Role of the low density lipoprotein receptor in the flux of cholesterol through the plasma and across the tissues of the mouse

Osono, Y; Woollett, L A; Herz, J; Dietschy, J M

doi:10.1172/jci117760

Cited by 169

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Role of the low density lipoprotein receptor in the flux of cholesterol through the plasma and across the tissues of the mouse

Osono, Y, Woollett, L A, Herz, J, Dietschy, J M·1995·Journal of Clinical Investigation

DOI 10.1172/jci117760

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Approximately 75% of circulating LDL particles are cleared by LDLR through receptor-mediated endocytosis.
“Approximately 75% of circulating LDL particles are cleared by LDLR through receptor-mediated endocytosis22,23.”
From ABCC4 impairs the clearance of plasma LDL cholesterol through suppressing LDLR expression in the liver (2025) · cites this paper as [22]
The paper’s opening summary reports that LDLR accounted for 88% of LDL-cholesterol turnover in normal mice, supporting a substantial role for LDLR in clearance. It does not support the stated figure of approximately 75%, an unqualified claim about circulating LDL particles, or the specified endocytosis mechanism. Section and page are not available in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measured
Low expression of LDLR in hepatocytes leads to hypercholesterolemia and contributes to atherosclerotic cardiovascular disease.
“Low expression level of low-density lipoprotein receptor (LDLR) in hepatocytes leads to hypercholesterolemia and eventually contributes to atherosclerotic cardiovascular disease (ASCVD).”
From ABCC4 impairs the clearance of plasma LDL cholesterol through suppressing LDLR expression in the liver (2025) · cites this paper as [22]
The paper’s Abstract (p. 1124) reports that most LDL-receptor-dependent transport occurs in the liver and that deleting LDLR in mice raises plasma LDL cholesterol 14-fold. It does not specifically test low LDLR expression in hepatocytes or establish the claimed progression to atherosclerotic cardiovascular disease. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Excessive cholesterol in the circulation, upon uptake by the liver via LDLR-mediated endocytosis, suppresses endogenous synthesis of cholesterol in the liver.
“Excessive cholesterol in the circulation, upon uptake by the liver via LDL receptor (LDLR)-mediated endocytosis, suppresses endogenous synthesis of cholesterol in the liver”
From Endocytic adaptors Arh and Dab2 control homeostasis of circulatory cholesterol (2016) · cites this paper as [8]
The study summary (section and page unavailable in our copy) reports that most LDL cholesterol returns to the liver and that the LDL receptor accounts for most receptor-dependent transport. It does not report that this uptake suppresses cholesterol synthesis in the liver; it reports no change in whole-animal synthesis after LDLR deletion, which does not settle the liver-specific effect. (LLM, conf=0.84)
Experimental — accuracy not yet measured
LDL clearance from the circulation by LDLR-mediated endocytosis by hepatic and peripheral tissues and subsequent feedback regulation of endogenous synthesis of cholesterol is a key determinant of serum LDL level.
“LDL clearance from the circulation by LDL receptor (LDLR)-mediated endocytosis by hepatic and peripheral tissues and subsequent feedback regulation of endogenous synthesis of cholesterol is a key determinant of serum LDL level”
From Endocytic adaptors Arh and Dab2 control homeostasis of circulatory cholesterol (2016) · cites this paper as [8]
The study summary (page not specified in our copy) reports that LDLR accounted for most LDL-cholesterol turnover in mice and that deleting it sharply raised plasma LDL-cholesterol. But most receptor-dependent transport occurred in the liver, and cholesterol synthesis did not change in extrahepatic organs or the whole animal. The claim's emphasis on peripheral clearance and subsequent feedback regulation of synthesis is therefore not supported by these findings. (LLM, conf=0.88)
Experimental — accuracy not yet measured
The balance of serum cholesterol level is determined by dietary intake, synthesis, and catabolism.
“The balance of serum cholesterol level is determined by dietary intake, synthesis, and catabolism”
From Endocytic adaptors Arh and Dab2 control homeostasis of circulatory cholesterol (2016) · cites this paper as [8]
The paper’s opening passage (page not available in our copy) examines cholesterol synthesis and LDL-cholesterol degradation in mice, and reports that altered LDL turnover changed plasma LDL-cholesterol levels. It does not establish dietary intake as a determinant or support the broader three-part account of serum cholesterol balance. (LLM, conf=0.82)
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Characterization of the sinusoidal transport process responsible for uptake of chylomicrons by the liver.
Sherrill, B. C., & Dietschy, J. M. (1978) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(19)62331-8 · Cited by 197
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Authors: Osono, Y., Woollett, L. A., Herz, J., & Dietschy, J. M.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 1995-03-01
Volume: 95
Issue: 3
Pages: 1124-1132
ISSN: 0021-9738
DOI: 10.1172/jci117760
Cited by: 169
References: 1
Language: en

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Role of the low density lipoprotein receptor in the flux of cholesterol through the plasma and across the tissues of the mouse

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