Project description:To assess the effect of steatosis and oxidative stress on progression of liver fibrosis, we have employed whole genome microarray expression profiling as a discovery platform to identify genes that are related with oxidative stress- and steatosis-induced hepatic fibrogenesis. When wild type mice were fed high-fat/high-sucrose diet for 24 weeks, expression of 69 genes was changed more than 10-fold compared with wild type animals fed normal diet, 11 of which were categorized to lipid metabolic process. Moreover, expression of 208 genes showed more than 5-fold changes in Tet-mev-1 mice fed high-fat/high-sucrose diet compared with the same transgenic animals fed normal diet, and gene ontology analyses indicated significant changes in chemokine activity and chemokine receptor binding as well as defense and immune responses. oxidative stress and high fat high calorie induced gene expression in wild type or Tet-mev-1 mouse liver tissue. wild type and Tet-mev-1 mice were fed either normal diet or high fat high sucrose diet for 4 months, and have been given doxycycline-containing water from embryo. Each group were perfomed by duplicate.
Project description:To assess the effect of steatosis and oxidative stress on progression of liver fibrosis, we have employed whole genome microarray expression profiling as a discovery platform to identify genes that are related with oxidative stress- and steatosis-induced hepatic fibrogenesis. When wild type mice were fed high-fat/high-sucrose diet for 24 weeks, expression of 69 genes was changed more than 10-fold compared with wild type animals fed normal diet, 11 of which were categorized to lipid metabolic process. Moreover, expression of 208 genes showed more than 5-fold changes in Tet-mev-1 mice fed high-fat/high-sucrose diet compared with the same transgenic animals fed normal diet, and gene ontology analyses indicated significant changes in chemokine activity and chemokine receptor binding as well as defense and immune responses.
Project description:The impact of high fat diet on secreted milk small RNA transcriptome was studied by isolating total RNA from milk fat fraction collected on lactation day 10 from control diet fed (C; n=5; 10% fat; 7% sucrose; Research Diets #D12450J, Brunswick, NJ) and high fat diet fed (HF; n=4; Research Diets #D12492, 60% of total kcal energy is fat and match 7% of total kcal is sucrose; Brunswick, NJ) mice.
Project description:The impact of high fat diet on secreted milk small RNA transcriptome was studied by isolating total RNA from milk fat fraction collected on lactation day 10 from control diet fed (C; n=5; 10% fat; 7% sucrose; Research Diets #D12450J, Brunswick, NJ) and high fat diet fed (HF; n=4; Research Diets #D12492, 60% of total kcal energy is fat and match 7% of total kcal is sucrose; Brunswick, NJ) mice.
Project description:The gene expression in the liver tumor tissues or non-tumor tissues of DMBA-treated, high fat diet-fed mouse livers compared with those of DMBA-treated, normal diet-fed mouse liver tissues were successfully analyzed through the expression profiling of a total of 23473 genes in mouse livers (three tumor bearing livers vs two normal mouse livers).
Project description:Xbp1 is an important regulator of unfolded protein response and lipid metabolism. Its dyregulation has been associcated in human NASH. Feeding a high fat diet with fructose/sucrose to mice causes progressive, fibrosing steatohepatitis. This study is to use RNA-Seq to identify differentially expressed genes in hepatic Xbp1 deficient mice livers fed with a high fat diet compared to controls.
Project description:Xbp1 is an important regulator of unfolded protein response and lipid metabolism. Its dyregulation has been associcated in human NASH. Feeding a high fat diet with fructose/sucrose to mice causes progressive, fibrosing steatohepatitis. This study is to use RNA-Seq to identify differentially expressed genes in hepatic Xbp1 deficient mice livers fed with a high fat diet compared to controls. Hepatic Xbp1 deficient mice or flox controls were fed either regular chow or a high fat diet (n=4). Samples from each cohort were pooled into two replicates.
Project description:This study sought to interrogate the effects of lipids and lipid metabolites on the hepatic proteome. Protein expression in high-fat diet (HFD) mouse livers vs. livers of normal chow fed (NC) mice were investigated using multiplexed quantitative LC-MS/MS (TMT labeling). This experiment contains additional replicates for normal chow and mice on high-fat diet for 16 weeks.
Project description:Age-related macular degeneration (AMD) is a leading cause of blindness. Metabolic disorders and diets are risk factors. We compared lipid profiles and retinal phenotypes with long-term feeding of four diets in male Chinchilla rabbits. Animals were fed a normal diet (ND), high-fat diet (HFD), high-sucrose diet (HSD) or a high-fat plus high-sucrose diet (HFSD) for 6 months. Eyes were examined using multimodal imaging modalities and electroretinograms. Retinal sections were analyzed using H&E staining, Toluidine Blue staining, immunostaining and transmission electron microscopy. Lipids and complement C3 protein (C3) in serum or aqueous humor were measured. RNA sequencing was performed to evaluate the retinal transcriptomes. HFD and HSD had minor effects on lipid profiles but, when fed concomitantly, synergistically induced severe dyslipidemia. None of the four diets caused obesity. HFSD induced retinal lesions, such as reticular pseudodrusen (RPDs) and other pigmentary abnormalities. RPD-like lesions were mainly lipid droplets around cells of the retinal pigment epithelium. HFSD also induced elevated levels of ocular C3 and reduced the density of retinal vessels. In conclusion, HFD and HSD can - when combined - induce normal-weight dyslipidemia and RPD-like retinal lesions. HFSD-fed male Chinchilla rabbits are a good model of early AMD.
Project description:Chronic high sugar feeding induces obesity, hyperglycemia, and insulin resistance in flies and mammals. These phenotypes are controlled by the fat body, a liver- and adipose- like tissue in Drosophila flies. To gain insight into the mechanisms underlying the connection between diet and insulin sensitivity, we used Illumina RNA-seq to profile gene expression in fat bodies isolated from chronically high sugar fed, wandering (post-prandial) third instar wild type larvae w(L3). These data were compared to control-fed wild-type wL3 fat bodies as well as those expressing transgenic interfering RNA (i) targeting CG18362 (Mio/dChREBP) in the fat body on both diets. Female VDRC w1118, cgGAL4, UAS-Dcr2 or UAS-ChREBPi(52606), cgGAL4, UAS-Dcr2 wandering third instar larvae were fed control (0.15M) or high (0.7M) sucrose and fat bodies isolated for RNA extraction.