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Updated: Feb 24, 2026

A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes
Published on: September 15, 2018
Glucose-dependent leucocyte activation in familial hypercholesterolemia
Natasja Koks1, Marijke A de Vries1, Erwin Birnie1,2,3
1Department of Internal Medicine, Center for Endocrinology, Diabetes and Vascular Medicine, Franciscus Gasthuis & Vlietland, Rotterdam, the Netherlands.
Familial hypercholesterolemia (FH) patients show higher post-oral glucose tolerance test (OGTT) glucose levels and monocyte activation compared to healthy individuals. This postprandial hyperglycemia may contribute to cardiovascular disease development in FH patients.
Area of Science:
- Cardiovascular Research
- Metabolic Disorders
- Immunology
Background:
- Leukocyte activation is crucial in atherosclerosis development.
- Postprandial states are linked to increased leukocyte activation in various disorders.
- Familial hypercholesterolemia (FH) is a genetic condition predisposing to cardiovascular disease.
Purpose of the Study:
- To investigate the effect of post-oral glucose tolerance test (OGTT) hyperglycemia on leukocyte activation in FH patients.
- To compare leukocyte activation markers between FH patients and healthy controls after an OGTT.
Main Methods:
- Heterozygous FH patients and healthy volunteers underwent an OGTT.
- Leukocyte activation markers (CD11b, CD66b) were measured using flow cytometry.
- Post-OGTT glucose excursions and leukocyte activation were analyzed using AUC and dAUC, with repeated measures analysis for time-dependent profiles.
Main Results:
- FH patients exhibited significantly higher post-OGTT glucose levels than healthy controls, irrespective of statin use.
- FH patients on statins had slightly higher HbA1c levels.
- Post-OGTT hyperglycemia was observed in FH patients.
Conclusions:
- FH patients demonstrate impaired post-OGTT glucose regulation compared to healthy individuals.
- Persistent post-OGTT monocyte activation in FH patients may be linked to hyperglycemia.
- This persistent activation could be a contributing factor to cardiovascular disease progression in FH.
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