We evaluated time course relationships between statin-mediated reduction in atherogenic apolipoprotein B (ApoB)-containing particles and dynamic intravascular remodeling of ApoAI-containing lipoprotein subpopulations in the mixed dyslipidemia of metabolic syndrome.
We evaluated if whey proteins (WP) consumed as a pre-meal before a fat-rich meal reduce postprandial triglyceride (TG) and apolipoprotein B-48 (ApoB-48) responses in subjects with the metabolic syndrome (MeS).
Serum apolipoprotein B is associated with increased risk of metabolic syndrome among middle-aged and elderly Chinese: A cross-sectional and prospective cohort study.
CEC was determined from THP-1 macrophage foam cells towards apolipoprotein B-depleted plasma among 639 subjects (454 men; 36 subjects with type 2 diabetes mellitus (T2D); 226 with MetS), participating in the Prevention of Renal and Vascular End-Stage Disease (PREVEND) study.
Across study pools, alirocumab-associated reductions in LDL-C, apolipoprotein B, and non-HDL-C were significant vs control, and did not vary by MetS status.
We used linear regression to compare MetS z-score and dietary factors with serum levels of low-density lipoprotein (LDL), apolipoprotein-B (ApoB), high-sensitivity C-reactive protein (hsCRP) and uric acid.
We investigated the association between the apolipoprotein B (ApoB)/apolipoprotein A1 (ApoA1) ratio and insulin resistance (IR), metabolic syndrome (MS) and its components in Chinese polycystic ovary syndrome (PCOS) adults.
Participants with or without the MetS exhibited contrasting responses to the modified breakfast: respectively, significant changes in DBP levels (-3.7 ± 6.9 versus -0.5 ± 6.9 mm Hg; P < 0.05), plasma glucose (-3 ± 7.3 versus 3 ± 7.4 mg/dL; P < 0.05), and apolipoprotein-B (-0.1 ± 0.6 versus 0.2 ± 0.3 mg/mL; P < 0.05), interferon-γ (-0.6 ± 1.2 versus 0.1 ± 1.3 pg/mL; P < 0.05), and tumor necrosis factor-α concentrations (0.4 ± 3.6 versus -0.8 ± 2.8 pg/mL; P < 0.05) were observed.
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.
In the present study, the case of an 18‑year‑old male who presented with MS characteristics with central obesity (overweight and a waist circumference of 95 cm) and dyslipidemia (high TG, low HDL levels and low apoA‑I/apoB‑100) was reported.
Genome-wide screen for metabolic syndrome susceptibility Loci reveals strong lipid gene contribution but no evidence for common genetic basis for clustering of metabolic syndrome traits.
Genome-wide screen for metabolic syndrome susceptibility Loci reveals strong lipid gene contribution but no evidence for common genetic basis for clustering of metabolic syndrome traits.
Furthermore, our transcript analyses of adipose RNA samples from 175 subjects in the Finnish Metabolic Syndrome in Men study indicate that rs7575840 alters expression of APOB (P=1.13×10(-10)) and a regional noncoding RNA (BU630349) (P=7.86×10(-6)) in adipose tissue.
Our results revealed that the Apo-B value may be considered as a predictive factor of lipidemic, atherogenic alterations, and it merits in this sense to be included in the diagnostic criteria of MS.
We assessed lipid levels and the frequencies of the cholesteryl ester transfer protein (CETP) Taq-1 B, lipoprotein lipase (LPL)S447X, -93 T/G, apolipoprotein B (APO B) 96bp ins/del, lipoprotein(a) (LP[a]) pentanucleotide repeat, and apolipoprotein E (APO) E epsilon 2/3/4 polymorphisms in relation to the metabolic syndrome using both National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) and International Diabetes Federation (IDF) definitions.
We sought to determine the effect of a potent and highly specific PPAR-alpha agonist, LY518674, on apoA-I, apoA-II, and apoB-100 kinetics in humans with metabolic syndrome and low levels of HDL cholesterol (C).
The present study has shown that the S1 allele of APOC3 SstI polymorphism and the H- allele of LPL HindIII polymorphism might have a small effect on apoB levels in the Central European Caucasian population with dyslipidemia of metabolic syndrome.
There were highly significant correlations with variables associated with the metabolic syndrome: plasma triglyceride, HDL- and LDL-cholesterol, apolipoprotein B and E, urate, and insulin concentrations; gamma-glutamyltransferase and aspartate and alanine aminotransferase activities; body mass index; and blood pressure.
Among the metabolic components of IRS, only triglyceride (TG) displayed an interaction with FABP2 polymorphism: compared with Thr/Ala and Ala/Ala, the Thr/Thr genotype was associated with a steeper increase in TC, LDL-C, and apoB parallel to TG concentrations (P <0.001).
The apoB-100 gene EcoRI polymorphism influences the relationship between features of the insulin resistance syndrome and the hyper-apoB and dense LDL phenotype in men.