Exploring the value of apoB48 as a marker for atherosclerosis in clinical practice

Alipour, Arash; Valdivielso, Pedro; Elte, J.W.F.; Janssen, Hans W.; Rioja, José; Meulen, N. van der; Mechelen, R. van; Njo, Tjin L.; González-Santos, Pedro; Rietveld, A.P.; Cabezas, Manuel Castro

doi:10.1111/j.1365-2362.2011.02635.x

Cited by 39 publications

(34 citation statements)

References 43 publications

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“…Our findings may have implications on the pathophysiology of insulin resistance–sociated hyperlipidemia. This condition has been associated with increased intestinal TLRs secretion and is proposed to be a pathogenic factor for atherosclerosis . Hayashi et al found that intestinal SR‐BI levels were increased in mice and hamsters that developed insulin resistance, hyperinsulinemia, and hyperlipidemia in response to a high‐fat and a high‐fructose diet, respectively .…”

Section: Discussionmentioning

confidence: 99%

Insulin increases cholesterol uptake, lipid droplet content, and apolipoprotein B secretion in CaCo‐2 cells by upregulating SR‐BI via a PI3K, AKT, and mTOR‐dependent pathway

Fuentes

Santander

Cortés

2018

J of Cellular Biochemistry

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The actions of insulin on intestinal cholesterol absorption and lipoprotein secretion are not well understood. Herein, we determined the effects of insulin on the levels of cholesterol transporter scavenger receptor, class B, type I (SR‐BI), cellular cholesterol uptake, intracellular lipid accumulation, and lipoprotein secretion in a cellular model of human intestinal epithelium. Methods: CaCo‐2 cells were cultured to postconfluency in Transwell filters and stimulated with glucose (25 mM) in the presence or absence of insulin (100 nM) at their basolateral surface. SR‐BI mRNA and protein levels were quantified by quantitative reverse transcription‐PCR and immunoblot, respectively. Polarized localization of SR‐BI was determined by cell surface proteins biotinylation and streptavidin precipitation. Activities of PI3K, AKT, mTOR, and SR‐BI were pharmacologically antagonized. Cholesterol uptake was assessed by NBD‐cholesterol incorporation. Apolipoprotein (apo) B concentration was quantified by ELISA. Subcellular localization of neutral lipids (BODIPY) and SR‐BI (immunofluorescence) was determined by confocal microscopy. Results: In polarized CaCo‐2 cells, insulin increased SR‐BI at the mRNA and protein levels. SR‐BI was exclusively present at apical cell surface, as indicated by biotinylation and confocal microscopy analysis. Glucose did not modify SR‐BI abundance or subcellular localization. Effects of insulin on SR‐BI levels were abrogated by PI3K, AKT, or mTOR pharmacological antagonism. Cholesterol uptake, neutral lipid abundance, and apo B secretion were increased by insulin in CaCo‐2 cells, and these effects were prevented by SR‐BI pharmacological antagonism with block lipid transport‐1. Conclusions: insulin promotes cholesterol uptake, intracellular lipid store, and apo B–containing lipoproteins secretion by SR‐BI‐dependent mechanisms in a model of human intestinal epithelium.

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Section: Discussionmentioning

confidence: 99%

Insulin increases cholesterol uptake, lipid droplet content, and apolipoprotein B secretion in CaCo‐2 cells by upregulating SR‐BI via a PI3K, AKT, and mTOR‐dependent pathway

Fuentes

Santander

Cortés

2018

J of Cellular Biochemistry

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“…These particles have been shown to be associated with impairment of endothelial function and asymptomatic peripheral arterial disease in patients with T2DM [16,17], and correlate with coronary artery disease and carotid intima-media thickness in subjects with normal serum TG levels [18,19]. The potential mechanisms by which lipoproteins such as apoB-48 play a role in the atherosclerotic process, besides mechanisms intrinsic to these particles such as inflammation may involve closely associated abnormalities in other lipoproteins such as HDL and LDL resulting in ‘atherogenic lipoprotein phenotype’ (low HDL and small dense LDL) [20,21]. …”

Section: Postprandial Dyslipidemia As a Risk Factormentioning

confidence: 99%

Lipoprotein effects of incretin analogs and dipeptidyl peptidase 4 inhibitors

Zhong

Maiseyeu

Rajagopalan

2015

Clinical Lipidology

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Elevated post-prandial lipoprotein levels are common in patients with type 2 diabetes. Post-prandial lipoprotein alterations in type 2 diabetics are widely believed to drive inflammation and are considered a major risk factor for cardiovascular disease in diabetic patients. The incretins glucagon like peptide-1 (GLP-1) and glucose insulinotropic peptide (GIP) modulate post-prandial lipoproteins through a multitude of pathways that are independent of insulin and weight loss. Evidence from both animal models and humans seems to suggest an important effect on triglyceride rich lipoproteins (Apo48 containing) with little to no effects on other lipoproteins at least in humans. Dipeptidyl peptidase-4 (DPP4) inhibitors also appear to share these effects suggesting an important role for incretins in these effects. In this review, we will summarize lipid modulating effects of incretin analogs and DPP-4 inhibitors in both animal models and human studies and provide an overview of mechanisms responsible for these effects.

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“…Alipour et al [144] reported postprandial accumulation of atherogenic remnants in patients with type 2 diabetes, familial combined hyperlipidemia (FCHL), familial hypercholesterolemia (FH), and CAD. ApoB-48 was highest in FCHL and atherosclerotic subjects with type 2 diabetes.…”

Section: The Value Of Apob-48 As a Marker For Atherosclerosis In Clinmentioning

confidence: 99%

Apolipoprotein B-48

Nakajima

Nagamine

Fujita

et al. 2014

Advances in Clinical Chemistry

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Exploring the value of apoB48 as a marker for atherosclerosis in clinical practice

Abstract: ApoB48 concentrations are highest in patients with FCH and in atherosclerotic subjects with T2DM. In patients not using statins, the surrogate atherosclerosis marker IMT correlates best with apoB48, suggesting that fasting apoB48 may help to detect subjects at risk.

Cited by 39 publications

References 43 publications

Insulin increases cholesterol uptake, lipid droplet content, and apolipoprotein B secretion in CaCo‐2 cells by upregulating SR‐BI via a PI3K, AKT, and mTOR‐dependent pathway

Insulin increases cholesterol uptake, lipid droplet content, and apolipoprotein B secretion in CaCo‐2 cells by upregulating SR‐BI via a PI3K, AKT, and mTOR‐dependent pathway

Lipoprotein effects of incretin analogs and dipeptidyl peptidase 4 inhibitors

Apolipoprotein B-48

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