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High density lipoproteins (HDL) are produced in the liver and intestine, with distinct apoprotein synthesis. Cholesterol feeding impacts HDL composition and introduces a new lipoprotein class.
Area of Science:
- Lipid metabolism
- Atherosclerosis research
- Biochemistry
Background:
- High density lipoproteins (HDL) play a crucial role in reverse cholesterol transport.
- HDL apoproteins are synthesized in the liver and intestine, with some exceptions.
Purpose of the Study:
- To investigate the synthesis and catabolism of HDL apoproteins.
- To examine the effects of cholesterol feeding on HDL metabolism and composition.
Main Methods:
- Radioiodination of HDL (125I-HDL) to trace its fate in circulation.
- Analysis of lipoprotein fractions and apoprotein composition following cholesterol administration.
Main Results:
- All HDL apoproteins, except C apoproteins, are synthesized in both liver and intestine.
- HDL apoproteins are removed from circulation at similar rates.
- Cholesterol feeding alters lipoprotein distribution, creating a new intermediate density class containing all HDL apoproteins and apo-B, and modifies HDL apoprotein composition.
Conclusions:
- The liver is the primary site for HDL catabolism and protein moiety degradation within lysosomes.
- Dietary cholesterol significantly impacts HDL metabolism, affecting its composition and introducing novel lipoprotein particles.
Abstract:
High density lipoproteins are synthesized both in the liver and intestine. All apoproteins can be synthesized in the liver and intestine except the "C" apoproteins which could not be synthesized by the intestine. After injection of 125I-HDL its different apoproteins are removed from the circulation at a similar rate. Most of the HDL is removed by the liver and the degradation of the protein moiety of HDL was localized to the lysozomes of the parenchymal cells. Cholesterol feeding alters the distribution of lipoprotein fractions and results in the appearance of a new intermediate density class, in which all HDL apoproteins are present in addition to apo-B. Cholesterol feeding also results in an alteration of apoprotein composition of HDL.