Rader HHDL and BioBank genotyping
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE100271 | GEO | 2017/06/21
SECONDARY ACCESSION(S): PRJNA391185
REPOSITORIES: GEO
Similar Datasets
Project description:The presence of a coding variant affecting plasma high density lipoprotein cholesterol (HDLC) levels was evaluated in subjects with elevated plasma levels of HDLC.
2015-12-17 | GSE76065 | GEO
Project description:The presence of a coding variant affecting plasma high density lipoprotein cholesterol (HDLC) levels was evaluated in subjects with elevated plasma levels of HDLC. 18 DNA samples from subjects with high plasma HDLC levels were analyzed. The samples were analyzed using the exome chip in three separate phases, with different samples in each phase. The same genotyping platform was used for each of the phases of the experiment under the same experimental conditions. Because different samples were run in different phases, raw intensity data was collected separately for each phase and genotypes were called separately for each phase. Raw intensity data is provided thus separately for the subjects by phase of genotyping. The experimental phase of each subject is also provided.
2015-12-17 | E-GEOD-76065 | biostudies-arrayexpress
Project description:Background---For decades, plasma lipid levels have been known risk factors of atherosclerosis. Recently, inflammation has gained acceptance as a crucial event in the pathogenesis and development of atherosclerosis. A number of studies have provided some insights into the relationships between the two aspects of atherosclerosis: plasma lipids --- the risk factors, and circulating leukocytes --- the effectors of inflammation. In this study, we investigate the relationships between plasma lipids and leukocytes. Methods and Results---No significant correlation was found between leukocyte counts and plasma lipid levels in 74 individuals. Profiling and analyzing the leukocyte gene expression of 32 individuals revealed distinctive patterns in response to plasma lipid levels: 1) genes involved in lipid metabolism and in the electron transport chain were positively correlated with triglycerides and low-density lipoprotein cholesterol levels, and negatively correlated with high-density lipoprotein cholesterol levels; 2) genes involved in platelet activation were negatively correlated with high-density lipoprotein cholesterol levels; 3) transcription factors regulating lipidgenesis-related genes were correlated with plasma lipid levels; 4) a number of genes correlated to plasma lipid levels were found located in the regions of known QTLs associated with hyperlipemia. Conclusions--- We discovered interesting patterns of leukocyte gene expression in response to plasma lipid levels. Most importantly, genes involved in lipid metabolism, the electron transportation chain, and platelet activation were found correlated with plasma lipid levels. We suggest that leukocytes respond to changing plasma lipid levels by regulating a network of genes, including genes involved in lipid and fatty acid metabolism, through the activation of key transcription factors, such as sterol regulatory element binding transcription factors and peroxisome proliferative activated receptors. Experiment Overall Design: 1. Profile gene expression in human peripheral blood cells. Experiment Overall Design: 2. Test blood biochemistry and blood cell differential counts Experiment Overall Design: 3. Examine the correlation between blood gene expression and blood lipid levels. Experiment Overall Design: 4. Explore possible pathways with significant genes. Experiment Overall Design: 5. Validate a number of significant genes with RT-PCR
2008-06-12 | E-GEOD-3059 | biostudies-arrayexpress
Project description:The effect of perfluoroalkyl sulfonates on lipoprotein metabolism was investigated in APOE*3-Leiden.CETP mice with a humanized lipoprotein profile. Perfluorohexane sulfonate and perfluorooctane sulfonate markedly reduced both plasma TG and TC by decreasing nonHDL-C and HDL-C accompanied by a reduction in apoAI. Mechanistic studies showed that these effects were mainly caused by impaired lipoprotein production. Male E3L.CETP mice on a C57Bl/6 background were fed a Western-type diet, containing 0.25% (w/w) cholesterol, 1% (w/w) corn oil and 14% (w/w) bovine fat (Western-type diet) (Hope Farms, Woerden, The Netherlands) for 4 to 6 weeks in three independent experiments. Upon randomization according to total plasma cholesterol (TC) and TG levels, mice received the Western-type diet without or with PFBS (30 mg/kg/day), PFHxS (6 mg/kg/day) or PFOS (3 mg/kg/day) during 4-6 weeks. The effects of these PFAS on plasma lipids and lipoproteins were determined. In addition, PFAS levels were determined in plasma and livers were isolated for hepatic lipid analysis and hepatic gene expression analysis using an Affymetrix technology platform and Affymetrix GeneChip® mouse genome 430 2.0 arrays.
2011-01-01 | E-GEOD-22940 | biostudies-arrayexpress
Project description:Background---For decades, plasma lipid levels have been known risk factors of atherosclerosis. Recently, inflammation has gained acceptance as a crucial event in the pathogenesis and development of atherosclerosis. A number of studies have provided some insights into the relationships between the two aspects of atherosclerosis: plasma lipids --- the risk factors, and circulating leukocytes --- the effectors of inflammation. In this study, we investigate the relationships between plasma lipids and leukocytes. Methods and Results---No significant correlation was found between leukocyte counts and plasma lipid levels in 74 individuals. Profiling and analyzing the leukocyte gene expression of 32 individuals revealed distinctive patterns in response to plasma lipid levels: 1) genes involved in lipid metabolism and in the electron transport chain were positively correlated with triglycerides and low-density lipoprotein cholesterol levels, and negatively correlated with high-density lipoprotein cholesterol levels; 2) genes involved in platelet activation were negatively correlated with high-density lipoprotein cholesterol levels; 3) transcription factors regulating lipidgenesis-related genes were correlated with plasma lipid levels; 4) a number of genes correlated to plasma lipid levels were found located in the regions of known QTLs associated with hyperlipemia. Conclusions--- We discovered interesting patterns of leukocyte gene expression in response to plasma lipid levels. Most importantly, genes involved in lipid metabolism, the electron transportation chain, and platelet activation were found correlated with plasma lipid levels. We suggest that leukocytes respond to changing plasma lipid levels by regulating a network of genes, including genes involved in lipid and fatty acid metabolism, through the activation of key transcription factors, such as sterol regulatory element binding transcription factors and peroxisome proliferative activated receptors. Keywords: Atherosclerosis, leukocyte, lipid, gene expression
2006-08-04 | GSE3059 | GEO
Project description:Specific mutations in Apolipoprotein A-I (ApoA-I) of high-density lipoprotein (HDL) are responsible for a late-onset systemic amyloidosis. Carriers do not exhibit increased cardiovascular disease risk despite reduced levels of ApoA-I/ HDL-cholesterol. To explain this paradox, we show that the HDL particle profile of L75P and L174S patients presents a higher relative abundance of the 8.4 nm vs 9.6 nm particles, and that serum from patients, as well as reconstituted 8.4 and 9.6 nm HDL particles (rHDL), possess increased capacity to catalyze cholesterol efflux from macrophages. Synchrotron radiation circular dichroism and hydrogen-deuterium exchange revealed that the variants in 8.4 nm rHDL have altered secondary structure composition and display a more flexible binding to lipids compared to their native counterpart. The reduced HDL-cholesterol levels of patients carrying ApoA-I amyloidogenic variants are thus balanced by higher proportion of small, dense HDL particles and better cholesterol efflux due to altered, region-specific protein structure dynamics.
2020-11-20 | PXD021266 | Pride
Project description:Chronic glucagon receptor inhibition with a glucagon receptor antibody decreases amino acid catabolism and ureagenesis, while increasing plasma triglyceride concentrations, plasma very-low density lipoprotein cholesterol concentrations, and liver triglyceride concentrations. To dissect the molecular mechanism underlying these effects, RNA sequencing of liver biopsies from female mice treated for eight weeks with the glucagon receptor antibody, REGN1193, or a control antibody, REGN1945, were performed.
2022-10-09 | E-MTAB-12048 | biostudies-arrayexpress
Project description:Dyslipidemia and inflammation play key roles in the pathogenesis of both nonalcoholic fatty liver disease (NAFLD) and atherosclerosis. NAFLD, particularly its severe form nonalcoholic steatohepatitis (NASH) is associated with increased cardiovascular disease (CVD) risk. HDL (high density lipoprotein- also a CVD risk) are decreased in NAFLD but whether HDL function is abnormal in NAFLD is unknown. Furthermore, it is unknown whether dyslipidemia contributes to reduced HDL function in NAFLD and whether hepatic inflammation further impairs HDL function in patients with NASH. Therefore, the aim of this study was to investigate HDL function and to examine the effect of dyslipidemia and inflammation on HDL metabolism in patients with biopsy-proven simple steatosis (SS) and NASH. RESULTS: Compared to controls, SS and NASH subjects had significantly higher levels of plasma triglyceride, insulin, and were more insulin resistant (HOMA, P<0.05) with no differences in total cholesterol, HDL cholesterol, ApoB100 and ApoAI levels. NAFLD patients had increased production and degradation rates of both HDLc and ApoAI that resulted in their levels remaining stable. The degradation rates also were increased of other HDL proteins, including ApoAII, ApoAIV, vitamin D-binding protein, and complement 3 (all P<0.05). NAFLD patients had increased activities of LCAT and CETP, indicating altered HDL lipidation. NAFLD induced alterations in HDL metabolism were associated with reduced anti-oxidant but increased pro-inflammatory activity of HDL. However, no differences were observed in either HDL function or the kinetics of HDLc and HDL proteins between SS and NASH subjects.
2019-08-12 | PXD010199 | Pride
Project description:The high-fat diet (HFD)-feeding significantly stimulated hypercholesterolemia in male SD rats. Simultaneous feeding of hawk tea extracts (HTE) reversed the hypercholesterolemia in rats by lowering the serum total cholesterol and low-density lipoprotein cholesterol levels. To understand the molecular mechanism underlying the cholesterol-lowering effects of HTE, we performed the RNA-seq analysis. Consequently, the change in mRNA levels of genes invovled in metabolism of lipid and lipoprotein, primary bile acid synthesis, and ABC transporters itriggered by HFD-feeding were reversed by the co-administration of HTE (200 mg/kg/day for 11 weeks).
2019-05-21 | GSE125084 | GEO
Project description:Stearoyl-CoA desaturase 1-deficient (SCD1-/-) mice have impaired monounsaturated fatty acid (MUFA) synthesis. When maintained on a very low-fat, high-carbohydrate (VLF-HC) diet, SCD1-/- mice develop severe hypercholesterolemia characterized by an increase in apolipoprotein B-containing lipoproteins and the appearance of lipoprotein-X. Additionally, high-density lipoprotein cholesterol is dramatically reduced in VLF-HC SCD1-/- mice. The concomitant presence of elevated plasma bile acids, bilirubin and aminotransferases in the VLF-HC SCD1-/- mouse are indicative of hepatic dysfunction. Supplementation of the VLF-HC diet with unsaturated fat (canola oil), but not saturated fat (coconut oil), prevents these plasma phenotypes. However, dietary oleate was not as effective as canola oil in reducing low-density lipoprotein cholesterol, signifying an additional role for dietary polyunsaturated fatty acid deficiency in the development of this phenotype. These results indicate that lack of SCD1 results in an increased requirement for dietary unsaturated fat to compensate for impaired MUFA synthesis and to prevent hypercholesterolemia and hepatic dysfunction. Experiment Overall Design: We used Affymetrix Mouse430v2.0 microarray chips to search for gene expression changes unique to the VLF-HC SCD1-/- group. These chips contain 45,101 probe sets representing over 39,000 transcripts and variants from over 34,000 mouse genes. We studied SCD1+/+ and SCD1-/- mice on chow or the VLF-HC diet, analyzing five individual livers from each subgroup for a total of twenty microarrays.
2007-11-01 | E-GEOD-3889 | biostudies-arrayexpress