scholarly journals The Effects of High Fat Diet-Induced Stress on Olfactory Sensitivity, Behaviors, and Transcriptional Profiling in Drosophila melanogaster

2018 ◽  
Vol 19 (10) ◽  
pp. 2855 ◽  
Author(s):  
Jewon Jung ◽  
Dong-In Kim ◽  
Gi-Youn Han ◽  
Hyung Kwon
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
High Fat Diet ◽  
Metabolic Regulation ◽  
Expression Profiles ◽  
Sensory System ◽  
Behavioral Responses ◽  
Olfactory Sensitivity ◽  
High Fat ◽  
Induced Stress

High-fat diet (HFD) often causes obesity and it has detrimental effects on the sensory system. In particular, sensory-mediated responses are crucial for maintaining energy balance, as they are involved in a metabolic regulation; however, there is still no clear explanation about the relationship between HFD-induced stress and sensory system. To gain insight on how HFD-induced stress affects olfactory sensitivity and behavioral responses, we have used a Drosophila melanogaster model for olfactory and nutrient-related signaling and accessed physiological, behavioral, and transcriptional changes. We demonstrated that lifespan and climbing ability in HFD-treated flies decreased and that olfactory sensitivity and behavioral responses to odorants were changed. Olfactory sensitivity to eight of ten odorants after 14 days on HFD treatment were reduced, while behavioral attraction was increased to benzaldehyde in flies that were treated with HFD. This behavioral and physiological modification in HFD-treated flies for 14 days was accompanied by a significant decrease in DmOrco gene expression in a peripheral olfactory organ, suggesting that is could be involved in the action of metabolic and sensory signal. Gene expression profiles of antennae showed significant differences on the olfactory receptors, odorant-binding proteins, and insulin signaling. Our results suggested that olfactory sensitivity and behavioral responses to HFD-induced stress are mediated through olfactory and nutrient-related signaling pathways.

scholarly journals Hepatic Gene Expression Profiling in Nrf2 Knockout Mice after Long-Term High-Fat Diet-Induced Obesity

2013 ◽  
Vol 2013 ◽  
pp. 1-17 ◽  
Author(s):  
Dionysios V. Chartoumpekis ◽  
Panos G. Ziros ◽  
Apostolos Zaravinos ◽  
Ralitsa P. Iskrenova ◽  
Agathoklis I. Psyrogiannis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Microarray Analysis ◽  
High Fat Diet ◽  
Metabolic Regulation ◽  
Expression Profiles ◽  
Related Factor ◽  
High Fat ◽  
Qrt Pcr ◽  
Nrf2 Knockout

Introduction. The transcription factor NFE2-related factor 2 (Nrf2) is a central regulator of antioxidant and detoxification gene expression in response to electrophilic or oxidative stress. Nrf2 has recently been shown to cross-talk with metabolic pathways, and its gene deletion protected mice from high-fat-diet-(HFD-) induced obesity and insulin resistance. This study aimed to identify potential Nrf2-regulated genes of metabolic interest by comparing gene expression profiles of livers of wild-type (WT) versus Nrf2 knockout (Nrf2-KO) mice after a long-term HFD.Methods. WT and Nrf2-KO mice were fed an HFD for 180 days; total RNA was prepared from liver and used for microarray analysis and quantitative real-time RT-PCR (qRT-PCR).Results. The microarray analysis identified 601 genes that were differentially expressed between WT and Nrf2-KO mice after long-term HFD. Selected genes, including ones known to be involved in metabolic regulation, were prioritized for verification by qRT-PCR:Cyp7a1andFabp5were significantly overexpressed in Nrf2-KO mice; in contrast,Car,Cyp2b10,Lipocalin 13,Aquaporin 8,Cbr3,Me1, andNqo1were significantly underexpressed in Nrf2-KO mice.Conclusion. Transcriptome profiling after HFD-induced obesity confirms thatNrf2is implicated in liver metabolic gene networks. The specific genes identified here may provide insights into Nrf2-dependent mechanisms of metabolic regulation.

scholarly journals Gene expression profiles of the colonic mucosa associated with phenotypic changes in mice fed high‐fat diet

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Yun Jung Bae ◽  
Youn-Kyung Bak ◽  
Taesun Park ◽  
Myung-Sook Choi ◽  
Jeongseon Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Colonic Mucosa ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
High Fat ◽  
Phenotypic Changes

scholarly journals A high-fat diet impacts memory and gene expression of the head in mated female Drosophila melanogaster

2019 ◽  
Vol 189 (2) ◽  
pp. 179-198 ◽  
Author(s):  
Osvaldo Rivera ◽  
Lara McHan ◽  
Bridget Konadu ◽  
Sumitkumar Patel ◽  
Silvienne Sint Jago ◽  
...  
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
High Fat Diet ◽  
High Fat ◽  
Mated Female

Hepatic gene expression profiles in a long-term high-fat diet-induced obesity mouse model

Gene ◽  
2004 ◽  
Vol 340 (1) ◽  
pp. 99-109 ◽  
Author(s):  
Sujong Kim ◽  
Insuk Sohn ◽  
Joon-Ik Ahn ◽  
Ki-Hwan Lee ◽  
Yeon Sook Lee ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mouse Model ◽  
High Fat Diet ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Hepatic Gene Expression ◽  
High Fat ◽  
Diet Induced Obesity

Gene expression profiles reveal effect of a high-fat diet on the development of white and brown adipose tissues

Gene ◽  
2015 ◽  
Vol 565 (1) ◽  
pp. 15-21 ◽  
Author(s):  
Hyeng-Soo Kim ◽  
Zae Young Ryoo ◽  
Sang Un Choi ◽  
Sanggyu Lee
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
High Fat ◽  
Adipose Tissues ◽  
Brown Adipose

scholarly journals High fat diet induces sex-specific differential gene expression in Drosophila melanogaster

PLoS ONE ◽  
2019 ◽  
Vol 14 (3) ◽  
pp. e0213474 ◽  
Author(s):  
Tsering Stobdan ◽  
Debashis Sahoo ◽  
Priti Azad ◽  
Iain Hartley ◽  
Erilynn Heinrichsen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Differential Gene Expression ◽  
High Fat Diet ◽  
High Fat ◽  
Differential Gene

Integrative study of diet-induced mouse models of NAFLD identifies PPARα as a sexually dimorphic drug target

Gut ◽  
2021 ◽  
pp. gutjnl-2020-323323
Author(s):  
Sarra Smati ◽  
Arnaud Polizzi ◽  
Anne Fougerat ◽  
Sandrine Ellero-Simatos ◽  
Yuna Blum ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Large Scale ◽  
Expression Profiles ◽  
Control Diet ◽  
Western Diet ◽  
Specific Response ◽  
Sexually Dimorphic ◽  
High Fat ◽  
Alcoholic Fatty Liver

ObjectiveWe evaluated the influence of sex on the pathophysiology of non-alcoholic fatty liver disease (NAFLD). We investigated diet-induced phenotypic responses to define sex-specific regulation between healthy liver and NAFLD to identify influential pathways in different preclinical murine models and their relevance in humans.DesignDifferent models of diet-induced NAFLD (high-fat diet, choline-deficient high-fat diet, Western diet or Western diet supplemented with fructose and glucose in drinking water) were compared with a control diet in male and female mice. We performed metabolic phenotyping, including plasma biochemistry and liver histology, untargeted large-scale approaches (liver metabolome, lipidome and transcriptome), gene expression profiling and network analysis to identify sex-specific pathways in the mouse liver.ResultsThe different diets induced sex-specific responses that illustrated an increased susceptibility to NAFLD in male mice. The most severe lipid accumulation and inflammation/fibrosis occurred in males receiving the high-fat diet and Western diet, respectively. Sex-biased hepatic gene signatures were identified for these different dietary challenges. The peroxisome proliferator-activated receptor α (PPARα) co-expression network was identified as sexually dimorphic, and in vivo experiments in mice demonstrated that hepatocyte PPARα determines a sex-specific response to fasting and treatment with pemafibrate, a selective PPARα agonist. Liver molecular signatures in humans also provided evidence of sexually dimorphic gene expression profiles and the sex-specific co-expression network for PPARα.ConclusionsThese findings underscore the sex specificity of NAFLD pathophysiology in preclinical studies and identify PPARα as a pivotal, sexually dimorphic, pharmacological target.Trial registration numberNCT02390232.

scholarly journals Analysis of gene expression in pancreatic islets from diet-induced obese mice

2008 ◽  
Vol 36 (1) ◽  
pp. 43-51 ◽  
Author(s):  
Yumi Imai ◽  
Hiral R. Patel ◽  
Nicolai M. Doliba ◽  
Franz M. Matschinsky ◽  
John W. Tobias ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Secretion ◽  
Pancreatic Islets ◽  
High Fat Diet ◽  
Expression Profiles ◽  
Inbred Mice ◽  
Gene Expression Profiles ◽  
Islet Function ◽  
High Fat ◽  
Islet Mass

In insulin-resistant status such as obesity, failure of pancreatic islets to increase insulin secretion leads to diabetes. We sought to screen for the islet genes that facilitate islet adaptation to obesity by comparing gene expression profiles between two strains of obesity-prone inbred mice with different propensities for hyperglycemia. C57BL/6J and AKR/J were fed regular rodent chow or high-fat diet, after which islet morphology, secretory function, and gene expression were assessed. AKR/J had lower blood glucose and higher insulin levels compared with C57BL/6J mice on regular rodent chow or high-fat diet. Insulin secretion was 3.2-fold higher in AKR/J than C57BL/6J mice following intraperitoneal glucose injection. Likewise, glucose-stimulated insulin secretion from isolated islets was higher in AKR/J. Additionally, islet mass was 1.4-fold greater in AKR/J compared with C57BL/6J. To elucidate the factors associated with the differences in islet function, we analyzed the gene expression profiles in islets in AKR/J and C57BL/6J mice. Of 14,000 genes examined, 202 were upregulated and 270 were downregulated in islets from diet-induced obese AKR/J mice compared with C57BL/6J mice. Key genes involved in islet signaling and metabolism, e.g., glucagon-like peptide-1 receptor, sterol Co-A desaturase 1 and 2, and fatty acid desaturase 2 were upregulated in obese AKR/J mice. The expression of multiple extracellular matrix proteins was also increased in AKR/J mice, suggesting a role in modulation of islet mass. Functional analyses of differentially regulated genes hold promise for elucidating factors linking obesity to alterations in islet function.

scholarly journals β-Cell Proliferation After a Partial Pancreatectomy Is Independent of IRS-2 in Mice

Endocrinology ◽  
2014 ◽  
Vol 155 (5) ◽  
pp. 1643-1652 ◽  
Author(s):  
Yu Togashi ◽  
Jun Shirakawa ◽  
Kazuki Orime ◽  
Mitsuyo Kaji ◽  
Eri Sakamoto ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
High Fat Diet ◽  
Expression Profiles ◽  
Cyclin B1 ◽  
Gene Set Enrichment Analysis ◽  
Sham Operation ◽  
High Fat ◽  
Β Cell ◽  
Partial Pancreatectomy

The glucokinase-induced up-regulation of insulin receptor substrate 2 (IRS-2) plays an important role in β-cell adaptive proliferation in response to high-fat diet-induced insulin resistance. This study aimed to investigate the role of IRS-2 in the proliferation of β-cells after a 60% partial pancreatectomy. IRS-2-deficient (IRS-2−/−) mice or wild-type mice were subjected to a pancreatectomy (60% partial pancreatectomy) or a sham operation (Sham). The β-cell proliferation and gene expression profiles of the islets were then assessed. Gene expression in islets from pancreatectomized and Sham C57BL/6J male mice was analyzed using a cDNA microarray analysis. To compare with β-cell proliferation induced by a high-fat diet, Gck+/− mice subjected to a pancreatectomy were also analyzed. The IRS-2−/− mice exhibited β-cell expansion and a significant increase in β-cell proliferation after the pancreatectomy, compared with the Sham group. Although glucose-stimulated insulin secretion from islets was not impaired, IRS-2−/− mice manifested severe hyperglycemia after the pancreatectomy. The expression levels of Aurora kinase B, Cyclin A, and Cyclin B1 in the pancreatectomized islets were also enhanced in the IRS-2−/− mice. A gene set enrichment analysis suggested an association between the genes that were up-regulated in the pancreatectomized islets and those involved in M phase progression in the cell cycle. β-Cell proliferation after a pancreatectomy was observed even in the Gck+/− mice. In conclusion, IRS-2 was not required for β-cell proliferation but might be needed for functional β-cell mass, after a pancreatectomy. A partial pancreatectomy in mice may be an attractive model for the development of new strategy for exploring the unique nature of β-cell proliferation.

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