Reverse Cholesterol Transport
Mostrando 13-24 de 53 artigos, teses e dissertações.
-
13. Hepatobiliary cholesterol transport is not impaired in Abca1-null mice lacking HDL
The ABC transporter ABCA1 regulates HDL levels and is considered to control the first step of reverse cholesterol transport from the periphery to the liver. To test this concept, we studied the effect of ABCA1 deficiency on hepatic metabolism and hepatobiliary flux of cholesterol in mice. Hepatic lipid contents and biliary secretion rates were determined in
American Society for Clinical Investigation.
-
14. A selective peroxisome proliferator-activated receptor δ agonist promotes reverse cholesterol transport
The peroxisome proliferator-activated receptors (PPARs) are dietary lipid sensors that regulate fatty acid and carbohydrate metabolism. The hypolipidemic effects of the fibrate drugs and the antidiabetic effects of the glitazone drugs in humans are due to activation of the α (NR1C1) and γ (NR1C3) subtypes, respectively. By contrast, the therapeutic po
The National Academy of Sciences.
-
15. Is it time to modify the reverse cholesterol transport model?
American Society for Clinical Investigation.
-
16. Tangier disease as a test of the reverse cholesterol transport hypothesis
American Society for Clinical Investigation.
-
17. Selective thyroid receptor modulation by GC-1 reduces serum lipids and stimulates steps of reverse cholesterol transport in euthyroid mice
Thyroid hormones [predominantly 3,5,3′-triiodo-l-thyronine (T3)] regulate cholesterol and lipoprotein metabolism, but cardiac effects restrict their use as hypolipidemic drugs. T3 binds to thyroid hormone receptors (TRs) α and β. TRβ is the predominant isoform in liver, whereas T3 effects on heart rate are mediated mostly by TRα. Drugs that target TRβ
National Academy of Sciences.
-
18. Activation of the Liver X Receptor Stimulates Trans-intestinal Excretion of Plasma Cholesterol*
Recent studies have indicated that direct intestinal secretion of plasma cholesterol significantly contributes to fecal neutral sterol loss in mice. The physiological relevance of this novel route, which represents a part of the reverse cholesterol transport pathway, has not been directly established in vivo as yet. We have developed a method to quantify the
American Society for Biochemistry and Molecular Biology.
-
19. Effects of postprandial lipemia on plasma cholesterol metabolism.
Cholesterol net transport, esterification, and cholesteryl ester transfer have been determined in plasma during fasting, and postprandially, after a high fat-cholesterol meal. Significant rises in plasma triglyceride, phospholipid, and free cholesterol were associated with increases in cholesterol net transport, esterification, and transfer (all P less than
-
20. Do DNA sequence variants in ABCA1 contribute to HDL cholesterol levels in the general population?
HDL has a key role in reverse cholesterol transport, mobilizing cholesterol from the peripheral tissues to liver. In this process, the ABC transporter A1 (ABCA1) protein controls the efflux of intracellular cholesterol to apoAI, the major apolipoprotein of HDL. Since ABCA1 mutations were discovered to cause Tangier disease, a rare recessive HDL deficiency, i
American Society for Clinical Investigation.
-
21. Annexin 2–caveolin 1 complex is a target of ezetimibe and regulates intestinal cholesterol transport
Modulation of cholesterol absorption in the intestine, the primary site of dietary cholesterol uptake in humans, can have profound clinical implications. We have undertaken a reverse genetic approach by disrupting putative cholesterol processing genes in zebrafish larvae by using morpholino (MO) antisense oligonucleotides. By using targeted MO injections and
National Academy of Sciences.
-
22. ABCG1 (ABC8), the human homolog of the Drosophila white gene, is a regulator of macrophage cholesterol and phospholipid transport
Excessive uptake of atherogenic lipoproteins such as modified low-density lipoprotein complexes by vascular macrophages leads to foam cell formation, a critical step in atherogenesis. Cholesterol efflux mediated by high-density lipoproteins (HDL) constitutes a protective mechanism against macrophage lipid overloading. The molecular mechanisms underlying this
The National Academy of Sciences.
-
23. Cyclodextrins as catalysts for the removal of cholesterol from macrophage foam cells.
Low concentrations of cyclodextrins (< 1.0 mM) added to serum act catalytically, accelerating the exchange of cholesterol between cells and lipoproteins. J774 macrophages incubated with serum and 2-hydroxypropyl-beta-cyclodextrin (< or = 1 mM) released fivefold more labeled cholesterol than with serum alone. Increased efflux was not accompanied by a change i
-
24. Increased coronary heart disease in Japanese-American men with mutation in the cholesteryl ester transfer protein gene despite increased HDL levels.
Plasma high density lipoprotein (HDL) levels are strongly genetically determined and show a general inverse relationship with coronary heart disease (CHD). The cholesteryl ester transfer protein (CETP) mediates the transfer of cholesteryl esters from HDL to other lipoproteins and is a key participant in the reverse transport of cholesterol from the periphery