Project description:Despite a variety of seasoning ingredients in diets, little is known about their cooperative effect on animal metabolism. We fed rats a diet containing 30 wt.% instant noodle with a 26% fat-to-energy ratio for 30 days (N-group). Compared with rats that were fed the same diet without seasonings (C-group), the N-group showed lower liver triacylglycerol levels and higher fecal cholesterol levels. To assess the mechanisms underlying this phenotype, we conducted transcriptome analyses of the hypothalamic–pituitary axis (HP), liver and white adipose tissue (WAT). Our results suggest that these ingredients may affect lipid homeostasis via the HP axis.
Project description:Despite a variety of seasoning ingredients in diets, little is known about their cooperative effect on animal metabolism. We fed rats a diet containing 30 wt.% instant noodle with a 26% fat-to-energy ratio for 30 days (N-group). Compared with rats that were fed the same diet without seasonings (C-group), the N-group showed lower liver triacylglycerol levels and higher fecal cholesterol levels. To assess the mechanisms underlying this phenotype, we conducted transcriptome analyses of the hypothalamic–pituitary axis (HP), liver and white adipose tissue (WAT). Our results suggest that these ingredients may affect lipid homeostasis via the HP axis.
Project description:Despite a variety of seasoning ingredients in diets, little is known about their cooperative effect on animal metabolism. We fed rats a diet containing 30 wt.% instant noodle with a 26% fat-to-energy ratio for 30 days (N-group). Compared with rats that were fed the same diet without seasonings (C-group), the N-group showed lower liver triacylglycerol levels and higher fecal cholesterol levels. To assess the mechanisms underlying this phenotype, we conducted transcriptome analyses of the hypothalamic–pituitary axis (HP), liver and white adipose tissue (WAT). Our results suggest that these ingredients may affect lipid homeostasis via the HP axis.
Project description:To investigate the effect of miR-503 in aging associated type 2 diabetes, target genes of miR-503 need to be investigated. The global miR-322-503-351 deletion (KO) mouse was constructed, and RNA-seq was then performed on aged mouse liver and white adipose tissue (WAT).
Project description:CD44 expression has been shown to be enhanced in the liver and white adipose tissue (WAT) during obesity, suggesting a possible regulatory role for CD44 in metabolic syndrome. To study this hypothesis, we compared the gene expression profiles in liver and in WAT between WT and CD44 knockout (CD44KO) mice fed a high-fat diet (HFD) for 21 weeks. This analysis demonstrated that several genes associated with triglyceride synthesis and accumulation, including Mogat2, Cidea, Cidea, Apoa4, and Elovl7, were decreased in the livers of CD44KO mice compared to WT mice. Many genes encoding pro-inflammatory chemokines and chemokine receptors also were decreased in the livers of CD44KO mice. Analysis with WAT showed that genes associated with triglyceride accumulation, including Fasn, Elovl6 and Mogat2, were increased in WAT of CD44KO(HFD) mice compared to WT(HFD) mice. Moreover, many genes associated with inflammation, including cytokines (Cxcl14, Cxcl12, Il33, and Il2), cytokine receptors (Ccr1, Il6ra, Il10rb), trypases (Tpsb2, Tpsab1, Tpsg1), and cellular matrix proteins (Integrin ?4 (Itga4), ItgaM, Itgb2), were decreased in WAT of CD44(HFD) compared to WT(HFD) mice. This study indicates that CD44 plays a critical role in regulating several aspects of metabolic syndrome. Liver and white adipose tissue (WAT) total RNAs were purified from 5 WT and 5 CD44 knockout mice fed with a high-fat diet for 21 weeks. Then, samples were applied on Agilent mouse genome chips.
Project description:Transcriptomic analysis on white adipose tissues (WAT), brown adipose tissues (BAT), skeletal muscles and liver from cold-exposed obese mice treated with KPT-330 or DMSO, and those from obese mice housed at ambient temperature indicated that KPT-330 profoundly modulates immune responses in these thermogenic tissues and organs.
Project description:We have modeled the Fnip2 rs2291007 genetic variant in the mouse genome. In this study we aimed to investigate the effect of this genetic variant in the transcriptome of two metabolically relevant tissues: liver and white adipose tissue (WAT)
Project description:We conducted expression profiling of white adipose tissue isolated from WT and miR-22 KO animals. The main work is analysis of the miR-22 function in striated muscle. White adipose tissue (WAT) was analyzed to look at effects in WAT, as that might be induced by metabolic changes in skeletal muscle.
Project description:Metabolism in mammals is regulated by the complex interplay among different organs. Fatty acid synthesis is increased in white adipose tissue (WAT) when it is inhibited in liver. Here we identify glycoprotein nonmetastatic melanoma protein B (Gpnmb) as one liver-WAT cross-talk factor in lipogenesis. Hepatic SREBP pathway inhibition leads to increased transcription of the Gpnmb and promotes the processing of the membrane protein to a secreted form. Gpnmb stimulates lipogenesis in WAT and exacerbates diet-induced obesity and insulin resistance. In humans, Gpnmb is tightly associated with body mass index and is a strong risk factor for obesity. Gpnmb inhibition by a neutralizing antibody or liver specific knockdown improves metabolic parameters including weight gain reduction and increased insulin sensitivity, likely by promoting the beiging of WAT. These results suggest that Gpnmb is a liver-secreted factor regulating lipogenesis in WAT, and that Gpnmb inhibition may provide a therapeutic strategy for obesity and diabetes. Hepatic SREBP pathway inhibition, such as liver-specific ablation of Scap (L-Scap-/-), decreases fatty acid synthesis in liver. Meanwhile, the fatty acid synthesis in white adipose tissue of L-Scap-/- is compensatorily increased. The microarray analysis using the liver RNAs of L-Scap-/- and wild type (WT) mice is performed to identify the up-regulated genes encoding secreted factors in L-Scap-/-.