Changes in the density distribution of pig high density lipoproteins during incubation in vitro

Ha, Y.C.; Gorjatschko, Ludmila; Barter, Philip J.

doi:10.1016/0021-9150(83)90043-6

Cited by 16 publications

(8 citation statements)

References 30 publications

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“…Potentially confounding factors such as fatty acid pool sizes and respiratory quotients have been considered and do not invalidate interpretations. Unlike rodents, HDL3 and cholesteryl ester transfer protein (CETP) are present in human plasma [24]. In man, the emulsion cholesteryl [ 13 C]oleate may be transferred to other lipoprotein fractions and breath test studies involving individuals with high and low CETP activity need to be performed to address this possibility.…”

Section: Human Obesitymentioning

confidence: 98%

Obesity and post-prandial lipid metabolism. Feast or famine?

Martins

Redgrave

2004

The Journal of Nutritional Biochemistry

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Section: Human Obesitymentioning

confidence: 98%

Obesity and post-prandial lipid metabolism. Feast or famine?

Martins

Redgrave

2004

The Journal of Nutritional Biochemistry

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“…These particles are assumed to be produced by CETP-mediated heterotypic transfer of lipids, but are also produced following transfers among HDL subclasses (homotypic transfer) (19). These small lipid-poor particles are involved in cellular cholesterol efflux (20) via ABCA1 that transports cholesterol and phospholipids to apoA-I (21, 22).…”

mentioning

confidence: 99%

Dalcetrapib and anacetrapib differently impact HDL structure and function in rabbits and monkeys

Brodeur

Rhainds

Charpentier

et al. 2017

Journal of Lipid Research

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Inhibition of cholesteryl ester transfer protein (CETP) increases HDL cholesterol (HDL-C) levels. However, the circulating CETP level varies and the impact of its inhibition in species with high CETP levels on HDL structure and function remains poorly characterized. This study investigated the effects of dalcetrapib and anacetrapib, the two CETP inhibitors (CETPis) currently being tested in large clinical outcome trials, on HDL particle subclass distribution and cholesterol efflux capacity of serum in rabbits and monkeys. New Zealand White rabbits and vervet monkeys received dalcetrapib and anacetrapib. In rabbits, CETPis increased HDL-C, raised small and large α-migrating HDL, and increased ABCA1-induced cholesterol efflux. In vervet monkeys, although anacetrapib produced similar results, dalcetrapib caused opposite effects because the LDL-C level was increased by 42% and HDL-C decreased by 48% (P < 0.01). The levels of α- and preβ-HDL were reduced by 16% (P < 0.001) and 69% (P < 0.01), resulting in a decrease of the serum cholesterol efflux capacity. CETPis modulate the plasma levels of mature and small HDL in vivo and consequently the cholesterol efflux capacity. The opposite effects of dalcetrapib in different species indicate that its impact on HDL metabolism could vary greatly according to the metabolic environment.

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“…Synthetic CETP inhibitors were optimized for the inhibition of neutral lipid transfer between HDL and apolipoprotein B (apoB)-containing lipoproteins (heterotypic transfer), but their effect on transfer of cholesteryl ester (CE) among HDL subparticles (homotypic transfer) and CETP-dependent HDL remodeling have not been studied. CETP facilitates the extensive remodeling of plasma HDL particles by promoting the interconversion of apoA-I-containing α-HDL to small, lipid-poor, pre-β-HDL (17, 18) and transfering CE among HDL subparticles (19, 20). This dynamic remodeling of HDL is a key aspect of its function in reverse cholesterol transport (RCT), leading to the removal of excess cholesterol from tissue and its delivery to the liver (21).…”

mentioning

confidence: 99%

Modulating cholesteryl ester transfer protein activity maintains efficient pre-β-HDL formation and increases reverse cholesterol transport

Niesor

Magg

Ogawa

et al. 2010

Journal of Lipid Research

151

119

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The mechanism by which cholesteryl ester transfer protein (CETP) activity affects HDL metabolism was investigated using agents that selectively target CETP (dalcetrapib, torcetrapib, anacetrapib). In contrast with torcetrapib and anacetrapib, dalcetrapib requires cysteine 13 to decrease CETP activity, measured as transfer of cholesteryl ester (CE) from HDL to LDL, and does not affect transfer of CE from HDL3 to HDL2. Only dalcetrapib induced a conformational change in CETP, when added to human plasma in vitro, also observed in vivo and correlated with CETP activity. CETP-induced pre-β-HDL formation in vitro in human plasma was unchanged by dalcetrapib ≤3 µM and increased at 10 µM. A dose-dependent inhibition of pre-β-HDL formation by torcetrapib and anacetrapib (0.1 to 10 µM) suggested that dalcetrapib modulates CETP activity. In hamsters injected with [3H]cholesterol-labeled autologous macrophages, and given dalcetrapib (100 mg twice daily), torcetrapib [30 mg once daily (QD)], or anacetrapib (30 mg QD), only dalcetrapib significantly increased fecal elimination of both [3H]neutral sterols and [3H]bile acids, whereas all compounds increased plasma HDL-[3H]cholesterol. These data suggest that modulation of CETP activity by dalcetrapib does not inhibit CETP-induced pre-β-HDL formation, which may be required to increase reverse cholesterol transport.

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Changes in the density distribution of pig high density lipoproteins during incubation in vitro

Cited by 16 publications

References 30 publications

Obesity and post-prandial lipid metabolism. Feast or famine?

Obesity and post-prandial lipid metabolism. Feast or famine?

Dalcetrapib and anacetrapib differently impact HDL structure and function in rabbits and monkeys

Modulating cholesteryl ester transfer protein activity maintains efficient pre-β-HDL formation and increases reverse cholesterol transport

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