scholarly journals High fat diet induced obesity alters ovarian phosphatidylinositol-3 kinase signaling gene expression

2013 ◽  
Vol 42 ◽  
pp. 68-77 ◽  
Author(s):  
J. Nteeba ◽  
J.W. Ross ◽  
J.W. Perfield II ◽  
A.F. Keating
2011 ◽  
Vol 85 (Suppl_1) ◽  
pp. 823-823
Author(s):  
Jackson Nteeba ◽  
Poulomi Bhattacharya ◽  
Jill A. Madden ◽  
Kelly Stromsdorfer ◽  
Jim W. Perfield ◽  
...  

2012 ◽  
Vol 61 (2) ◽  
pp. 89-101 ◽  
Author(s):  
Natthanan Nukitrangsan ◽  
Takafumi Okabe ◽  
Takayoshi Toda ◽  
Masashi Inafuku ◽  
Hironori Iwasaki ◽  
...  

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 503-503
Author(s):  
Zhiji Huang ◽  
Yafang Ma ◽  
Chunbao Li

Abstract Objectives Kappa-Carrageenan(CGN) is a widely used food additive in the meat industry and a highly viscous soluble dietary fiber which can hardly be fermented. It has been shown to be able to regulate the energy metabolism and inhibit diet-induced obesity. However, the mechanism is not well understood. The purpose of this study is to investigate the mechanisms of κ-carrageenan to inhibit the body weight gain. Methods A high-fat diet incorporated with lard, pork protein and CGN (2% or 4%, w/w) was given to C57BL/6J mice for 90 days. The energy intake and weight changes were measured every three days. After the dietary intervention, mice were sacrificed, liver and epididymal adipose tissues were taken for real-time polymerase chain reaction (RT-qPCR) analysis. Results The CGN in the high-fat diet restricted weight gain by decreasing liver and adipose mass without inhibiting energy intake.  The genes involving energy expenditure such as Acox1, Acadl, CPT-1A and Sirt1 were upregulated in the mice fed with carrageenan. However, the genes responsible for lipid synthesis were not significantly different compared to the diet-induced obese model. Conclusions The anti-obesity effect of the CGN in high-fat diet could be highly related to the enhancement of energy expenditure through up-regulating the downstream genes which promote β-oxidation by increasing the Sirt1 gene expression in liver. Funding Sources Ministry of Science and Technology of the People's Republic of China (10000 Talent Project)


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.


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 ◽  
...  

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Lingli Chen ◽  
Jiaqiang Huang ◽  
Yuanyuan Wu ◽  
Fazheng Ren ◽  
Xin Gen Lei

Abstract Objectives Metabolic function of selenoprotein V (SELENOV) remains unknown, although we previously showed a strong correlation of its gene expression with the high-fat diet-induced obesity in pigs. This study was conducted to explore the role and mechanism of SELENOV in body fat metabolism. Methods We applied the CRISPR/Cas9 gene-targeting deletion to generate Selenovknockout (KO) mice (C57BL/6 J background). Male KO and their wild-type (WT) (8 weeks old, n = 10 per genotype by treatment group) were fed a normal diet (NF, 10% calories coming from fat) or a high-fat diet (HF, 60% calories coming from fat) for 27 weeks. At the end, body weights and composition of mice were recorded, and tissues were collected to assay for gene expression and protein production related to lipid metabolism. Results Body weights of the KO mice fed the NF or HF diet were 16–19% higher (P < 0.05) than those of the WT mice. Total fat mass of the KO mice was 54% higher (P < 0.05) than the WT mice fed either diet, whereas total lean mass of the KO mice was 5 and 35% lower (P < 0.05) than that of WT mice fed the NF and HF diets, respectively. Gene expression of key enzymes (Fasn, Acaca, Dgat1, and Lpl) involved in lipogenesis was elevated (P < 0.05) in the white adipose tissue of the KO mice compared with the WT mice. In contrast, differences in gene expression of enzymes related to lipolysis and fatty acid oxidation (Atgl, Hsl, Ces1d, and Cpt1a) between the two genotypes were exactly the opposite (P < 0.05). Consistently, levels of proteins related to lipid accumulation (pACC, ACC, FAS, and LPL) were upregulated (P < 0.05) and proteins related to lipolysis (ATGL, HSL, and pHSL) were down-regulated (P < 0.05) in the KO mice compared with the WT mice. Conclusions Knockout of Selenov predisposed the male mice to elevated lipogenesis and attenuated lipolyis, leading to the body fat accumulation. This illustrated role and mechanism of SELENOV helps explain our previously-reported correlation between its gene expression and the high-fat diet-induced obesity in pigs. Funding Sources This research was supported in part by a NSFC grant #31,320,103,920.


2014 ◽  
Vol 1842 (9) ◽  
pp. 1870-1878 ◽  
Author(s):  
Zhibo Gai ◽  
Christian Hiller ◽  
Siew Hung Chin ◽  
Lia Hofstetter ◽  
Bruno Stieger ◽  
...  

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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