|
Hypertriglyceridemia
|
0.100 |
GeneticVariation
|
phenotype |
LHGDN |
Effect of SstI polymorphism of the apolipoprotein CIII gene and environmental factors on risks of hypertriglyceridemia in Taiwan aborigines.
|
16864937 |
2006 |
|
Hypertriglyceridemia
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Various population studies have reported the association of rare S2 allele of apolipoprotein C3 (APOC3) SstI polymorphism with hypertriglyceridemia (HTG) and coronary artery disease (CAD).
|
15124908 |
2004 |
|
Hypertriglyceridemia
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Therefore, although the individual risk of hypertriglyceridemia is increased in women with the haplotype T, C at -482, -455, it appears that the -482, -455 and SstI APOC-III gene polymorphisms are not major contributors to the risk of dyslipidemia in the population of northern France.
|
10781646 |
2000 |
|
Hypertriglyceridemia
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
We assessed, in the Quebec City population, the allele frequency and haplotype distributions of mutations in genes related to HTG, such as the apolipoprotein E (APOE) (C112R and C158R), the apolipoprotein CIII (APOC3) (C-482T and C3238G) and the peroxisome proliferator-activated receptor alpha (PPARalpha) (L162V) genes.
|
15549499 |
2004 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
To analyze the association between genetic polymorphisms of apolipoprotein genes APOA5, APOC3, and APOE and the severity of hypertriglyceridemia during bexarotene therapy and to optimize patient selection for bexarotene therapy based on adverse effect profile.
|
30422238 |
2018 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Higher apoCIII concentrations were associated (P < .0001) with increased triglycerides (r = 0.78), total (r = 0.61) and low-density lipoprotein (LDL) (r = 0.40) cholesterol, apoA-I (r = 0.26), and apoB (r = 0.50), and these relationships persisted after controlling for age, gender, body mass index (BMI), and hemoglobin A1c (HbA1c).
|
15375785 |
2004 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
In summary, hypertriglyceridemia in HuCIIITg mice appears to result primarily from decreased tissue uptake of triglyceride-rich particles from the circulation, which is most likely due to increased apo CIII and decreased apo E on VLDL particles. the HuCIIITg mouse appears to be a suitable animal model of primary familial hypertriglyceridemia, and these studies suggest a possible mechanism for this common lipoprotein disorder.
|
1430212 |
1992 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
A cross experiment was done to determine the genetic background of hypertriglyceridemia observed in FLS mice. cDNA sequences of apoC-II and apoC-III of FLS mice were determined.
|
14506831 |
2003 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
To investigate whether hypertriglyceridemia subtypes affect acute pancreatitis progression, we analyzed two genetically modified hypertriglyceridemia mouse models-namely, glycosylphosphatidylinositol high-density lipoprotein binding protein 1 knockout (Gpihbp1-/-) and apolipoprotein C3 transgenic (ApoC3-tg) mice.
|
31570698 |
2019 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
These results indicate that apoCIII and/or hypertriglyceridemia plays a major role in liver inflammation and cell death, which in turn increases susceptibility to and the severity of diet-induced NAFLD.
|
28163820 |
2017 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
apoB = apolipoprotein B; apoC-III = apolipoprotein CIII; ASO = antisense oligonucleotide; FCS = familial chylomicronemia syndrome; HTG = hypertriglyceridemia; LPL = lipoprotein lipase; LPLD = lipoprotein lipase deficiency.
|
30183397 |
2018 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Higher apoCIII concentrations were associated (P<.0001) with increased triglycerides (r=.78), total (r=.61) and LDL (r=.40) cholesterol, apoAI (r=.26), and apoB (r=.50), AER (r=.08), and the severity of retinopathy (ETDRS score, r=.11), and these relationships persisted after controlling for age, gender, body mass index (BMI), and HbA1c level.
|
15642486 |
2005 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Furthermore, RNAi-mediated ApoC3 inhibition lowered plasma TG concentrations in animals with diet-induced hypertriglyceridemia.
|
30723097 |
2019 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The variant apo CIII promoter is common in the human population and may represent a major contributing factor to the development of hypertriglyceridemia.
|
8675624 |
1995 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Increases in postprandial apoCIII after fructose, but not glucose consumption, are positively associated with elevated triglycerides in large triglyceride-rich lipoproteins and increased small dense LDL levels.
|
31789670 |
2020 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
These results indicate that the metabolic response to HTG in human apolipoprotein C-III overexpressing mice may support a high TG production rate and that the cytosol of hepatocytes is subjected to an important oxidative stress, probably as a result of FFA over-accumulation, iron overload and enhanced activity of some ROS-producing catabolic enzymes.
|
25047818 |
2014 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Apolipoprotein C-III has been referred to as an important participant in the metabolism of triglyceride-rich lipoproteins, leading to hypertriglyceridemia and thereafter cardiovascular disease.
|
27770802 |
2016 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Here, we review the pathophysiological role of apoC-III in TG metabolism and the evidence supporting this apolipoprotein as an emerging target for hypertriglyceridemia (HTG) and associated cardiovascular disorders.
|
26435212 |
2015 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Therefore, VLDL particles with apoC-III may play a central role in identifying the high risk of coronary heart disease in hypertriglyceridemia, but their substantial prevalence in normolipidemics may be of clinical significance as well.
|
11483625 |
2001 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Several therapies for regulating TRL metabolism, including inhibitors of diacylglycerol O-acyltransferase and microsomal triglyceride transfer protein, and apoC-III antisense oligonucleotides, merit further investigation in patients with hypertriglyceridaemia.
|
24060958 |
2013 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
While loss of insulin response is associated with unrestrained apoC-III production and impaired triglyceride metabolism, these data suggest that Foxo1 provides a molecular link between insulin deficiency or resistance and aberrant apoC-III production in the pathogenesis of diabetic hypertriglyceridemia.
|
15546000 |
2004 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
We showed that ApoC3-transgenic mice, as opposed to age/sex-matched wild-type littermates, develop hypertriglyceridemia with concomitant elevations in plasma cholesterol and non-esterified fatty acid levels.
|
27226540 |
2016 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Unlike the human apo CII (HuCII)- and apo CIII (HuCIII)-transgenic mouse models of hypertriglyceridemia, plasma cholesterol was disproportionately elevated (95 +/- 23 vs 73 +/- 23, P = 0.002, fasted and 90 +/- 24 vs 61 +/- 14, P < 0.0001, fed).
|
8698877 |
1996 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Therefore, there appears to be a need for effective TG-lowering agents.<b>Areas covered</b>: This review presents the most recent advances in hypertriglyceridemia treatment; specifically, it discusses the results of clinical trials and critically comments on apolipoprotein C-III inhibitors, angiopoietin-like 3 inhibitors, alipogene tiparvovec, pradigastat, pemafibrate and novel formulations of omega-3 fatty acids.<b>Expert opinion</b>: In the era of extreme lowering of LDL-C levels with several agents, there seems to be space for novel therapeutic options to combat parameters responsible for residual CVD risk, among which are elevated TGs.
|
31738617 |
2020 |
|
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
We show that expression of a mouse apoC-III transgene can also cause hypertriglyceridemia with a similar accumulation of a VLDL-like particle with increased apoC-III and decreased apoE.
|
8864964 |
1996 |