Maternal high-fat diet during gestation and lactation alters hepatic gene expression in male rat offspring

Appetite ◽  
2011 ◽  
Vol 57 ◽  
pp. S15
Author(s):  
E.R. Ewald ◽  
B. Sun ◽  
R.H. Purcell ◽  
R.S. Lee ◽  
J.B. Potash ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Male Rat ◽  
Hepatic Gene Expression ◽  
High Fat ◽  
Rat Offspring

scholarly journals Maternal High-Fat Diet Modulates Cnr1 Gene Expression in Male Rat Offspring

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2885
Author(s):  
Dawid Gawliński ◽  
Kinga Gawlińska ◽  
Irena Smaga
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Cpg Islands ◽  
Male Offspring ◽  
Epigenetic Mechanism ◽  
Male Rat ◽  
High Fat ◽  
Rat Offspring ◽  
Pregnancy And Lactation ◽  
Cnr1 Gene

In recent years, strong evidence has emerged that exposure to a maternal high-fat diet (HFD) provokes changes in the structure, function, and development of the offspring’s brain and may induce several neurodevelopmental and psychiatric illnesses. The aims of this study were to evaluate the effects of a maternal HFD during pregnancy and lactation on depressive-like behavior and Cnr1 gene expression (encoding the CB1 receptor) in brain structures of rat offspring and to investigate the epigenetic mechanism involved in this gene expression. We found that a maternal HFD during pregnancy and lactation induced a depressive-like phenotype at postnatal days (PNDs) 28 and 63. We found that a maternal HFD decreased the Cnr1 mRNA levels in the prefrontal cortex with the increased levels of miR-212-5p and methylation of CpG islands at the Cnr1 promoter and reduced the level of Cnr1 gene expression in the dorsal striatum with an increased level of miR-154-3p in adolescent male offspring. A contrasting effect of a maternal HFD was observed in the hippocampus, where upregulation of Cnr1 gene expression was accompanied by a decrease of miR-154-3p (at PNDs 28 and 63) and miR-212-5p (at PND 63) expression and methylation of CpG islands at the Cnr1 promoter in male offspring. In summary, we showed that a maternal HFD during pregnancy and lactation triggered several epigenetic mechanisms in the brains of rat offspring, which may be related to long-lasting alterations in the next generation and produce behavioral changes in offspring, including a depressive-like phenotype.

scholarly journals Container-aided Integrative QTL and RNA-seq Analysis of Collaborative Cross Mice Supports Distinct Sex-Oriented Molecular Modes of Response in Obesity

2019 ◽  
Author(s):  
Ilona Binenbaum ◽  
Hanifa Abu-Toamih Atamni ◽  
Georgios Fotakis ◽  
Georgia Kontogianni ◽  
Theodoros Koutsandreas ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Complex Traits ◽  
Hepatic Gene Expression ◽  
High Fat ◽  
Mouse Population ◽  
Male And Female ◽  
Female Mice ◽  
Diet Induced Obesity ◽  
Genetic Mechanisms

Abstract Background: The CC mouse population is a valuable resource to study the genetic basis of complex traits, such as obesity. Although the development of obesity is influenced by environmental factors, the underlying genetic mechanisms play a crucial role in the response to these factors. The interplay between the genetic background and the gene expression pattern can provide further insight into this response, but we lack robust and easily reproducible workflows to integrate genomic and transcriptomic information in the CC mouse population. Results: We established an automated and reproducible integrative workflow to analyse complex traits in the CC mouse genetic reference panel at the genomic and transcriptomic levels. We implemented the analytical workflow to assess the underlying genetic mechanisms of host susceptibility to diet induced obesity and integrate these results with diet induced changes in the hepatic gene expression of susceptible and resistant mice. Hepatic gene expression differs significantly between obese and non-obese mice, with a significant sex effect, where male and female mice exhibit different responses and coping mechanisms. Conclusion: Integration of the data showed that different genes but similar pathways are involved in the genetic susceptibility and disturbed in diet induced obesity. Genetic mechanisms underlying susceptibility to high-fat diet induced obesity differ in female and male mice. The clear distinction we observe in the systemic response to the high-fat diet challenge and to obesity between male and female mice points to the need for further research into distinct sex-related mechanisms in metabolic disease.

scholarly journals Maternal high-fat diet induces sex-specific changes to glucocorticoid and inflammatory signaling in response to corticosterone and lipopolysaccharide challenge in adult rat offspring

2019 ◽  
Author(s):  
Sanoji Wijenayake ◽  
Mouly F. Rahman ◽  
Christine M.W. Lum ◽  
Wilfred C. De Vega ◽  
Aya Sasaki ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Maternal Obesity ◽  
Inflammatory Responses ◽  
Physiological Stress ◽  
High Fat ◽  
Inflammatory Gene Expression ◽  
Inflammatory Genes ◽  
Inflammatory Gene ◽  
Rat Offspring

ABSTRACTBackgroundAcute elevations in endogenous corticosterone (CORT) with psychosocial stress or exogenous administration potentiate inflammatory gene expression. Maternal obesity as a result of high-fat diet (HFD) consumption has been linked to higher basal levels of neuroinflammation, including increased expression of pro-inflammatory genes in the amygdala. These findings suggest that exposure to maternal HFD may elicit pro-inflammatory responses in the presence of an immune stressor such as lipopolysaccharide (LPS), a component of gram-negative bacteria, as well as acute elevated CORT.MethodsRat offspring were exposed to maternal HFD or control diet (CHD) throughout pre and postnatal development until weaning, when all offspring were provided CHD until adulthood. In adulthood, offspring were ‘challenged’ with administration of exogenous CORT, to simulate an acute physiological stress, LPS, to induce an immune stress, or both. qPCR was used to measure transcript abundance of CORT receptors and downstream inflammatory genes in the amygdala, hippocampus and prefrontal cortex, brain regions that mediate neuroendocrine and behavioral responses to stress.ResultsHFD female offspring exhibited elevations in anti-inflammatory transcripts, whereas HFD male offspring responded with greater pro-inflammatory gene expression to simultaneous CORT and LPS administration.ConclusionsThese findings suggest that exposure to maternal HFD leads to sex-specific alterations that may alter inflammatory responses in the brain, possibly as an adaptive response to basal inflammation.

scholarly journals Maternal high-fat diet results in cognitive impairment and hippocampal gene expression changes in rat offspring

2019 ◽  
Vol 318 ◽  
pp. 92-100 ◽  
Author(s):  
Zachary A. Cordner ◽  
Seva G. Khambadkone ◽  
Gretha J. Boersma ◽  
Lin Song ◽  
Tyler N. Summers ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cognitive Impairment ◽  
High Fat Diet ◽  
High Fat ◽  
Rat Offspring

scholarly journals Raspberry Polyphenol Extracts Modify Physiological Parameters and the Hepatic Transcriptome of C57BL/6J Mice Fed a High-Fat Diet

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 452-452
Author(s):  
Gavin Pierce ◽  
Mariana Buranelo Egea ◽  
Neil Shay
Keyword(s):  
Gene Expression ◽  
Energy Efficiency ◽  
Expression Analysis ◽  
High Fat Diet ◽  
Fasting Blood Glucose ◽  
Differential Expression Analysis ◽  
Hepatic Gene Expression ◽  
High Fat ◽  
Treatment Groups ◽  
Hepatic Transcriptome

Abstract Objectives Red raspberries are rich in polyphenols, fiber, and volatile compounds, and have been demonstrated to have favorable effects on energy homeostasis in mice. We made two extracts from red raspberries, enriched in either hydrophilic (R25) or hydrophobic (R80) polyphenols. We tested the hypothesis that these polyphenol extracts would differentially alter and improve physiological measures and the hepatic transcriptome of C57BL/6J male mice fed a obesigenic high fat diet (HF). Methods Raspberry polyphenol extracts were obtained using FPX-66 resin, and eluting with 25% (R25) and 80% (R80) ethanol (v/v); eluates were then dried. Mice were provided a low fat diet (LF, 10% kcal fat, n = 12), high fat diet (HF, 45% kcal fat, n = 12), HF with raspberry puree concentrate (RPC, n = 8), HF with R25 (n = 8), or HF with R80 (n = 8) ad libitum for 10 weeks. Body weights, food intake, and fasting glucose levels were measured. Post mortem, serum was collected for ELISA, organ weights were recorded, and liver tissue was collected for triglyceride analysis and differential expression analysis. Results Energy efficiency and liver weights in the R25 and R80 groups were intermediate to the LF and HF controls. Fasting blood glucose, serum triglycerides, and adipose tissue weights did not differ between treatment groups. A trend toward significance was seen in reduction of weight gain in the raspberry treatment groups. Differential gene expression analysis revealed that the R25 diet acted agonistically towards the constitutive androstane receptor (CAR) and reduced the relative levels of several sterol regulatory binding protein-regulated genes. Notably, the R80 diet robustly increased levels of Cyp4a14, a peroxisome proliferator-activated receptor alpha (PPAR-α)-regulated gene. Conclusions Supplementation of a high fat diet with raspberry polyphenol extracts modified hepatic gene expression and energy efficiency in C57BL/6J mice. The two extracts had a differential impact on hepatic gene expression. For example, the R25 extract behaved as an agonist for CAR, while the R80 extract behaved as an agonist for PPAR-α. These findings suggest that select polyphenols found within red raspberries may serve as nutraceuticals that specifically act via PPAR-α, CAR, and other targets in liver. Funding Sources National Processed Raspberry Commission and Washington Red Raspberry Commission.

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