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Glucocorticoids upregulate high-affinity, high-density lipoprotein binding sites in rat hepatocytes
A V Bocharov1, W Huang, T G Vishniakova
1Cardiology Research Center, Moscow, Russia.
Metabolism: Clinical and Experimental
|June 1, 1995
Summary
Glucocorticoid hormones (GL) regulate high-density lipoprotein (HDL) uptake by liver cells. Dexamethasone (DEX) treatment increases HDL binding sites on hepatocytes, suggesting a role for GL in HDL processing.
Area of Science:
- Biochemistry
- Endocrinology
- Hepatology
Background:
- Glucocorticoid hormones (GL) influence high-density lipoprotein (HDL) plasma levels by affecting liver synthesis and secretion.
- The impact of GL on HDL uptake and processing by hepatocytes (HEP) remains largely uncharacterized.
Purpose of the Study:
- To investigate the effect of dexamethasone (DEX), a synthetic glucocorticoid, on the expression of HDL-binding sites in cultured rat hepatocytes.
- To determine the role of DEX in the specific binding and internalization of HDL3 by hepatocytes.
Main Methods:
- Cultured rat hepatocytes were treated with varying concentrations of DEX.
- Specific binding and internalization of iodine-labeled apolipoprotein E-free HDL3 were measured.
- Hepatocytes were isolated from adrenalectomized rats to study glucocorticoid deficiency in vivo.
Main Results:
- Hepatocytes cultured without DEX showed a 60% decrease in HDL3 binding and internalization.
- DEX treatment (10^-7 and 10^-5 mol/L) prevented this decrease, maintaining HDL3 binding and internalization.
- DEX demonstrated a dose-dependent effect on HDL binding capacity, with saturation at 10^-7 mol/L.
Conclusions:
- Glucocorticoids, such as DEX, upregulate high-affinity HDL-binding sites on hepatocytes.
- These findings suggest that glucocorticoids play a significant role in regulating the liver's uptake and processing of HDL.
- Glucocorticoid deficiency impairs HDL uptake by hepatocytes.