| http://purl.uniprot.org/citations/25495645 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/25495645 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/25495645 | http://www.w3.org/2000/01/rdf-schema#comment | "Homozygosity of loss-of-function mutations in ANGPTL3 (angiopoietin-like protein 3)-gene results in FHBL2 (familial combined hypolipidaemia, OMIM #605019) characterized by the reduction of all major plasma lipoprotein classes, which includes VLDL (very-low-density lipoprotein), LDL (low-density lipoprotein), HDL (high-density lipoprotein) and low circulating NEFAs (non-esterified fatty acids), glucose and insulin levels. Thus complete lack of ANGPTL3 in humans not only affects lipid metabolism, but also affects whole-body insulin and glucose balance. We used wild-type and ANGPTL3-silenced IHHs (human immortalized hepatocytes) to investigate the effect of ANGPTL3 silencing on hepatocyte-specific VLDL secretion and glucose uptake. We demonstrate that both insulin and PPARγ (peroxisome-proliferator-activated receptor γ) agonist rosiglitazone down-regulate the secretion of ANGPTL3 and TAG (triacylglycerol)-enriched VLDL1-type particles in a dose-dependent manner. Silencing of ANGPTL3 improved glucose uptake in hepatocytes by 20-50% and influenced down-regulation of gluconeogenic genes, suggesting that silencing of ANGPTL3 improves insulin sensitivity. We further show that ANGPTL3-silenced cells display a more pronounced shift from the secretion of TAG-enriched VLDL1-type particles to secretion of lipid poor VLDL2-type particles during insulin stimulation. These data suggest liver-specific mechanisms involved in the reported insulin-sensitive phenotype of ANGPTL3-deficient humans, featuring lower plasma insulin and glucose levels."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.org/dc/terms/identifier | "doi:10.1042/bsr20140115"xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.org/dc/terms/identifier | "doi:10.1042/bsr20140115"xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/author | "Ehnholm C."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/author | "Ehnholm C."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/author | "Jauhiainen M."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/author | "Jauhiainen M."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/author | "Laurila P.P."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/author | "Laurila P.P."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/author | "Metso J."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/author | "Metso J."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/author | "Soronen J."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/author | "Soronen J."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/author | "Tikka A."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/author | "Tikka A."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/name | "Biosci. Rep."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/name | "Biosci. Rep."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/pages | "E00160"xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/pages | "E00160"xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/title | "Silencing of ANGPTL 3 (angiopoietin-like protein 3) in human hepatocytes results in decreased expression of gluconeogenic genes and reduced triacylglycerol-rich VLDL secretion upon insulin stimulation."xsd:string |
| http://purl.uniprot.org/citations/25495645 | http://purl.uniprot.org/core/title | "Silencing of ANGPTL 3 (angiopoietin-like protein 3) in human hepatocytes results in decreased expression of gluconeogenic genes and reduced triacylglycerol-rich VLDL secretion upon insulin stimulation."xsd:string |