Coordinated regulation of hepatic and adipose tissue transcriptomes by the oral administration of an amino acid mixture simulating the larval saliva of Vespa species

Genes mapped on Fig. 3. (XLSX 13 kb

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

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

The effects of compression load to the trunk on lipid metabolism in an inactive phase.

The effects of compression load to a specific body part, e.g. leg, arm, or trunk, evoke many functions and are applied in various fields including clinical medicine, sports, and general health care. Nevertheless, little is known about the functional mechanism of compression load, especially regarding its effects on metabolic function. We investigated the effects of compression load to the trunk on the metabolism. We designed adjustable compression clothes for mice and attached them to ten-week-old C57BL/6N male mice in a controlled environment. The mice were divided into compression and no-compression groups, the latter only wearing the clothes without added compression. The evoked metabolic changes were evaluated using indirect calorimetry and transcriptomics with liver tissue to investigate the mechanism of the metabolic changes induced by the compression load. The results indicated decreases in body weight gain, food intake, and respiratory exchange ratio in the compression group compared to the no-compression group, but these effects were limited in the "light period" which was an inactive phase for mice. As a result of the transcriptome analysis after eight hours of compression load to the trunk, several DEGs, e.g., Cpt1A, Hmgcr, were classified into functional categories relating to carbohydrate metabolism, lipid metabolism, or immune response. Lipid metabolism impacts included suppression of fatty acid synthesis and activation of lipolysis and cholesterol synthesis in the compression group. Taken together, our results showed that activation of lipid metabolism processes in an inactive phase was induced by the compression load to the trunk

Influence of a short-term iron-deficient diet on hepatic gene expression profiles in rats.

Iron is an essential mineral for the body, and iron deficiency generally leads to anemia. However, because non-anemic iron deficiency can exist, we performed a comprehensive transcriptome analysis of the liver to define the effects of this condition on the body. Four-week-old male rats were fed a low-iron diet (approximately 3 ppm iron) for 3 days and compared with those fed a normal diet (48 ppm iron) by pair feeding as a control. The rats in the iron-deficient diet group developed a non-anemic iron-deficient state. DNA microarray analysis revealed that during this short time, this state conferred a variety of effects on nutrient metabolism in the liver. In comparison with long-term (17 days) iron-deficiency data from a previous study, some of the changed genes were found to be common to both short- and long-term iron deficiency models, some were specific to the short-term iron deficiency model, and the others were oppositely regulated between the two feeding terms. Taken together, these data suggest that although the blood hemoglobin level itself remains unchanged during non-anemic iron deficiency, a variety of metabolic processes involved in the maintenance of the energy balance are altered

GO terms associated with the genes that were up-regulated in the iron-deficient group.

<p>FDR-corrected <i>P</i>-values were defined by the modified Fisher's exact test with the Benjamini and Hochberg FDR correction. FDR-corrected <i>P</i>-values<0.05 are shaded in gray.</p

Total cholesterol, triacylglycerol and total bile acid levels in the liver and total cholesterol, triacylglycerol, glucose and pyruvate levels in serum.

<p>The values represent the mean ± SEM (n = 5).</p

List of genes with expression changes in livers of rats fed an iron-deficient diet.

<p>White arrows: up-regulated gene expression, black arrows: down-regulated gene expression, gray arrows: no change.</p