Chronic treatment with bark infusion fromCroton cajucaralowers plasma triglyceride levels in genetic hyperlipidemic mice

2004 ◽  
Vol 82 (6) ◽  
pp. 387-392 ◽  
Author(s):  
Eliete J.B Bighetti ◽  
Alba R.M Souza-Brito ◽  
Eliana C. de Faria ◽  
Helena C.F Oliveira
Keyword(s):  
Essential Oil ◽  
Transgenic Mice ◽  
Gene Knockout ◽  
Receptor Gene ◽  
Ldl Receptor ◽  
Plasma Lipid ◽  
Lipid Lowering ◽  
Biochemical Tests ◽  
Vldl Fraction ◽  
Croton Cajucara

Aqueous infusion and preparations containing dehydrocrotonin (DHC) and essential oil from Croton cajucara bark were tested for plasma lipid-lowering effects in genetically modified hyperlipidemic mice. Two mouse models were tested: 1) primary hypercholesterolemia resulting from the LDL-receptor gene knockout, and 2) combined hyperlipidemia resulting from crosses of LDL-receptor knockout mice with transgenic mice overexpressing apolipo protein (apo) CIII and cholesteryl ester-transfer protein. Mice treated with bark infusion, DHC, essential oil, or placebos for 25 days showed no signals of toxicity as judged by biochemical tests for liver and kidney functions. The bark infusion reduced triglyceride plasma levels by 40%, while essential oil and DHC had no significant effects on plasma lipid levels. The bark infusion treatment promoted a redistribution of cholesterol among the lipoprotein fractions in combined hyperlipidemic mice. There was a marked reduction in the VLDL fraction and an increase in the HDL fraction, in such a way that the (VLDL + LDL)/HDL ratio was reduced by half. The bark infusion treatment did not modify cholesterol distribution in hypercholesterolemic mice. In conclusion, C. cajucara bark infusion reduced plasma triglycerides levels and promoted a redistribution of cholesterol among lipoproteins in genetically combined hyperlipidemic mice. These changes modify risk factors for the development of atherosclerotic diseases.Key words: hyperlipidemia, transgenic mice, Croton cajucara, dehydrocrotonin, cholesterol.

scholarly journals Current Treatment of Familial Hypercholesterolaemia

2014 ◽  
Vol 9 (2) ◽  
pp. 76 ◽  
Author(s):  
Cameron T Lambert ◽  
Pratik Sandesara ◽  
Ijeoma Isiadinso ◽  
Maria Carolina Gongora ◽  
Danny Eapen ◽  
...  
Keyword(s):  
Familial Hypercholesterolaemia ◽  
Lifestyle Modification ◽  
Receptor Gene ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Lipid Lowering ◽  
Atherosclerotic Cardiovascular Disease ◽  
Lipid Lowering Therapy ◽  
Pcsk9 Inhibitors ◽  
Autosomal Dominant Disorder

Familial hypercholesterolaemia is an autosomal-dominant disorder associated with mutations in the LDL receptor gene resulting in markedly elevated plasma low-density lipoprotein cholesterol levels. FH is significantly underrecognised with as many as 1 in 300 having the heterozygous form and 1 in 1 million having the homozygous form of the disease. Early diagnosis and treatment of FH is paramount to reduce the risk of premature atherosclerotic cardiovascular disease and death. The goal of treatment is to reduce LDL-C by 50 % from baseline levels with lifestyle modification, pharmacologic lipid-lowering therapy, LDL apheresis and in rare cases, liver transplantation. Pharmacologic treatment ranges from statin medications to newer agents such as lomitapide, mipomersin and PCSK9 inhibitors. Combination therapy is frequently required to achieve goal lipoprotein level reductions and prevent complications.

scholarly journals Detection of the Low Density Lipoprotein Receptor Gene Pvuii Intron 15 Polymorphism Using the Polymerase Chain Reaction: Association With Plasma Lipid Traits in Healthy Men and Women

1998 ◽  
Vol 13 (4) ◽  
pp. 209-220 ◽  
Author(s):  
V. Gudnason ◽  
T. Zhou ◽  
K. Thormar ◽  
S. Baehring ◽  
J. Cooper ◽  
...  
Keyword(s):  
Receptor Gene ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Splice Acceptor Site ◽  
Low Density ◽  
Lipid Levels ◽  
Men And Women ◽  
The Impact

We have used anchored PCR to amplify and sequence 1400bp of the 15th intron of the Low Density Lipoprotein (LDL) receptor gene, and have determined oligonucleotides and conditions for the genotyping of the previously reported Pvull polymorphism. The cutting site (CAGCTG) is created by the transition of a CpG to a TpG within the sequence CAGCCG at a position roughly 600bp 5' from the splice acceptor site of exon 16. Genotype was determined in three populationbased samples of healthy individuals. In a group of 318 men and women from Iceland the frequencies of the Intron-15 T (cutting) allele was 0.23 (95% CI, 0.19-0.28) and was similar in men and women. In two groups of men from England (n=385) and Scotland (n=320), the frequency was similar, being 0.23 (0.19-0.27) and 0.25 (0.22-0.28) respectively. Individuals who were homozygous for the T allele had lower levels oftotal-cholesterol triglycerides and apolipoprotein B, than those with other genotypes, and in the combined group of UK men this effect reached statistical significance; compared to the CIC group, the TIT group had 6% lower cholesterol (p=0.02) and 15% lower triglycerides (p=0.03). The lowering effect associated with the TIT genotype was greater in men who were in the lowest terti Ie of body mass index (<25kg/m2) and for the trait of apoB levels, this genotype x obesity interaction was statistically significant (p=0.01). We thus confirm the association between this allele and lower levels of plasma lipid levels previously reported. The availability of a PCR-based method to detect this polymorphism will facilitate further investigation of the impact of LDL-receptor gene variation in determining lipid levels.

scholarly journals Tempol improves lipid profile and prevents left ventricular hypertrophy in LDL receptor gene knockout (LDLr-/-) mice on a high-fat diet

2017 ◽  
Vol 36 (9) ◽  
pp. 629-638 ◽  
Author(s):  
Igor Cândido Viana Gonçalves ◽  
Cláudio Daniel Cerdeira ◽  
Eduardo Poletti Camara ◽  
José Antônio Dias Garcia ◽  
Maísa Ribeiro Pereira Lima Brigagão ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Lipid Profile ◽  
High Fat Diet ◽  
Ventricular Hypertrophy ◽  
Gene Knockout ◽  
Receptor Gene ◽  
Ldl Receptor ◽  
Left Ventricular ◽  
High Fat

The A370T Variant (StuI Polymorphism) in the LDL Receptor Gene is not Associated with Plasma Lipid Levels or Cardiovascular Risk in UK Men

2006 ◽  
Vol 70 (6) ◽  
pp. 697-704 ◽  
Author(s):  
José Ricardo S. Vieira ◽  
Ros A. Whittall ◽  
Jackie A. Cooper ◽  
George J. Miller ◽  
Steve E. Humphries
Keyword(s):  
Cardiovascular Risk ◽  
Receptor Gene ◽  
Ldl Receptor ◽  
Plasma Lipid ◽  
Lipid Levels

scholarly journals Tempol improves lipid profile and prevents left ventricular hypertrophy in LDL receptor gene knockout (LDLr-/-) mice on a high-fat diet

2017 ◽  
Vol 36 (9) ◽  
pp. 629-638
Author(s):  
Igor Cândido Viana Gonçalves ◽  
Cláudio Daniel Cerdeira ◽  
Eduardo Poletti Camara ◽  
José Antônio Dias Garcia ◽  
Maísa Ribeiro Pereira Lima Brigagão ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Lipid Profile ◽  
High Fat Diet ◽  
Ventricular Hypertrophy ◽  
Gene Knockout ◽  
Receptor Gene ◽  
Ldl Receptor ◽  
Left Ventricular ◽  
High Fat

scholarly journals Japanese familial hypercholesterolaemia with a 327insC mutation in the LDL receptor gene

2002 ◽  
Vol 39 (5) ◽  
pp. 526-530 ◽  
Author(s):  
Ryoji Hirota ◽  
Nobuhiko Kubo ◽  
Kazumasa Hikiji ◽  
Kumiko Nakajima ◽  
Yoshiya Hata ◽  
...  
Keyword(s):  
Heart Disease ◽  
Ischaemic Heart Disease ◽  
Familial Hypercholesterolaemia ◽  
Receptor Gene ◽  
Ldl Receptor ◽  
Premature Termination Codon ◽  
Lipid Lowering ◽  
Ldlr Gene ◽  
Plasma Total Cholesterol ◽  
Low Incidence

Mutations in the LDL receptor (LDLR) cause familial hypercholesterolaemia (FH) in an autosomal dominant manner. The condition frequently progresses to coronary atherosclerosis. We describe a patient with FH, but without ischaemic heart disease, who had a novel frameshift mutation (327insC) in exon 4 of the LDLR gene. This mutation introduced a premature termination codon (TGA, codon 158). The patient was a 59-year-old man who had presented with hypercholesterolaemia and a plasma total cholesterol (TC) concentration of 12·2 mmol/L at age 44 years. The mutation 327insC in this patient was heterozygous and hypercholesterolaemia was common within his family. Despite taking lipid-lowering medications (probucol and pravastatin) for more than 20 years, his TC concentration hardly fell below 7·8 mmol/L. However, neither the patient nor anyone else in his family developed characteristic symptoms of ischaemic heart disease or xanthoma. This patient was discovered by an intensive mutation survey among 22 unrelated Japanese with FH mainly in the Kanto area of Japan, suggesting a low incidence of the mutation in the area.

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