Mouse ApoB100(Apoliprotein B100) ELISA Kit

Objective Ataxia-telangiectasia (A-T) is an autosomal recessive neurodegenerative disease caused by mutations in the ataxia-telangiectasia mutated (ATM) gene. The parents do not manifest the disease but are heterozygous carriers of a pathogenicATMmutation that may be associated with coronary atherosclerosis and increased cholesterol levels. The objective of this study was to verify whether there is an agreement between the biomarkers of the lipid profile and the carotid intima-media thickness (IMT) of mothers and their children with A-T. Methods This cross-sectional study included A-T patients (n = 11), their mothers (n = 9), and controls (n = 20). Anthropometric data, lipid profile markers, and apolipoproteins (Apo) A-1 and B were collected and carotid IMT was performed. Results Dyslipidemia was found in 7/11 of patients with A-T and 6/9 of mothers with a strong level of agreement (p(o) = 1.00; Kappa = 1.00;p = 0.001). Regarding the variables of the lipid profile, only NHDL-c (ICC = 0.64;p = 0.01) and the ApoB/ApoA-1 ratios (p(o) = 0.72;Kappa = 0.14;p = 0.62) and TG/HDL-c (ICC = 0.54;p = 0.04) showed agreement between mothers and children. A significant difference (p < 0.001) of the carotid IMT was found in A-T patients when compared to their mothers. Conclusion The agreement for lipid metabolism biomarkers associated with cardiovascular risk between children with A-T and their mothers emphasizes the importance of continuous monitoring of both.

Atherogenic LDL particles are physicochemically and metabolically heterogeneous. Can bioactive lipid cargo differentiate LDL subclasses, and thus potential atherogenicity? What is the effect of statin treatment? Obese hypertriglyceridemic hypercholesterolemic males [n = 12; lipoprotein (a) <10 mg/dl] received pitavastatin calcium (4 mg/day) for 180 days in a single-phase unblinded study. The lipidomic profiles (23 lipid classes) of five LDL subclasses fractionated from baseline and post-statin plasmas were determined by LC-MS. At baseline and on statin treatment, very small dense LDL (LDL5) was preferentially enriched (up to 3-fold) in specific lysophospholipids {LPC, lysophosphatidylinositol (LPI), lysoalkylphosphatidylcholine [LPC(O)]; 9, 0.2, and 0.14 mol per mole of apoB, respectively; all P < 0.001 vs. LDL1-4}, suggesting elevated inflammatory potential per particle. In contrast, lysophosphatidylethanolamine was uniformly distributed among LDL subclasses. Statin treatment markedly reduced absolute plasma concentrations of all LDL subclasses (up to 33.5%), including LPC, LPI, and LPC(O) contents (up to -52%), consistent with reduction in cardiovascular risk. Despite such reductions, lipotoxic ceramide load per particle in LDL1-5 (1.5-3 mol per mole of apoB; 3-7 mmol per mole of PC) was either conserved or elevated. Bioactive lipids may constitute biomarkers for the cardiometabolic risk associated with specific LDL subclasses in atherogenic dyslipidemia at baseline, and with residual risk on statin therapy.