Gene Expression Patterns Are Altered in Athymic Mice and Metabolic Syndrome Factors Are Reduced in C57BL/6J Mice Fed High-Fat Diets Supplemented with Soy Isoflavones

2016 ◽  
Vol 64 (40) ◽  
pp. 7492-7501 ◽  
Author(s):  
Ting Luo ◽  
Sarah M. Snyder ◽  
Bingxin Zhao ◽  
Debra K. Sullivan ◽  
Jill Hamilton-Reeves ◽  
...  
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Expression Patterns ◽  
Soy Isoflavones ◽  
Gene Expression Patterns ◽  
Athymic Mice ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets

scholarly journals Maternal and Post-weaning High-Fat Diets Produce Distinct DNA Methylation Patterns in Hepatic Metabolic Pathways within Specific Genomic Contexts

2019 ◽  
Vol 20 (13) ◽  
pp. 3229 ◽  
Author(s):  
Moody ◽  
Wang ◽  
Jung ◽  
Chen ◽  
Pan
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Metabolic Pathways ◽  
Expression Patterns ◽  
Sprague Dawley ◽  
High Fat ◽  
Differentially Methylated Genes ◽  
High Fat Diets ◽  
Diet Intake ◽  
Fat Diets

Calorie-dense high-fat diets (HF) are associated with detrimental health outcomes, including obesity, cardiovascular disease, and diabetes. Both pre- and post-natal HF diets have been hypothesized to negatively impact long-term metabolic health via epigenetic mechanisms. To understand how the timing of HF diet intake impacts DNA methylation and metabolism, male Sprague–Dawley rats were exposed to either maternal HF (MHF) or post-weaning HF diet (PHF). At post-natal week 12, PHF rats had similar body weights but greater hepatic lipid accumulation compared to the MHF rats. Genome-wide DNA methylation was evaluated, and analysis revealed 1744 differentially methylation regions (DMRs) between the groups with the majority of the DMR located outside of gene-coding regions. Within differentially methylated genes (DMGs), intragenic DNA methylation closer to the transcription start site was associated with lower gene expression, whereas DNA methylation further downstream was positively correlated with gene expression. The insulin and phosphatidylinositol (PI) signaling pathways were enriched with 25 DMRs that were associated with 20 DMGs, including PI3 kinase (Pi3k), pyruvate kinase (Pklr), and phosphodiesterase 3 (Pde3). Together, these results suggest that the timing of HF diet intake determines DNA methylation and gene expression patterns in hepatic metabolic pathways that target specific genomic contexts.

scholarly journals Metabolic Syndrome and Hepatic Steatosis is Reduced in C57BL/6J Mice Fed High‐fat Diets Supplemented with Soy Isoflavones

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Ting Luo ◽  
Sarah Smith ◽  
Bingxin Zhao ◽  
Jill Hamiton‐Reeves ◽  
Debra Sullivan ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Hepatic Steatosis ◽  
Soy Isoflavones ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets

High-fat diets promote insulin resistance through cytokine gene expression in growing female rats

2008 ◽  
Vol 19 (8) ◽  
pp. 505-513 ◽  
Author(s):  
Anne M. Flanagan ◽  
Jackie L. Brown ◽  
Consuelo A. Santiago ◽  
Pauline Y. Aad ◽  
Leon J. Spicer ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Female Rats ◽  
Cytokine Gene Expression ◽  
Cytokine Gene ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets

The combination of maternal and offspring high-fat diets causes marked oxidative stress and development of metabolic syndrome in mouse offspring

Life Sciences ◽  
2016 ◽  
Vol 151 ◽  
pp. 70-75 ◽  
Author(s):  
Junya Ito ◽  
Kiyotaka Nakagawa ◽  
Shunji Kato ◽  
Taiki Miyazawa ◽  
Fumiko Kimura ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets

scholarly journals The intake of high-fat diets induces the acquisition of brown adipocyte gene expression features in white adipose tissue

2015 ◽  
Vol 39 (11) ◽  
pp. 1619-1629 ◽  
Author(s):  
E García-Ruiz ◽  
B Reynés ◽  
R Díaz-Rúa ◽  
E Ceresi ◽  
P Oliver ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Brown Adipocyte ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets

scholarly journals Lasting Effects on Body Weight and Mammary Gland Gene Expression in Female Mice upon Early Life Exposure to n-3 but Not n-6 High-Fat Diets

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e55603 ◽  
Author(s):  
Mirjam Luijten ◽  
Amar V. Singh ◽  
Caleb A. Bastian ◽  
Anja Westerman ◽  
M. Michele Pisano ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Mammary Gland ◽  
Early Life ◽  
High Fat ◽  
Female Mice ◽  
Early Life Exposure ◽  
High Fat Diets ◽  
Fat Diets

scholarly journals Metabolic imprinting: critical impact of the perinatal environment on the regulation of energy homeostasis

2006 ◽  
Vol 361 (1471) ◽  
pp. 1107-1121 ◽  
Author(s):  
Barry E Levin
Keyword(s):  
Metabolic Syndrome ◽  
Energy Homeostasis ◽  
Perinatal Period ◽  
Neural Pathways ◽  
High Fat ◽  
Maternal Undernutrition ◽  
The Metabolic Syndrome ◽  
Obesity And Diabetes ◽  
High Fat Diets ◽  
Fat Diets

Epidemiological studies in humans suggest that maternal undernutrition, obesity and diabetes during gestation and lactation can all produce obesity in offspring. Animal models have allowed us to investigate the independent consequences of altering the pre- versus post-natal environments on a variety of metabolic, physiological and neuroendocrine functions as they effect the development in the offspring of obesity, diabetes, hypertension and hyperlipidemia (the ‘metabolic syndrome’). During gestation, maternal malnutrition, obesity, type 1 and type 2 diabetes and psychological, immunological and pharmacological stressors can all promote offspring obesity. Normal post-natal nutrition can reduce the adverse impact of some of these pre-natal factors but maternal high-fat diets, diabetes and increased neonatal access to food all enhance the development of obesity and the metabolic syndrome in offspring. The outcome of these perturbations of the perinatal environmental is also highly dependent upon the genetic background of the individual. Those with an obesity-prone genotype are more likely to be affected by factors such as maternal obesity and high-fat diets than are obesity-resistant individuals. Many perinatal manipulations appear to promote offspring obesity by permanently altering the development of central neural pathways, which regulate food intake, energy expenditure and storage. Given their strong neurotrophic properties, either excess or an absence of insulin and leptin during the perinatal period are likely to be effectors of these developmental changes. Because obesity is associated with an increased morbidity and mortality and because of its resistance to treatment, prevention is likely to be the best strategy for stemming the tide of the obesity epidemic. Such prevention should begin in the perinatal period with the identification and avoidance of factors which produce permanent, adverse alterations in neural pathways which control energy homeostasis.

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