Project description:Affymetrix SNP array analysis was performed on DNA extracted from whole blood samples of 7 Taiwanese patients with hyperlipidemia. Three copy number variant (CNV) regions associated significantly with hyperlipidemia were identified through genomic segmentation analysis (P<0.001).
Project description:Pulsatilla chinensis (PC) is a traditional Chinese medicinewith detoxification activities. It has been used for dysentery, vaginal trichomoniasis, bacterial infections and malignant tumor treatment. Gavage administration of PC in hyperlipidemia rats for 11 weeks resulted in obviously reduced serum total cholesterol, LDL-cholesterol and ameliorated fatty liver. So we wanted to further investigate the relationship between PC and lipid metabolism related pathways or genes
Project description:Pulsatilla chinensis (PC) is a traditional Chinese medicinewith detoxification activities. It has been used for dysentery, vaginal trichomoniasis, bacterial infections and malignant tumor treatment. Gavage administration of PC in hyperlipidemia rats for 11 weeks resulted in obviously reduced serum total cholesterol, LDL-cholesterol and ameliorated fatty liver. So we wanted to further investigate the relationship between PC and lipid metabolism related pathways or genes
Project description:Affymetrix SNP array analysis was performed on DNA extracted from whole blood samples of 7 Taiwanese patients with hyperlipidemia. Three copy number variant (CNV) regions associated significantly with hyperlipidemia were identified through genomic segmentation analysis (P<0.001). 7 male Taiwanese hyperlipidemia patients.
Project description:Colesevelam is a bile acid sequestrant approved to treat both hyperlipidemia and type 2 diabetes, but the mechanism for its glucose lowering effects is not fully understood. The aim of this study was to investigate the role of hepatic microRNA’s as regulators of metabolic disease and to investigate the link between the cholesterol and glucose lowering effects of colesevelam. To quantify the impact of colesevelam treatment in rodent models of diabetes, metabolic studies were performed in Zucker Diabetic Fatty (ZDF) rats and db/db mice. Colesevelam treatments significantly decreased plasma glucose levels and increased glycolysis in the absence of changes to insulin levels in ZDF rats and db/db mice. High-throughput sequencing and real-time PCR were used to quantify hepatic miRNA and mRNA changes, and the cholesterol-sensitive miR-96/182/183 cluster was found to be significantly increased in livers from ZDF rats treated with colesevelam compared to vehicle controls. In summary, these results support that colesevelam likely improves glycemic control through hepatic miR-96/182/183, a mechanism that directly links cholesterol and glucose metabolism.
Project description:To investigate effects of intake of mulberry leaves on hyperlipidemia, we performed gene expression profiling on rat liver by microarray analysis. Microarray analysis revealed that mulberry leaves up-regulated the genes involved in alpha-, beta-, and omega-oxidation of fatty acids, mainly relating to peroxisome proliferator-activated receptor signaling pathway, and down-regulated the gene expression involved in lipogenesis. Furthermore, the genes relating to response to oxidative stress were up-regulated in rats administrated mulberry leaves.
Project description:To investigate effects of intake of Eucommia ulmoides leaves on hyperlipidemia, we performed gene expression profiling on rat liver by microarray analysis. Microarray analysis revealed that Eucommia ulmoides leaves up-regulated the gene expression involved in alpha-, beta-, and omega-oxidation of fatty acids, mainly relating to peroxisome proliferator-activated receptor signaling pathway. Rats were fed a high-fat diet and high-fructose water without/with orally administration of Eucommia ulmoides leaves for 5 weeks. Livers were taken for RNA extraction and hybridization on Agilent microarrays.
Project description:Hyperlipidemia is accompanied by increased systemic inflammation. However, how hyperlipidemia affects T cell biology is still unclear. We aimed to detail the effects of hyperlipidemia on the T cell’s transcriptome, metabolome and lipidome. Low-density lipoprotein receptor-deficient (LDLR-/-) mice were subjected to a 0.15% high cholesterol diet (HCD), a normal chow diet (NCD) and T cells were analyzed. Hyperlipidemia induced an increase in CXCR3 on and IFN in CD4+ T cells, which was accompanied by transcriptomic changes in interleukin-mediated JAK/STAT signaling, interferon-γ signaling and a general pro-inflammatory immune response, suggesting that hyperlipidemia induces a Th1-like response. In these T cells, hyperlipidemia did not affect levels of metabolites involved in glycolysis or fatty acid oxidation, but enhanced amino acids levels. CD4+ T-cells of mice fed a HCD exhibited increased cellular cholesterol accumulation and an increased arachidonic acid (AA) to Docosahexaenoic acid (DHA) ratio, which was associated with T cell activation and IFN signaling. In vitro, T cell exposure to VLDL, but not LDL phenocopied these results. The effect of hyperlipidemia on T cell activation is reversible as transcriptional- and lipid profiles in LDLr-/ mice normalized 6 weeks after switching the HCD to NCD. In conclusion, hyperlipidemia induces a Th1-like response in CD4+ T cells, which is associated with an AA/DHA ratio in these cells. VLDL, but not LDL is the main lipid component driving hyperlipidemia induced T cell activation.
Project description:Hyperlipidemia is accompanied by increased systemic inflammation. However, how hyperlipidemia affects T cell biology is still unclear. We aimed to detail the effects of hyperlipidemia on the T cell’s transcriptome, metabolome and lipidome. Low-density lipoprotein receptor-deficient (LDLR-/-) mice were subjected to a 0.15% high cholesterol diet (HCD), a normal chow diet (NCD) and T cells were analyzed. Hyperlipidemia induced an increase in CXCR3 on and IFN in CD4+ T cells, which was accompanied by transcriptomic changes in interleukin-mediated JAK/STAT signaling, interferon-γ signaling and a general pro-inflammatory immune response, suggesting that hyperlipidemia induces a Th1-like response. In these T cells, hyperlipidemia did not affect levels of metabolites involved in glycolysis or fatty acid oxidation, but enhanced amino acids levels. CD4+ T-cells of mice fed a HCD exhibited increased cellular cholesterol accumulation and an increased arachidonic acid (AA) to Docosahexaenoic acid (DHA) ratio, which was associated with T cell activation and IFN signaling. In vitro, T cell exposure to VLDL, but not LDL phenocopied these results. The effect of hyperlipidemia on T cell activation is reversible as transcriptional- and lipid profiles in LDLr-/ mice normalized 6 weeks after switching the HCD to NCD. In conclusion, hyperlipidemia induces a Th1-like response in CD4+ T cells, which is associated with an AA/DHA ratio in these cells. VLDL, but not LDL is the main lipid component driving hyperlipidemia induced T cell activation.