual rotifer Brachionus calyciflorus, we test how environmental complexity affects the evolution of sex by adapting replicate populations to various environments that differ from the original along one, two, or three environmental dimensions. Three different estimates of fitness (growth, lifetime reproduction, and population density) confirmed that populations adapted to their new environment. Growth measures revealed an intriguing cost of complex adaptations: populations that adapted to more complex environments lost greater amounts of fitness in the original environment. Furthermore, both experiments showed that B. calyciflorus became more sexual when adapting to a greater number of environmental dimensions. Common garden experiments confirmed that observed changes in sex were heritable. As environments in nature are inherently complex these findings help explain why sex is maintained in natural populations.

show abstract

Accumulation of endoplasmic reticulum stress and lipogenesis in the liver through generational effects of high fat diets

Cited by 146 publications

References 48 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

Dynamics of epigenetic phenomena: intergenerational and intragenerational phenotype ‘washout’

Higher rates of sex evolve during adaptation to more complex environments

Contact Info

Product

Resources

About