Publications by authors named "Leonie C Van Vark-Van Der Zee"

Background: Proprotein convertase subtilisin kexin type 9 (PCSK9) monoclonal antibodies (mAbs) reduce fasting and post fat load cholesterol in non-HDL and intermediate density lipoprotein (IDL) in familial dysbetalipoproteinemia (FD). However, the effect of PCSK9 mAbs on the distribution and composition of atherogenic lipoproteins in patients with FD is unknown.

Objective: To evaluate the effect of the PCSK9 mAb evolocumab added to standard lipid-lowering therapy in patients with FD on fasting and post fat load lipoprotein distribution and composition.

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Article Synopsis
  • The study aimed to compare different methods for measuring LDL-C concentrations against a reference standard in patients with Familial Dysbetalipoproteinemia (FD).
  • It analyzed data from 28 FD patients using the Friedewald formula, Martin-Hopkins formula, direct assay, and PGGE, comparing results to density gradient ultracentrifugation.
  • The findings revealed that all four LDL-C measurement methods had significant inaccuracies compared to ultracentrifugation, while non-HDL-C measurements were more reliable, suggesting a preference for using non-HDL-C in FD patients.
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  • Familial dysbetalipoproteinemia (FD) is a lipid disorder affecting about 1 in 850-3500 people, linked to a higher risk of cardiovascular disease due to lipid imbalances, with many patients not reaching their cholesterol treatment goals.* -
  • A study assessed the effectiveness of adding the PCSK9 monoclonal antibody evolocumab to standard lipid-lowering therapy in FD patients, using a randomized, placebo-controlled, double-blind design over two 12-week periods.* -
  • Results showed that evolocumab significantly lowered levels of non-HDL cholesterol and apolipoprotein B, potentially reducing cardiovascular risk, although it did not prevent a rise in lipid levels after fat consumption.*
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  • Sodium-glucose cotransporter 2 inhibitors (SGLT2i), like dapagliflozin, may help improve cardiovascular outcomes in type 2 diabetes but their exact protective mechanisms are not fully understood.
  • * In a study involving 14 male patients with type 2 diabetes, dapagliflozin led to a significant reduction in the daily insulin dose but did not change fasting or postprandial glucose or insulin levels.
  • * Results indicated that dapagliflozin increased postprandial ketone bodies and decreased fasting chylomicron remnants, suggesting it may enhance fat oxidation without affecting lipid levels or inflammatory markers.*
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Background: The first 6 months of life are a critical window for adiposity programming. Appetite-regulating hormones (ARH) are involved in food intake regulation and might, therefore, play a role in adiposity programming. Studies examining ARH in early life are limited.

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Aim: Type 2 diabetes mellitus (T2DM) is associated with an increased risk of cardiovascular disease (CVD) linked to atherogenic dyslipidaemia and postprandial hyperlipidaemia. Alirocumab, a proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor, improves CVD risk by reducing the concentration of low-density lipoprotein-cholesterol (LDL-C). However, effects of PCK9 inhibitors on other aspects of diabetic dyslipidaemia, particularly in the postprandial situation, are less clear.

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Introduction: Body composition in early life influences development of obesity during childhood and beyond. Appetite-regulating hormones (ARH) play a role in regulation of food intake and might thus influence body composition in later life. Studies on associations between ARH and body composition in early life are limited.

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Red wine polyphenols may preserve endothelial function during aging. Endothelial cell senescence enhances age-related endothelial dysfunction. We investigated whether RWE (red wine extract) prevents oxidative-stress-induced senescence in HUVECs (human umbilical-vein endothelial cells).

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Plant sterols such as sitosterol and campesterol are frequently applied as functional food in the prevention of atherosclerosis. Recently, it became clear that plasma derived plant sterols accumulate in murine brains. We questioned whether plant sterols in the brain are associated with alterations in brain cholesterol homeostasis and subsequently with brain functions.

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Disturbances in cerebral cholesterol metabolism have been implicated in the pathogenesis of Alzheimer's disease (AD). Here, we provide evidence that alterations in brain cholesterol homeostasis also can be a consequence of disease progression. We found that APPSLxPS1mut mice, at the age of 9 months when AD-like pathology starts to develop, display increased levels of the cholesterol precursor desmosterol and of the cholesterol metabolite 27-hydroxy(OH)cholesterol in their cerebellum in comparison with wild-type controls.

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Alterations in cerebral cholesterol metabolism are thought to play a role in the progression of Alzheimer's disease (AD). Liver X receptors (LXRs) are key regulators of cholesterol metabolism. The synthetic LXR activator, T0901317 has been reported to improve memory functions in animal models for AD and to reduce amyloid-β (Aβ) deposition in the brain.

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Introduction: Fasting and postprandial hypertriglyceridemia are essential features of metabolic syndrome. Statins decrease fasting lipid levels but fail to reduce fat load induced hypertriglyceridemia. We established whether ezetimibe combined with simvastatin differently influences post fat load lipid levels and lipoprotein composition as compared to simvastatin 80mg monotherapy in obese male metabolic syndrome patients.

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Introduction: The postprandial lipid metabolism in metabolic syndrome patients is disturbed and may add to the increased cardiovascular risk in these patients. It is not known whether postprandial high density lipoprotein-cholesterol (HDL-c) metabolism is also affected and whether this can be influenced by statin and/or ezetimibe treatment.

Methods: Prospective, randomized, double blind, crossover trial comparing simvastatin 80 mg with simvastatin/ezetimibe 10 mg/10 mg treatment for 6 weeks on postprandial HDL-c metabolism in 15, nonsmoking, male, obese metabolic syndrome patients (Adult Treatment Panel III, ATPIII).

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