Cellular cholesterol efflux to plasma from moderately hypercholesterolaemic type 1 diabetic patients is enhanced, and is unaffected by simvastatin treatment

Vries, R. de; Kerstens, Michiel N.; Sluiter, Wim J.; Groen, Albert K.; Tol, Arie van; Dullaart, Robin P. F.

doi:10.1007/s00125-005-1760-0

Cited by 49 publications

(39 citation statements)

References 56 publications

(70 reference statements)

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“…In the present study, human skin fibroblasts, obtained from a single normolipidemic donor, were used to assess the ability of plasma to promote cholesterol efflux. These cells abundantly express ABCA1 (20), and probably also ABCG1 (31), but contain negligible SR-BI (21). Thus, it is most likely that several pathways including ABCA1-mediated cholesterol transport contribute to fibroblast cholesterol efflux, although their relative contribution is still unknown.…”

Section: Discussionmentioning

confidence: 99%

“…Cholesterol efflux to plasma was determined using human fibroblasts as cholesterol donor, essentially as described (20,30). In brief, fibroblasts were obtained from a normolipidemic control and were cultured (until passages 5-15) in 24-well culture plates to full confluency.…”

Section: Laboratory Measurementsmentioning

confidence: 99%

“…The cells were cultured in Dulbecco's Modified Eagle's Medium (DMEM) supplemented with 10% vol/vol fetal calf serum (FCS). After washing them with DMEM, they were loaded with [ 3 H]cholesterol (0.5 mCi/ml) during 24 h in the presence of added unlabelled cholesterol (30 mg/ml), thereby inducing ABCA1 (20). After cholesterol loading, cells were washed three times with 0.2% PBS/BSA (weight/vol).…”

Section: Laboratory Measurementsmentioning

confidence: 99%

“…One study in MetS subjects has demonstrated a normal potential of individual skin fibroblasts, a cell system that expresses ABCA1 but hardly any SR-BI (11,12,20,21), to transport cholesterol to purified apo A-I, acting as a cholesterol acceptor (22). On the other hand, cholesterol efflux from monocyte-derived macrophages to apo A-I is defective in a considerable number of subjects with isolated low HDL cholesterol, even in the absence of mutations in ABCA1 (23).…”

Section: Introductionmentioning

confidence: 99%

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Fibroblast cholesterol efflux to plasma from metabolic syndrome subjects is not defective despite low high-density lipoprotein cholesterol

Dullaart¹,

Groen

Dallinga‐Thie

et al. 2008

European Journal of Endocrinology

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Objective: We tested whether in metabolic syndrome (MetS) subjects the ability of plasma to stimulate cellular cholesterol efflux, an early step in the anti-atherogenic reverse cholesterol transport pathway, is maintained despite low high-density lipoprotein (HDL) cholesterol. Design: In 76 subjects with and 94 subjects without MetS based on the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria, we determined plasma (apo)lipoproteins, pre-b-HDL formation, phospholipid transfer protein (PLTP) activity, cholesterol esterification (EST), cholesteryl ester transfer (CET), adiponectin, and the ability of plasma from each subject to stimulate cholesterol efflux out of cultured fibroblasts obtained from a single donor. Results: Apo E, PLTP activity, EST, and CET were higher (PZ0.04 to !0.001), whereas adiponectin was lower in MetS subjects (P!0.01). Pre-b-HDL and pre-b-HDL formation were not different between subjects with and without MetS. Cellular cholesterol efflux to plasma from MetS subjects was slightly higher versus plasma from subjects without MetS (8.8G1.0 vs 8.5G0.9%, PZ0.05), but the difference was not significant after age, sex, and diabetes adjustment. Cellular cholesterol efflux was positively related to pre-b-HDL formation, EST, PLTP activity, and apo E (P!0.05 for all by multiple linear regression analysis), without an independent association with MetS and diabetes status. Conclusions: The ability of plasma from MetS subjects to promote fibroblast cholesterol efflux is not defective, although HDL cholesterol is decreased. Higher cholesterol esterification, PLTP activity, and apo E levels may contribute to the maintenance of cholesterol efflux in MetS.European Journal of Endocrinology 158 53-60

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Section: Discussionmentioning

confidence: 99%

Section: Laboratory Measurementsmentioning

confidence: 99%

Section: Laboratory Measurementsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Fibroblast cholesterol efflux to plasma from metabolic syndrome subjects is not defective despite low high-density lipoprotein cholesterol

Dullaart¹,

Groen

Dallinga‐Thie

et al. 2008

European Journal of Endocrinology

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“…Increased oxidation of plasma LDL (7) and accumulation of oxidatively modified LDL in macrophages in the arterial wall (8) are characteristic of the early stage of atherogenesis. HDL has a protective role against atherosclerosis: it removes lipid peroxides (LPOs) and cholesterol from oxidized LDL (9,10) and from cell membranes through the reverse cholesterol transport pathway (11,12). Once LPOs are absorbed by HDL, they are either transported to the liver, where they are detoxified and excreted into the bile (13)(14)(15), or they are reduced directly by HDL to hydroxylipids (16,17).…”

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confidence: 99%

Increased methionine sulfoxide content of apoA-I in type 1 diabetes

Brock

Jenkins

Lyons

et al. 2008

Journal of Lipid Research

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Cardiovascular disease is a major cause of morbidity and premature mortality in diabetes. HDL plays an important role in limiting vascular damage by removing cholesterol and cholesteryl ester hydroperoxides from oxidized low density lipoprotein and foam cells. Methionine (Met) residues in apolipoprotein A-I (apoA-I), the major apolipoprotein of HDL, reduce peroxides in HDL lipids, forming methionine sulfoxide [Met(O)]. We examined the extent and sites of Met(O) formation in apoA-I of HDL isolated from plasma of healthy control and type 1 diabetic subjects to assess apoA-I exposure to lipid peroxides and the status of oxidative stress in the vascular compartment in diabetes. Three tryptic peptides of apoA-I contain Met residues: Q 84 -M 86 -K 88 , W 108 -M 112 -R 116 , and L 144 -M 148 -R 149 . These peptides and their Met(O) analogs were identified and quantified by mass spectrometry. Relative to controls, Met(O) formation was significantly increased at all three locations (Met 86 , Met 112 , and Met 148 ) in diabetic patients. The increase in Met(O) in the diabetic group did not correlate with other biomarkers of oxidative stress, such as N : -malondialdehyde-lysine or N : -(carboxymethyl)lysine, in plasma or lipoproteins. The higher Met(O) content in apoA-I from diabetic patients is consistent with increased levels of lipid peroxidation products in plasma in diabetes. Using the methods developed here, future studies can address the relationship between Met(O) in apoA-I and the risk, development, or progression of the vascular complications of diabetes.-Brock, J.

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Current literature in diabetes

2006

Diabetes Metabolism Res

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In order to keep subscribers up‐to‐date with the latest developments in their field, John Wiley & Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of diabetes/metabolism. Each bibliography is divided into 26 sections: 1 Reviews & Symposia; 2 General; 3 Genetics; 4 Epidemiology; 5 Immunology; 6 Obesity; 7 Prediction and Prevention; 8 Intervention: a) General; b) Care; c) Drug Therapy; d)Economics; e) Gene therapy; f) Nursing; g) Nutrition; h) Surgery; i) Transplantation; 9 Pathology and Complications: a) General; b) Cardiovascular; c) Eye disease; d) Gestational and fetal; e) Neurological; f) Podiatrical; g) Renal; 10 Endocrinology & Metabolism; 11 Experimental Studies; 12 Diagnosis and Techniques. Within each section, articles are listed in alphabetical order with respect to author

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Cellular cholesterol efflux to plasma from moderately hypercholesterolaemic type 1 diabetic patients is enhanced, and is unaffected by simvastatin treatment

Cited by 49 publications

References 56 publications

Fibroblast cholesterol efflux to plasma from metabolic syndrome subjects is not defective despite low high-density lipoprotein cholesterol

Fibroblast cholesterol efflux to plasma from metabolic syndrome subjects is not defective despite low high-density lipoprotein cholesterol

Increased methionine sulfoxide content of apoA-I in type 1 diabetes

Current literature in diabetes

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