Transcriptomic responses of the liver and adipose tissues to altered carbohydrate-fat ratio in diet: an isoenergetic study in young rats

Tanaka, Mitsuru; Yasuoka, Akihito; Shimizu, Manae; Saito, Yoshikazu; Kumakura, Kei; Asakura, Tomiko; Nagai, Tadashi

doi:10.1186/s12263-017-0558-2

Cited by 8 publications

(5 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…“Metabolic memory” and “persistent epigenetic modification” [ 48 , 49 ] are well known contributors in this controversial weight loss theory. To address the aberrant upregulation of hepatic lipogenic genes after a diet change from HF to chow, we need to account for the HFD-induced disruption of daily rhythm, chromatin modification, carbohydrate to fat ratio in the diet, genetic modification/strain of the mice and overall “metabolic memory” of the cells [ 47 , 48 , 49 , 50 ]. There are contradictory studies reporting both reversal of HF-induced lipogenic genes to normal (in chow fed mice) upon diet change and vice-versa.…”

Section: Discussionmentioning

confidence: 99%

E4orf1 Prevents Progression of Fatty Liver Disease in Mice on High Fat Diet

Afruza

Dhurandhar

Hegde

2022

IJMS

View full text Add to dashboard Cite

Non-alcoholic fatty liver disease (NAFLD) covers a broad spectrum of liver diseases ranging from steatosis to cirrhosis. There are limited data on prevention of hepatic steatosis or its progression to liver disease. Here, we tested if either transgenic (Tg) doxycycline-induced expression in adipose tissue of E4orf1 (E4), an adenoviral protein, or dietary fat restriction attenuated hepatic steatosis or its progression in mice. Twelve to fourteen-week-old TgE4 mice (E4 group) and control mice were exposed to a 60% (Kcal) high fat diet (HFD) for 20 weeks, while another group of mice on HFD for 10 weeks were switched to a chow diet (chow group) for another 10 weeks. Glycemic control was determined at weeks 10 and 20. Tissues were collected for gene and protein analysis at sacrifice. Compared to control, diet reversal significantly reduced body weight in the chow group, whereas E4 expression attenuated weight gain, despite HFD. E4 mice evinced significantly improved glucose clearance, lower endogenous insulin secretion, reduced serum triglycerides, attenuated hepatic steatosis and inflammation. Interestingly, in spite of weight loss and lower liver fat, chow mice showed significant upregulation of hepatic genes involved in lipid metabolism. Despite HFD, E4 prevents hepatic lipid accumulation and progression of hepatic steatosis, while diet reversal maintains hepatic health, but is unable to improve molecular changes.

show abstract

Section: Discussionmentioning

confidence: 99%

E4orf1 Prevents Progression of Fatty Liver Disease in Mice on High Fat Diet

Afruza

Dhurandhar

Hegde

2022

IJMS

View full text Add to dashboard Cite

show abstract

“…The strain dependent results underscore the importance of studying obesity in multiple strains of mice instead of basing conclusions off of one strain. Differences in duration of diet treatment [ 61 ], type of fat [ 62 ], and percent of fat in the diets [ 63 ] also can affect gene expression and may contribute to variation across studies.…”

Section: Discussionmentioning

confidence: 99%

A high-fat diet alters genome-wide DNA methylation and gene expression in SM/J mice

et al. 2018

View full text Add to dashboard Cite

BackgroundWhile the genetics of obesity has been well defined, the epigenetics of obesity is poorly understood. Here, we used a genome-wide approach to identify genes with differences in both DNA methylation and expression associated with a high-fat diet in mice.ResultsWe weaned genetically identical Small (SM/J) mice onto a high-fat or low-fat diet and measured their weights weekly, tested their glucose and insulin tolerance, assessed serum biomarkers, and weighed their organs at necropsy. We measured liver gene expression with RNA-seq (using 21 total libraries, each pooled with 2 mice of the same sex and diet) and DNA methylation with MRE-seq and MeDIP-seq (using 8 total libraries, each pooled with 4 mice of the same sex and diet). There were 4356 genes with expression differences associated with diet, with 184 genes exhibiting a sex-by-diet interaction. Dietary fat dysregulated several pathways, including those involved in cytokine-cytokine receptor interaction, chemokine signaling, and oxidative phosphorylation. Over 7000 genes had differentially methylated regions associated with diet, which occurred in regulatory regions more often than expected by chance. Only 5–10% of differentially methylated regions occurred in differentially expressed genes, however this was more often than expected by chance (p = 2.2 × 10− 8).ConclusionsDiscovering the gene expression and methylation changes associated with a high-fat diet can help to identify new targets for epigenetic therapies and inform about the physiological changes in obesity. Here, we identified numerous genes with altered expression and methylation that are promising candidates for further study.Electronic supplementary materialThe online version of this article (10.1186/s12864-018-5327-0) contains supplementary material, which is available to authorized users.

show abstract

“…To examine the kind of molecular change that underlies these biochemical and behavioral phenotypes, we analyzed the transcriptome of the amygdala, hypothalamus, and liver in the mice raised in SH condition. We chose these tissues according to their contribution to the perception of social stimuli by the brain and to the regulation of metabolic status (Tanaka et al, 2017(Tanaka et al, , 2018. Especially in the social interaction context, stimuli from the other individuals seemed to be evaluated primarily by the amygdala, and the resulting emotional change of the brain may descend through the HPA axis to regulate metabolism.…”

Section: Analysis Of Tissue Transcriptomes and Cecal Microbiomementioning

confidence: 99%

Mouse Model of Weak Depression Exhibiting Suppressed cAMP Signaling in the Amygdala, Lower Lipid Catabolism in Liver, and Correlated Gut Microbiota

Yasuoka

Shimada

Nohara

et al. 2022

Front. Behav. Neurosci.

Self Cite

View full text Add to dashboard Cite

To establish a mouse model of weak depression, we raised 6-week-old C57BL/6N mice in single (SH) or group housing (GH) conditions for 2 weeks. The SH group showed less social interaction with stranger mice, learning disability in behavioral tests, and lower plasma corticosterone levels. The cecal microbiota of the SH group showed significant segregation from the GH group in the principal coordinate analysis (PCoA). Transcriptome analysis of the amygdala and liver detected multiple differentially expressed genes (DEGs). In the amygdala of SH mice, suppression of the cyclic adenine monophosphate (cAMP) signal was predicted and confirmed by the reduced immunoreactivity of phosphorylated cAMP-responsive element-binding protein. In the liver of SH mice, downregulation of beta-oxidation was predicted. Interestingly, the expression levels of over 100 DEGs showed a significant correlation with the occupancy of two bacterial genera, Lactobacillus (Lactobacillaceae) and Anaerostipes (Lachnospiraceae). These bacteria-correlated DEGs included JunB, the downstream component of cAMP signaling in the amygdala, and carnitine palmitoyltransferase 1A (Cpt1a), a key enzyme of beta-oxidation in the liver. This trans-omical analysis also suggested that nicotinamide adenine dinucleotide (NAD) synthesis in the liver may be linked to the occupancy of Lactobacillus through the regulation of nicotinamide phosphoribosyltransferase (NAMPT) and kynureninase (KYNU) genes. Our results suggested that SH condition along with the presence of correlated bacteria species causes weak depression phenotype in young mice and provides a suitable model to study food ingredient that is able to cure weak depression.

show abstract

Transcriptomic responses of the liver and adipose tissues to altered carbohydrate-fat ratio in diet: an isoenergetic study in young rats

Cited by 8 publications

References 49 publications

E4orf1 Prevents Progression of Fatty Liver Disease in Mice on High Fat Diet

E4orf1 Prevents Progression of Fatty Liver Disease in Mice on High Fat Diet

A high-fat diet alters genome-wide DNA methylation and gene expression in SM/J mice

Mouse Model of Weak Depression Exhibiting Suppressed cAMP Signaling in the Amygdala, Lower Lipid Catabolism in Liver, and Correlated Gut Microbiota

Contact Info

Product

Resources

About