Propagule Powder of Japanese Yam ( Dioscorea Japonica ) Reduces High‐Fat Diet‐Induced Metabolic Stress in Mice through the Regulation of Hepatic Gene Expression

2020 ◽  
Vol 64 (17) ◽  
pp. 2000284
Author(s):  
Fumika Shinozaki ◽  
Asuka Kamei ◽  
Yuki Watanabe ◽  
Akihito Yasuoka ◽  
Kousuke Shimada ◽  
...  
Appetite ◽  
2011 ◽  
Vol 57 ◽  
pp. S15
Author(s):  
E.R. Ewald ◽  
B. Sun ◽  
R.H. Purcell ◽  
R.S. Lee ◽  
J.B. Potash ◽  
...  

2019 ◽  
Author(s):  
Ilona Binenbaum ◽  
Hanifa Abu-Toamih Atamni ◽  
Georgios Fotakis ◽  
Georgia Kontogianni ◽  
Theodoros Koutsandreas ◽  
...  

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.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 452-452
Author(s):  
Gavin Pierce ◽  
Mariana Buranelo Egea ◽  
Neil Shay

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.


BMC Genomics ◽  
2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Ilona Binenbaum ◽  
Hanifa Abu-Toamih Atamni ◽  
Georgios Fotakis ◽  
Georgia Kontogianni ◽  
Theodoros Koutsandreas ◽  
...  

Abstract Background The Collaborative Cross (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, 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 integrated 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 are different in female and male mice. The clear distinction we observed 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.


Gene ◽  
2004 ◽  
Vol 340 (1) ◽  
pp. 99-109 ◽  
Author(s):  
Sujong Kim ◽  
Insuk Sohn ◽  
Joon-Ik Ahn ◽  
Ki-Hwan Lee ◽  
Yeon Sook Lee ◽  
...  

2020 ◽  
Author(s):  
Ilona Binenbaum ◽  
Hanifa Abu-Toamih Atamni ◽  
Georgios Fotakis ◽  
Georgia Kontogianni ◽  
Theodoros Koutsandreas ◽  
...  

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.


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