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[Reduced cell sensitivity to glucocorticoid hormones in hypercholesterolemia]
Biokhimiia (Moscow, Russia)
|November 1, 1989
Summary
Subjects with hypercholesterolemia exhibit decreased glucocorticoid receptor sensitivity in lymphocytes and fibroblasts. This reduced sensitivity, linked to lipoproteins, may explain how high cholesterol contributes to atherosclerosis and heart disease.
Area of Science:
- Endocrinology
- Cell Biology
- Lipid Metabolism
Context:
- Hypercholesterolemia (HCS) is associated with cardiovascular disease.
- Glucocorticoid hormones play crucial roles in cellular function and immune response.
- Understanding cellular sensitivity to hormones in HCS is vital for disease mechanism elucidation.
Purpose:
- To investigate the effect of hypercholesterolemia on glucocorticoid receptor binding and sensitivity in human cells.
- To identify specific blood components in HCS that may alter glucocorticoid receptor function.
- To explore the potential link between altered glucocorticoid sensitivity and the pathogenesis of atherosclerosis.
Summary:
- Lymphocytes from hypercholesterolemia subjects showed reduced 3H-dexamethasone binding sites and diminished response to dexamethasone.
- Human skin fibroblasts exposed to hypercholesterolemia sera exhibited decreased glucocorticoid receptor availability and affinity.
- Very low-density lipoproteins (VLDL) and low-density lipoproteins (LDL) from HCS sera significantly inhibited 3H-dexamethasone binding, suggesting a role in reduced hormone sensitivity.
Impact:
- Findings suggest a cellular mechanism for hypercholesterolemia, involving impaired glucocorticoid signaling.
- This reduced sensitivity may contribute to the development of atherosclerosis and coronary heart disease.
- Identifies lipoproteins as key modulators of glucocorticoid receptor function in hypercholesterolemia.