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High density lipoprotein catabolism before and after partial hepatectomy.
Atherosclerosis
|April 1, 1978
Summary
Partial hepatectomy in rats did not alter high density lipoprotein (HDL)-apoprotein degradation rates. Reduced serum HDL levels after liver removal are likely due to impaired hepatic synthesis, not increased catabolism.
Area of Science:
- Biochemistry
- Physiology
- Hepatic Metabolism
Background:
- High density lipoprotein (HDL) plays a crucial role in reverse cholesterol transport.
- Understanding HDL metabolism is vital for cardiovascular health.
- The impact of liver resection on HDL catabolism requires further investigation.
Purpose of the Study:
- To investigate the effect of partial hepatectomy on the serum decay and tissue distribution of HDL-apoproteins in rats.
- To determine if liver mass reduction influences HDL-apoprotein fractional catabolic rate (FCR).
- To elucidate the mechanisms behind decreased serum HDL levels post-hepatectomy.
Main Methods:
- Development of a continuous blood sampling method in rats without anticoagulants or anesthetics.
- Iodine-labeling of HDL-apoproteins for tracking serum decay and tissue distribution.
- Measurement of HDL-apoprotein serum decay kinetics and tissue uptake 2-8 hours after partial hepatectomy or sham-operation.
Main Results:
- HDL-apoprotein serum decay exhibited a biexponential pattern, unaffected by partial hepatectomy.
- Fractional catabolic rate (FCR) of HDL-apoproteins remained unchanged post-liver resection.
- Serum HDL levels decreased significantly after partial hepatectomy, while HDL chemical composition remained constant.
- Liver showed a significant decrease in HDL radioactivity uptake post-hepatectomy, while other tissues were largely unaffected.
Conclusions:
- In vivo degradation rate of HDL-apoproteins is not influenced by the removal of two-thirds of the liver.
- Reduced serum HDL concentration following partial hepatectomy is attributed to impaired hepatic synthesis.
- Results suggest potential for extrahepatic HDL-apoprotein catabolism or stimulated degradation in remaining liver lobes.