Chylomicrons or their remnants penetrate rabbit thoracic aorta as efficiently as do smaller macromolecules, including low-density lipoprotein, high-density lipoprotein, and albumin

Mamo, John; Wheeler, James R.

doi:10.1097/00019501-199408000-00008

Cited by 103 publications

(91 citation statements)

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“…In a series of studies with rabbits and rats, it has been shown that chylomicrons are able to penetrate arteries as efficiently as smaller macromolecules, including LDL, HDL and albumin [20,21,23,49,50]. Whole-VLDL-particle uptake has also been demonstrated in mice, whereby whole-particle lipoprotein uptake in muscle increases by transgenic expression of catalytically inactive LPL in the presence of active LPL [51,52].…”

Section: Discussionmentioning

confidence: 99%

Human triglyceride-rich lipoproteins impair glucose metabolism and insulin signalling in L6 skeletal muscle cells independently of non-esterified fatty acid levels

et al. 2005

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Aims/hypothesis: Elevated fasting and postprandial plasma levels of triglyceride-rich lipoproteins (TGRLs), i.e. VLDL/remnants and chylomicrons/remnants, are a characteristic feature of insulin resistance and are considered a consequence of this state. The aim of this study was to investigate whether intact TGRL particles are capable of inducing insulin resistance. Methods: We studied the effect of highly purified TGRLs on glycogen synthesis, glycogen synthase activity, glucose uptake, insulin signalling and intramyocellular lipid (IMCL) content using fully differentiated L6 skeletal muscle cells. Results: Incubation with TGRLs diminished insulin-stimulated glycogen synthesis, glycogen synthase activity, glucose uptake and insulin-stimulated phosphorylation of Akt and glycogen synthase kinase 3. Insulin-stimulated tyrosine phosphorylation of IRS-1, and IRS-1-and IRS-2-associated phosphatidylinositol 3-kinase (PI3K) activity were not impaired by TGRLs, suggesting that these steps were not involved in the lipoprotein-induced effects on glucose metabolism. The overall observed effects were time-and dose-dependent and paralleled IMCL accumulation. NEFA concentration in the incubation media did not increase in the presence of TGRLs indicating that the effects observed were solely due to intact lipoprotein particles. Moreover, co-incubation of TGRLs with orlistat, a potent active-site inhibitor of various lipases, did not alter TGRL-induced effects, whereas co-incubation with receptor-associated protein (RAP), which inhibits interaction of TGRL particles with members of the LDL receptor family, reversed the TGRL-induced effects on glycogen synthesis and insulin signalling. Conclusions/ interpretation: Our data suggest that the accumulation of TGRLs in the blood stream of insulin-resistant patients may not only be a consequence of insulin resistance but could also be a cause for it.

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Section: Discussionmentioning

confidence: 99%

Human triglyceride-rich lipoproteins impair glucose metabolism and insulin signalling in L6 skeletal muscle cells independently of non-esterified fatty acid levels

et al. 2005

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“…Large CM are excluded from entry into the arterial intima (26) and the transfer of lipoproteins across the endothelium appears to be a non-receptormediated process of transcytosis or molecular sieving. Despite their size, chylomicron remnants and VLDL have been shown to penetrate arterial tissue, although, at a lower rate than LDL or HDL (27,28). Studies on lipoprotein efflux showed that after entry into the intima, triglyceridecontaining lipoproteins can become trapped (25) and it has been postulated by Williams and Tabas (12) that subendothelial retention of atherogenic lipoproteins may be an initiating pathogenic event in atherogenesis.…”

Section: Direct Involvement Of Chylomicron Remnants In Atherogenesis mentioning

confidence: 99%

Induction of Atherosclerosis by Human Chylomicron Remnants: A Hypothesis

Wilhelm

Cooper

2003

JAT

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“…Ž . 1996 andin vivo Mamo andWheeler, 1994 . LDL has also been shown to be taken up by the rat aorta in vivo Ž .…”

Section: Introductionmentioning

confidence: 96%

“…1991 . Furthermore, Mamo andWheeler 1994 have demonstrated that chylomicron remnants accumulate in the thoracic aortae of conscious rabbits and that this uptake by the artery wall is non-specific, its rate being dependent on plasma concentration. In addition, at high concentrations chylomicron remnants have been shown to be cytotoxic to arterial smooth muscle cells in vitro which may be a Ž possible cause of cell death in atherosclerotic plaques Yu .…”

Section: Introductionmentioning

confidence: 99%

Effects of chylomicrons and chylomicron remnants on endothelium-dependent relaxation of rat aorta

Grieve

Avella

Botham

et al. 1998

European Journal of Pharmacology

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. (1998). Effects of chylomicrons and chylomicron remnants on endothelium-dependent relaxation of rat aorta. European Journal of Pharmacology, 348(2-3)(2-3), 181-190. DOI: 10.1016181-190. DOI: 10. /S0014-2999 AbstractThe effects of chylomicrons and chylomicron remnants on endothelium-dependent relaxation of rat aorta were studied in vitro. Chylomicrons and chylomicron remnants were prepared in vivo. Aortic rings were incubated with the lipoproteins for 45 min before the vessels were constricted with phenylephrine and concentration relaxation response curves constructed to carbachol, ATP, A23187 and S-nitroso-N-acetylpenicillamine. Maximum % relaxations to carbachol were significantly reduced by both chylomicrons and chylomicron remnants but responses to ATP and S-nitroso-N-acetylpenicillamine were unaffected. In addition, chylomicrons significantly inhibited A23187-induced relaxation, causing an increase in the EC value. Chylomicron remnants cause selective inhibition of carbachol-induced 50 relaxation suggesting an action at the receptor or G protein-coupled component of the receptor-mediated activation of the L-arginine-nitric oxide pathway. Chylomicrons appear to be less selective in their inhibition of the endothelium-dependent relaxation. This study demonstrates that lipoprotein particles of dietary origin may cause endothelial cell dysfunction. q 1998 Elsevier Science B.V. All rights reserved. Ž .Ž .

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Chylomicrons or their remnants penetrate rabbit thoracic aorta as efficiently as do smaller macromolecules, including low-density lipoprotein, high-density lipoprotein, and albumin

Cited by 103 publications

References 0 publications

Human triglyceride-rich lipoproteins impair glucose metabolism and insulin signalling in L6 skeletal muscle cells independently of non-esterified fatty acid levels

Human triglyceride-rich lipoproteins impair glucose metabolism and insulin signalling in L6 skeletal muscle cells independently of non-esterified fatty acid levels

Induction of Atherosclerosis by Human Chylomicron Remnants: A Hypothesis

Effects of chylomicrons and chylomicron remnants on endothelium-dependent relaxation of rat aorta

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