Regulation of serum apolipoprotein E metabolism: role of chylomicron metabolism.

DeLamatre, John G.; Krause, Brian R.; Roheim, Paul S.

doi:10.1073/pnas.79.4.1282

Cited by 12 publications

(8 citation statements)

References 31 publications

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“…227 W.,%;; 11 0-0.-.-than decreased hepatic synthesis. In support of this concept are data showing that a single feeding of the same cholesterol-rich diet used in our study, rapidly (within 9 h) decreased the serum concentration of apolipoprotein E by 35% (DeLamatre et al, 1982). These results were interpreted by DeLamatre and co-workers to indicate that cholesterol-rich chylomicrons associate with serum apolipoprotein E and the complexed apolipoprotein E is selectively removed via the hepatic chylomicron receptor.…”

Section: Discussionsupporting

confidence: 85%

Dietary cholesterol does not affect the synthesis of apolipoproteins B and E by rat hepatocytes

Davis¹,

Malone-McNeal²

1985

Biochemical Journal

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To examine the unproved hypothesis that dietary cholesterol affects the synthesis of apolipoprotein B and E, we fed rats a cholesterol-rich diet that has been shown to alter dramatically the serum concentrations of these apolipoproteins. Rats fed for 4 weeks on a cholesterol-rich diet accumulate increased concentrations of low Mr apolipoprotein B (+2.7-fold) and decreased concentrations of apolipoprotein E (-40%) in their serum. Hepatocytes obtained from similarly treated rats were placed in monolayer culture and the rate of synthesis de novo of apolipoproteins was determined. Although cells from cholesterol-fed rats remained filled with lipid droplets throughout the experimental period, there was no difference in plating efficiency or viability, compared with cells obtained from chow-fed control rats. Both groups of cells synthesized and secreted immunoprecipitable apolipoproteins B and E at similar rates throughout the 18 h experiment. Thus there was a discordance between the effects of dietary cholesterol on serum apolipoprotein concentrations and hepatocyte synthesis and secretion. The data indicate that altered hepatic apolipoprotein synthesis cannot account for the changes in serum apolipoprotein concentrations caused by dietary cholesterol.

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Section: Discussionsupporting

confidence: 85%

Dietary cholesterol does not affect the synthesis of apolipoproteins B and E by rat hepatocytes

Davis¹,

Malone-McNeal²

1985

Biochemical Journal

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“…55 Furthermore, high-lipid food intake was reported to result in the production of more CMs; thus, more CMassociated apoE was absorbed by the liver and removed from the serum. 55 The pork group exposed to the PFAAs showed that the level of apoE decreased the most relative to water (28.4%). Since the cholesterol in the liver can be recovered almost completely, 55 its concentration was measured to indicate the amount of CMs absorbed in mouse liver.…”

Section: ■ Materials and Methodsmentioning

confidence: 91%

“…54 ApoE is important in lipoprotein recognition and is also one of the hepatic recognition sites on CM remnants. 55 Thus, the concentration of apoE in mouse blood may reflect the content of CM remnants. As shown in Figure 4f, the level of apoE in all the exposure groups was significantly higher than that in the control group.…”

Section: ■ Materials and Methodsmentioning

confidence: 99%

“…This might be because the cholesterol-rich CM remnants in the pork group had a greater affinity to retain apoE. 55 Furthermore, high-lipid food intake was reported to result in the production of more CMs; thus, more CMassociated apoE was absorbed by the liver and removed from the serum. 55 The pork group exposed to the PFAAs showed that the level of apoE decreased the most relative to water (28.4%).…”

Section: ■ Materials and Methodsmentioning

confidence: 99%

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Mechanisms Underlying the Impacts of Lipids on the Diverse Bioavailability of Per- and Polyfluoroalkyl Substances in Foods

Zhu

Jia

Wang

et al. 2022

Environ. Sci. Technol.

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Food is a major source of human exposure to per- and polyfluoroalkyl substances (PFASs), yet little is known about their bioavailability in food matrices. Here, the relative bioavailability (RBA) of PFASs in foods was determined using an in vivo mouse model. Pork, which had the highest lipid content, exhibited the greatest effect on bioavailability by increasing the RBAs of perfluoroalkyl acids (PFAAs) while reducing those of fluorotelomer phosphate diesters (diPAPs). During intestinal digestion of lipids, the bioaccessibility of PFAAs increased due to their greater partition into the stable mixed micelles. However, diPAPs were more likely to partition into the undigested oil phase due to their strong hydrophobicity. Both in vitro incubation and molecular docking results indicated that the PFAAs exhibited stronger binding affinities with mouse blood chylomicrons (CMs) than with diPAPs. Collectively, both lipid digestion in the intestine and the carrier effect of CMs played important roles in modulating the bioavailability of PFASs in food. More attention should be given to further evaluating the health risks of PFASs associated with the intake of high-lipid foods.

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“…Al though both diets induced hypercholesterol emia, as previously reported [ 15], the most impressive difference was seen for the (HDL|-rich) LDL2 fraction since a distinct LDL2 peak appeared after cystine feeding whereas the shoulder existing at the same density for control rats disappeared after cholesterol feeding. The elevation of the TRL level after cholesterol feeding is well known, whereas the decrease in the HDL| level has only been mentioned by some au thors [22,23]. It is noteworthy that hyper cholesterolemia induced in rats by a choles terol-enriched diet containing propylthio uracil is associated with a high level of large apoE-rich HDL [24,25], but this effect is probably due to hypothyroidism induced by the drug [26,27], Therefore in the conditions of the present study, the change in the HDL, level after cholesterol feeding (without pro pylthiouracil) strongly contrasts with that observed after cystine feeding.…”

Section: Discussionmentioning

confidence: 99%

Lipolytic Activities in Rats Fed a Sucrose-Rich Diet Supplemented with either Cystine or Cholesterol: Relationships with Lipoprotein Profiles

Mathé¹,

Sérougne²,

Férézou³

et al. 1991

Ann Nutr Metab

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To study the relationships between lipolytic activities and plasma lipoprotein levels in rats, three diets were given for 8 weeks: a semipurifïed diet (based on sucrose, casein and lard) and this diet enriched with 5% cystine or with 1 % cholesterol. Both supplemented diets induced hypercholesterolemia. Lipoprotein analysis by density gradient ultracentrifugation of plasma indicated that hypercholesterolemia of cystine-fed rats (+52%) was characterized by an increased cholesterol level in high-density lipoprotein (HDL; +131 %) and low-density lipoprotein 2 (LDL₂; +147%), the lipoprotein fraction containing essentially apolipoprotein-E-rich high-density lipoproteins (HDLi), and was associated with a decreased cholesterol level in triglyceride-rich lipoproteins (TRL; -69%). That obtained by cholesterol feeding (+28%) was due to a large increase in the TRL cholesterol level (+315%) whereas cholesterol was reduced in HDL (-40%) and in LDL₂ (-60%). Under these dietary conditions, the activity of hepatic lipase (HL) was measured in liver homogenates and those of both HL and lipoprotein lipase were measured in plasma after heparin injection. The activity of HL (1,783 ± 132 mU/g liver in control rats) was increased by 48% in cystine-fed rats and decreased by 40% in cholesterol-fed rats. Similar changes were observed in the activity of both lipases measured in postheparin plasma. Highly significant positive correlations linked each lipolytic activity with the level of cholesterol, phospholipids and proteins in LDL₂ (HDL₁-rich fraction) and in HDL. In contrast, significant negative correlations were found between all of the TRL components and the activity of the lipases. These results suggest that the accumulation in plasma of HDL and of their final products of transformation in the rat, the HDL₁, is closely dependent on the intensity of the TRL lipolysis.

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Regulation of serum apolipoprotein E metabolism: role of chylomicron metabolism.

Cited by 12 publications

References 31 publications

Dietary cholesterol does not affect the synthesis of apolipoproteins B and E by rat hepatocytes

Dietary cholesterol does not affect the synthesis of apolipoproteins B and E by rat hepatocytes

Mechanisms Underlying the Impacts of Lipids on the Diverse Bioavailability of Per- and Polyfluoroalkyl Substances in Foods

Lipolytic Activities in Rats Fed a Sucrose-Rich Diet Supplemented with either Cystine or Cholesterol: Relationships with Lipoprotein Profiles

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