Effect of apoproteins on hepatic uptake of triglyceride emulsions in the rat.

Shelburne, F; Hanks, John B.; Meyers, William C.; Quarfordt, Steven H.

doi:10.1172/jci109710

Cited by 356 publications

(114 citation statements)

References 33 publications

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“…Apo-CIII provides a strong negative charge on the surface of lipoproteins preventing nonspecific interactions with the cell surface (29) and perhaps with other lipoproteins. This may act to reduce futile cycles in TG transport by preserving the particles for high affinity interactions such as with lipoprotein lipase or specific cell surface receptors, such as those binding to apo E or apo B.…”

Section: Resultsmentioning

confidence: 99%

Apolipoprotein CIII polymorphism and triglyceride levels of a Japanese population living in Southern Brazil

Parzianello

Oliveira

Coelho

2008

Braz J Med Biol Res

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Apolipoprotein CIII (apo-CIII) participates in the regulation of triglyceride-rich lipoprotein metabolism. Several polymorphic sites have been detected within and around the apo-CIII gene. Here, we examined the relationship between apo-CIII Sst I polymorphism (CC, CG, GG genotypes) and plasma triglyceride (TG) levels in a group of 159 Japanese individuals living in Southern Brazil. The sample was divided into a group of Japanese descendants (N = 51) with high TG (HTG; >200 mg/dL) and a group of Japanese descendants (N = 108) with normal TG (NTG; <200 mg/dL). TG and total cholesterol levels were analyzed by an enzymatic method using the Labtest-Diagnostic kit and high-and low-density lipoproteins by a direct method using the Labtest-Diagnostic kit and DiaSys Diagnostic System International kit, respectively. A 428-bp sequence of apo-CIII gene was amplified using oligonucleotide primers 5' GGT GAC CGA TGG CTT CAG TTC CCT GA 3' and 5' CAG AAG GTG GAT AGA GCG CTG GCC T 3'. The PCR products were digested with a restriction endonuclease Sst I. Rare G allele was highly prevalent in our study population (0.416) compared to Caucasians (0.00-0.11). G allele was almost two times more prevalent in the HTG group compared to the NTG group (P < 0.001). The genotype distribution was consistent with the Hardy-Weinberg equilibrium. There was a significant association between rare G allele and HTG in Japanese individuals living in Southern Brazil as indicated by one-way ANOVA, P < 0.05.

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Section: Resultsmentioning

confidence: 99%

Apolipoprotein CIII polymorphism and triglyceride levels of a Japanese population living in Southern Brazil

Parzianello

Oliveira

Coelho

2008

Braz J Med Biol Res

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“…In vitro, apoC-III can inhibit the hydrolysis of triglyceride 68,69 and reduce TRL clearance. 70,71 In vivo, transgenic mice overexpressing human apoC-III develop a marked hypertriglyceridemia resulting from impaired clearance of TRL due to apoE insufficiency. 72,73 In contrast, homozygous apoC-III knockout mice have hypotriglyceridemia and enhanced TRL clearance.…”

Section: Burnett Et Al December 1998mentioning

confidence: 99%

The HMG-CoA Reductase Inhibitor Atorvastatin Increases the Fractional Clearance Rate of Postprandial Triglyceride-Rich Lipoproteins in Miniature Pigs

Burnett

Barrett

Vicini

et al. 1998

ATVB

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Abstract-We have previously shown in vivo that the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor atorvastatin decreases hepatic apolipoprotein B (apoB) secretion into plasma. To test the hypothesis that atorvastatin modulates exogenous triglyceride-rich lipoprotein (TRL) metabolism in vivo, an oral fat load (2 g fat/kg body wt) containing retinol (50 000 IU) was given to 6 control miniature pigs and to 6 animals after 28 days of treatment with atorvastatin 3 mg ⅐ kg Ϫ1 ⅐ d Ϫ1. A multicompartmental model was developed by use of SAAM II and kinetic analysis performed on the plasma retinyl palmitate (RP) data. Peak TRL (dϽ1.006 g/mL; S f Ͼ20) triglyceride concentrations were decreased 29% by atorvastatin, and the time to achieve this peak was delayed (5.2 versus 2.3 hours; PϽ0.01). The TRL triglyceride 0-to 12-hour area under the curve was decreased by 24%. In contrast, atorvastatin treatment had no effect on peak TRL RP concentrations, time to peak, or its rate of appearance into plasma; however, the TRL RP 0-to 12-hour area under the curve was decreased by 20%. Analysis of the RP kinetic parameters revealed that the TRL fractional clearance rate was increased significantly, 1.4-fold (3.093 versus 2.276 pools/h; Pϭ0.012), with atorvastatin treatment. The percent conversion of TRL RP from the rapid-turnover to the slow-turnover compartment was decreased by 47% with atorvastatin treatment. The TRL RP fractional clearance rate was negatively correlated with very low density lipoprotein apoB production rate measured in the fasting state (rϭϪ0.49). Thus, although atorvastatin had no effect on intestinal TRL assembly and secretion, plasma TRL clearance was significantly increased, an effect that may relate to a decreased competition for removal processes by hepatic very low density lipoprotein.

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“…Clearance and liver uptake are apoE dependent (3)(4)(5)(6)(7)(8). On the basis of a large body of evidence from cell culture (9,10) and in vivo (11) studies it has been postulated that the initial sequestration of lipoprotein particles is mediated mainly by hepatic heparan sulfate proteoglycans (HSPGs), and that this facilitates their subsequent interiorization by the low density lipoprotein receptor (LDLR), and the LDLR-related 1Abbreviations used in this paper: apoE, apoliprotein E; CS, circumsporozoite protein; EEF, exoerythrocytic forms; GAG, glycosaminoglycan; HPRT, hypoxanthine phosphorybosyl transferase; HSPG, heparan sulfate proteoglycan; LDLR, low density lipoprotein receptor; LRP, LDLRrelated protein; RT, reverse transcriptase; TBS, Tris-buffered saline; TRAP/SSP2, thrombospondin-related adhesive protein/sporozoite surface protein 2; VLDL, very low density lipoprotein.…”

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confidence: 99%

Remnant lipoproteins inhibit malaria sporozoite invasion of hepatocytes.

Sinnis

Willnow

Briones

et al. 1996

The Journal of Experimental Medicine

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SummaryRemnants oflipoproteins, intestinal chylomicrons, and very low density lipoproteins (VLDL), are rapidly cleared from plasma and enter hepatocytes. It has been suggested that remnant lipoproteins are initially captured in the space of Disse by heparan sulfate proteoglycans (HSPGs), and that their subsequent internalization into hepatocytes is mediated by members of the LDLreceptor gene family. Similarly to lipoprotein remnants, malaria sporozoites are removed from the blood circulation by the liver within minutes after injection by Anopheles mosquitoes. The sporozoite's surface is covered by the circumsporozoite protein (CS), and its region II-plus has been implicated in the binding of the parasites to glycosaminoglycan chains of hepatocyte HSPGs. Lactoferrin, a protein with antibacterial properties found in breast milk and neutrophil granules, is also rapidly cleared from the circulation by hepatocytes, and can inhibit the hepatic uptake of lipoprotein remnants. Here we provide evidence that sporozoites, lactoferrin, and remnant lipoproteins are cleared from the blood by similar mechanisms. CS, lactoferrin, and remnant lipoproteins compete in vitro and in vivo for binding sites on liver cells. The relevance of this binding event for sporozoite infectivity is highlighted by our demonstration that apoliprotein E-enriched [3-VLDL and lactoferrin inhibit sporozoite invasion of HepG2 cells. In addition, malaria sporozoites are less infective in LDL-receptor knockout (LDLR-/-) mice maintained on a high fat diet, as compared with littermates maintained on a normal diet. We conclude that the clearance oflipoprotein remnants and sporozoites from the blood is mediated by the same set of highly sulfated HSPGs on the hepatocyte plasma membrane.

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Effect of apoproteins on hepatic uptake of triglyceride emulsions in the rat.

Cited by 356 publications

References 33 publications

Apolipoprotein CIII polymorphism and triglyceride levels of a Japanese population living in Southern Brazil

Apolipoprotein CIII polymorphism and triglyceride levels of a Japanese population living in Southern Brazil

The HMG-CoA Reductase Inhibitor Atorvastatin Increases the Fractional Clearance Rate of Postprandial Triglyceride-Rich Lipoproteins in Miniature Pigs

Remnant lipoproteins inhibit malaria sporozoite invasion of hepatocytes.

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