The role of endoplasmic reticulum stress in hippocampal insulin resistance.
Ann Arbor, United States. In Exp Neurol, Feb 2016
In the current study, we investigated ER stress in the hippocampus of 3 different mouse models of metabolic syndrome: the C57BL6 mouse on a high fat (HF) diet; apolipoprotein E, leptin, and apolipoprotein B-48 deficient (ApoE 3KO) mice; and the low density lipoprotein receptor, leptin, and apolipoprotein B-48 deficient (LDLR 3KO) mice.
Adzuki bean ameliorates hepatic lipogenesis and proinflammatory mediator expression in mice fed a high-cholesterol and high-fat diet to induce nonalcoholic fatty liver disease.
Seoul, South Korea. In Nutr Res, Jan 2016
The transcriptional factors of hepatic lipogenesis, such as adiponectin, AMP-activated protein kinase α, sterol regulatory element-binding protein 1c, fatty acid synthase, carnitine palmitoyltransferase 1, 3-hydroxy-3-methyl-glutaryl-CoA reductase, and apolipoprotein B, as well as proinflammatory mediators, such as tumor necrosis factor α, nuclear factor κB, and caspase-3, improved in both experimental groups (P < .05).
Lipoprotein apheresis: present and future uses.
Kansas City, United States. In Curr Opin Lipidol, Dec 2015
RECENT FINDINGS: Lipoprotein apheresis lowers not only plasma levels of apolipoprotein B lipoproteins but also markers of vascular inflammation and blood rheology.
Non-high-density lipoprotein cholesterol: current status as cardiovascular marker.
Amsterdam, Netherlands. In Curr Opin Lipidol, Dec 2015
PURPOSE OF REVIEW: In this review, we summarize the evidence with regard to the rationale of using nonhigh density lipoprotein cholesterol (non-HDL-C) as a cardiovascular disease (CVD) risk factor, in relation to low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apoB).
Meta-analysis of lipid-traits in Hispanics identifies novel loci, population-specific effects, and tissue-specific enrichment of eQTLs.
Houston, United States. In Sci Rep, Dec 2015
Genome-wide significant signals were observed in or near CELSR2, ZNF259/APOA5, KANK2/DOCK6 and NCAN/MAU2 for total cholesterol, LPL, ABCA1, ZNF259/APOA5, LIPC and CETP for HDL cholesterol, CELSR2, APOB and NCAN/MAU2 for LDL cholesterol, and GCKR, TRIB1, ZNF259/APOA5 and NCAN/MAU2 for triglycerides.
Hypermutation in human cancer genomes: footprints and mechanisms.
More papers using
In Nat Rev Cancer, 2014
This major expansion of cancer mutation data sets has provided unprecedented statistical power for the analysis of mutation spectra, which has confirmed several classical sources of mutation in cancer, highlighted new prominent mutation sources (such as apolipoprotein B mRNA editing enzyme catalytic polypeptide-like (APOBEC) enzymes) and empowered the search for cancer drivers.