1.P.78 Role of human apolipoproteins in cell cholesterol efflux: Studies with transgenic mice

Chiesa, Giulia; Parolini, Cinzia; Canavesi, M.; Colombo, N.; Rubin, Edward M.; Franceschini, Guido; Zimetti, Francesca

doi:10.1016/s0021-9150(97)88260-3

Cited by 2 publications

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“…It seems that human ApoA2 has different performances between animals and humans 53 . Moreover, very high secretion of ApoA2 might has been led to elevated ApoB‐containing lipoprotein concentrations that can promote hyperlipidaemia and inflammation 54 …”

Section: Discussionmentioning

confidence: 99%

“…53 Moreover, very high secretion of ApoA2 might has been led to elevated ApoB-containing lipoprotein concentrations that can promote hyperlipidaemia and inflammation. 54 Moreover based on the findings of Lai et al, there were defects in BCAA metabolism pathway in mice with CC genotype and high SFA intake compared to TT genotype with the same diet which were not present between TT and CC carriers with low SFA intakes.…”

Section: Ta B L E 4 (Continued)mentioning

confidence: 99%

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A personalised diet study: The interaction between ApoA2 −265T > C polymorphism and dietary inflammatory index on oxidative and inflammatory markers and lipid profile in patients with type 2 diabetes mellitus: A cross‐sectional study

et al. 2021

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Background: This study aimed to investigate the interaction between dietary inflammatory index (DII) and apolipoproteinA2 265T > C (ApoA2 −265T > C) polymorphism on inflammatory and oxidative markers and lipid profile in type 2 diabetes mellitus (T2DM) patients. Methods:In this cross-sectional study, 157 patients with T2DM were recruited. A food-frequency questionnaire was used for DII calculation. Inflammatory, oxidative and lipid biomarkers were measured. Real-time polymerase chain reaction (PCR) method was used for ApoA2 genotyping determination.Results: In the current study, serum 8-iso-PGF2α and CRP were significantly higher, and serum SOD activity was significantly lower in subjects with CC genotype than TT homozygous in both crude and adjusted (for DII and AAs intake) models. Also, C-allele carriers compared with people with TT genotype had lower PTX3 in both models. In addition, serum TG level was significantly higher in TC genotype than TT homozygous in adjusted model. Moreover, subjects with CC homozygous and high DII level had significantly higher 8-iso-PGF2α level compared to those with TT genotype and low DII (reference group) in adjusted (for BMI, age, sexuality and AAs intake) model. Our results also showed that in TC genotypes with low DII and CC homozygous with both low and high DII, PTX3 concentrations were significantly lower than the reference group. In addition, CC carriers with low DII had significantly higher CRP level compared to the reference group. Moreover, our results reported significant How to cite this article: Karimi E, Tondkar P, Sotoudeh G, Qorbani M, Rafiee M, Koohdani F. A personalised diet study:The interaction between ApoA2 −265T > C polymorphism and dietary inflammatory index on oxidative and inflammatory markers and lipid profile in patients with type 2 diabetes mellitus: A cross-sectional study. Int J Clin Pract.

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Section: Discussionmentioning

confidence: 99%

Section: Ta B L E 4 (Continued)mentioning

confidence: 99%

A personalised diet study: The interaction between ApoA2 −265T > C polymorphism and dietary inflammatory index on oxidative and inflammatory markers and lipid profile in patients with type 2 diabetes mellitus: A cross‐sectional study

et al. 2021

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“…31 On the other hand, apoA-I knockout (AI-KO) mice have very low plasma HDL levels but are not at increased risk of aortic lesion development, even after administration of the atherogenic diet. 32 Chiesa et al 33 expressed hapo A-I, hapo A-II, and both hapo A-I and A-II in the AI-KO background, and they measured cholesterol efflux from Fu5AH cells. Efflux was equally low in plasma from AI-KO and AI-KO/hAIItg mice, whereas it increased appreciably in plasma from AI-KO/hAItg mice, with or without the concomitant expression of hapo A-II.…”

Section: Fournier Et Al Cholesterol Efflux Modulation By Human Apoa-iimentioning

confidence: 99%

Opposite Effects of Plasma From Human Apolipoprotein A-II Transgenic Mice on Cholesterol Efflux From J774 Macrophages and Fu5AH Hepatoma Cells

Fournier

Cogny

Atger

et al. 2002

ATVB

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Abstract-Overexpression of human apolipoprotein A-II (hapo A-II) in transgenic mice (hAIItg mice) induced marked hypertriglyceridemia and low levels of plasma high density lipoprotein (HDL) with a high hapo A-II content. We sought to determine whether cholesterol efflux to plasma and HDL from these mice would be affected. In the Fu5AH cell system, plasma from hAIItg mice induced a markedly lower cholesterol efflux than did control plasma, in accordance with the dependence of efflux on HDL concentration. Moreover, HDLs from hAIItg mice were less effective acceptors than were control HDLs. In the J774 macrophage cell system, pretreatment with cAMP, which upregulates ATP binding cassette transporter 1, induced a marked increase in the efflux to hAIItg plasma as well as to purified hapo A-I and hapo A-II, whereas it had no effect on cholesterol efflux to control plasma. T he negative correlation between plasma HDL concentration and the risk of cardiovascular disease has been partly attributed to the ability of HDL to stimulate reverse cholesterol transport (RCT) from peripheral tissues to the liver for recycling. 1,2 The first step of RCT is efflux of free cholesterol from cell membranes to the extracellular medium. A major research effort these last decades has established that at least 3 mechanisms are involved: a nonspecific and relatively inefficient aqueous diffusion pathway, which operates in all cells, and 2 regulated pathways, which are modulated by phospholipid (PL)-containing acceptor particles (such as HDL) or lipid-poor apolipoproteins. 3 On the other hand, controversial results were obtained regarding the effect of the apolipoprotein composition of HDL, with some studies reporting a stimulation of cholesterol efflux by HDLs containing only apoA-I 4 and other studies reporting HDL carrying apoA-I and apoA-II. 5 Recently, the type of the acceptor particles was linked to the type of the receptors present in the various cells, 3 thus identifying the following 2 specific efflux mechanisms involving (1) the scavenger receptor class B type I (SR-BI) and (2) the ATP binding cassette transporter 1 (ABCA1). Cholesterol molecules that desorb from cell membranes rich in SR-BI diffuse through the aqueous phase and associate with PL-containing acceptor particles, in proportion to PL content. 6 Moreover, the ability of HDL and serum to stimulate cholesterol efflux from different cell types was correlated with the expression level of SR-BI. 7 SR-BI is equally efficient at mediating the import and export of cholesterol to and from cells to lipoproteins and other acceptors. 7,8 By contrast, the unidirectional efflux of membrane cholesterol and PL of cells expressing ABCA1 is promoted by apolipoproteins in lipid-poor form but is little affected by HDLs, small unilamellar vesicles, bile acid micelles, or cyclodextrin. 9 -11 ApoA-I is the major apolipoprotein component of HDL, and its role in RCT has been extensively studied. ApoA-II is the second most abundant HDL apolipoprotein, but its contribution to the function of H...

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1.P.78 Role of human apolipoproteins in cell cholesterol efflux: Studies with transgenic mice

Cited by 2 publications

References 0 publications

A personalised diet study: The interaction between ApoA2 −265T > C polymorphism and dietary inflammatory index on oxidative and inflammatory markers and lipid profile in patients with type 2 diabetes mellitus: A cross‐sectional study

A personalised diet study: The interaction between ApoA2 −265T > C polymorphism and dietary inflammatory index on oxidative and inflammatory markers and lipid profile in patients with type 2 diabetes mellitus: A cross‐sectional study

Opposite Effects of Plasma From Human Apolipoprotein A-II Transgenic Mice on Cholesterol Efflux From J774 Macrophages and Fu5AH Hepatoma Cells

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