Familial combined hyperlipidemia or FCHL is one of the most common genetic causes of hyperlipidemia and is associated with elevation of cholesterol, triglycerides or both, and increased serum apolipoprotein B (apoB).
Fasting Apolipoprotein B48 (ApoB48) is reported to be a well surrogate marker for postprandial lipidemia and have been repeatedly associated with cardiovascular disease.
Liraglutide Reduces Postprandial Hyperlipidemia by Increasing ApoB48 (Apolipoprotein B48) Catabolism and by Reducing ApoB48 Production in Patients With Type 2 Diabetes Mellitus.
The multivariate analysis showed that age (OR = 2.62, 95%CI: 1.51-4.56, P = 0.001), hyperlipidemia (OR = 1.89, 95%CI: 1.07-3.36, P = 0.029), high-density lipoprotein cholesterol (HDL-C) (OR = 0.46, 95%CI: 0.24-0.87, P = 0.02), the ratio of total cholesterol to high-density lipoproteincholesterol (TC/HDL-C) (OR = 0.69, 95%CI: 0.50-0.94, P = 0.02), apolipoprotein B (apoB) (OR = 3.08, 95%CI: 1.50-6.32, P = 0.002), and adiponectin (OR = 0.37, 95%CI: 0.19-0.74, P = 0.005) were independently associated with the presence of high risk plaques.
Apolipoprotein B (ApoB), as the only essential scaffolding protein in the assembly of very-low-density lipoproteins, is a target to treat hyperlipidemia and atherosclerosis.
Diagnosis of dysbetalipoproteinaemia should be considered in mixed hyperlipidaemias for which the apolipoprotein B concentration is relatively low in relation to the total cholesterol concentration or when there is significant disparity between the calculated LDL and directly measured LDL cholesterol concentrations.
Microsomal triglyceride transfer protein (MTP) plays a key role in the lipidation of nascent apoB and the secretion of apoB-containing lipoproteins enriched with triglycerides and is thus a promising target for the treatment of hyperlipidemia.
Mipomersen displayed dose-dependent efficacy in lowering LDL-C, ApoB, triglycerides, total cholesterol and other low-density lipoproteins in healthy volunteers with mild hyperlipidemia.
Combined hyperlipidemia results from overproduction of hepatically synthesized apolipoprotein B in very low-density lipoproteins in association with reduced lipoprotein lipase activity.
In FCHL relatives (n = 618) and spouses (n = 297), prevalence data of hyperlipidemia and high apolipoprotein B levels and their age and gender-corrected odds ratios (ORs) were calculated for sex-adjusted categories of waist-to-hip ratio (WHR), waist circumference, and BMI.
Hammerhead ribozyme as a therapeutic agent for hyperlipidemia: production of truncated apolipoprotein B and hypolipidemic effects in a dyslipidemia murine model.
The only significant differences found among the groups, regardless of the presence of hyperlipemia, were the increased levels of total and high-density lipoprotein phospholipids, and lower levels of apolipoprotein B, found in the group with xanthelasmas.