The exchangeable apolipoproteins present in small, dense LDL (sdLDL) and large, buoyant LDL subclasses were evaluated with a quantitative proteomic approach in patients with the metabolic syndrome and with type 2 diabetes, both with subclinical atherosclerosis and the B LDL phenotype. The analyses included surface-enhanced laser adsorption/ionization, time-of-flight mass spectrometry, and subsequent identification by mass spectrometry or immunoblotting and were carried out in LDL subclasses isolated by ultracentrifugation in deuterium oxide gradients with near physiological salt concentrations. The sdLDLs of both types of patients were enriched in apolipoprotein C-III (apoC-III) and were depleted of apoC-I, apoA-I, and apoE compared with matched healthy controls with the A phenotype. The LDL complexes formed in serum from patients with diabetes with the arterial proteoglycan (PG) versican were also enriched in apoC-III. In addition, there was a significant correlation between the apoC-III content in sdLDL in patients and the apparent affinity of their LDLs for arterial versican.The unique distribution of exchangeable apolipoproteins in the sdLDLs of the patients studied, especially high apoC-III, coupled with the augmented affinity with arterial PGs, may contribute to the strong association of the dyslipidemia of insulin resistance with increased risk for cardiovascular disease. The exchangeable apolipoproteins present in small, dense LDL (sdLDL) and large, buoyant LDL subclasses were evaluated with a quantitative proteomic approach in patients with the metabolic syndrome and with type 2 diabetes, both with subclinical atherosclerosis and the B LDL phenotype. The analyses included surface-enhanced laser adsorption/ionization, time-of-flight mass spectrometry, and subsequent identification by mass spectrometry or immunoblotting and were carried out in LDL subclasses isolated by ultracentrifugation in deuterium oxide gradients with near physiological salt concentrations. The sdLDLs of both types of patients were enriched in apolipoprotein C-III (apoC-III) and were depleted of apoC-I, apoA-I, and apoE compared with matched healthy controls with the A phenotype. The LDL complexes formed in serum from patients with diabetes with the arterial proteoglycan (PG) versican were also enriched in apoC-III. In addition, there was a significant correlation between the apoC-III content in sdLDL in patients and the apparent affinity of their LDLs for arterial versican. The unique distribution of exchangeable apolipoproteins in the sdLDLs of the patients studied, especially high apoC-III, coupled with the augmented affinity with arterial PGs, may contribute to the strong association of the dyslipidemia of insulin resistance with increased risk for cardiovascular disease. Most of the interactions of LDL with other macromolecules and cells, including those that contribute to its atherogenicity, are controlled by segments of the nonexchangeable apolipoprotein B-100 (apoB-100) exposed at the particle surface (1Chan L. Apolipoprotein B, the major protein component of triglyceride-rich and low-density lipoproteins.J. Biol. Chem. 1992; 267: 25621-25624Google Scholar, 2Camejo G. Hurt-Camejo E. Wiklund O. Bondjers G. Association of lipoproteins with arterial proteoglycans: pathological significance.Atherosclerosis. 1998; 139: 205-222Google Scholar, 3Gustafsson M. Borén J. Mechanisms of lipoprotein retention by the extracellular matrix.Curr. Opin. Lipidol. 2004; 15: 505-514Google Scholar, 4Tannock L.R. Chait A. Lipoprotein-matrix interactions in macrovascular disease in diabetes.Front. Biosci. 2004; 9: 1728-1742Google Scholar). However, exchangeable apolipoproteins can also modulate some of these interactions when adsorbed at the LDL surface, as suggested in the pioneering work of Alaupovic (5Alaupovic P. Significance, structure, function and classification of plasma lipoprotein families.Methods Enzymol. 1996; 263: 32-60Google Scholar) and Campos and colleagues (6Campos H. Perlov D. Khoo C. Sacks F.M. Distinct patterns of lipoproteins with apoB defined by presence of apoE or apoC-III in hypercholesterolemia and hypertriglyceridemia.J. Lipid Res. 2001; 42: 1239-1249Google Scholar). The lipoprotein class with densities of 1.019–1.063 is a collection of particles that differ in size, lipid, and apolipoprotein composition (7Lund-Katz S. Laplaud S. Phillips M. Chapman M.J. Apolipoprotein B-100 conformation and particle surface charge in human LDL subspecies: implications for LDL receptor interaction.Biochemistry. 1998; 37: 12867-12874Google Scholar). Elevated levels of the small, dense LDL (sdLDL) subclass are strongly associated with coronary disease progression, and this phenotype is a marker of the atherogenic dyslipidemia of insulin resistance and type 2 diabetes (8Krauss R.M. Genetic, metabolic, and dietary influences on the atherogenic lipoprotein phenotype.World Rev. Nutr. Diet. 1997; 80: 22-43Google Scholar, 9Krauss R.M. Lipids and lipoproteins in patients with type 2 diabetes.Diabetes Care. 2004; 27: 1496-1504Google Scholar, 10Taskinen M-R. Diabetic dyslipidemia: from basic research to clinical practice.Diabetologia. 2003; 46: 733-749Google Scholar). Furthermore, the prevalence of sdLDL is high in subjects with preclinical femoral and carotid atherosclerosis (11Hulthe J. Bokemark L. Wikstrand J. Fagerberg B. The metabolic syndrome, LDL particle size, and atherosclerosis: the Atherosclerosis and Insulin Resistance (AIR) study.Arterioscler. Thromb. Vasc. Biol. 2000; 20: 2140-2147Google Scholar).These particles have increased affinity for arterial proteoglycans (PGs) and once associated with them become more easily modifiable by enzymatic and oxidative processes than larger, more buoyant LDLs, causing increased uptake by macrophages (12Hurt-Camejo E. Camejo G. Rosengren B. López F. Wiklund O. Bondjers G. Differential uptake of proteoglycan-selected subfractions of low density lipoprotein by human macrophages.J. Lipid Res. 1990; 31: 1387-1398Google Scholar). Such alterations may lead to preferential entrapment and modifications of sdLDL in the intima PG layer, a critical initial step in atherogenesis (2Camejo G. Hurt-Camejo E. Wiklund O. Bondjers G. Association of lipoproteins with arterial proteoglycans: pathological significance.Atherosclerosis. 1998; 139: 205-222Google Scholar, 3Gustafsson M. Borén J. Mechanisms of lipoprotein retention by the extracellular matrix.Curr. Opin. Lipidol. 2004; 15: 505-514Google Scholar, 13Williams K.J. Tabas I. The response-to-retention hypothesis of early atherogenesis.Arterioscler. Thromb. Vasc. Biol. 1995; 15: 551-561Google Scholar, 14Steinberg D. Atherogenesis in perspective: hypercholesterolemia and inflammation as partners in crime.Nat. Med. 2002; 8: 1211-1217Google Scholar, 15Khalil M.F. Wagner W.D. Goldberg I.J. Molecular interactions leading to lipoprotein retention and the initiation of atherosclerosis.Arterioscler. Thromb. Vasc. Biol. 2004; 24: 2211-2218Google Scholar). High apoC-III content in LDL is receiving much attention because subjects with this phenotype are at much higher risk of cardiovascular events than those with a low content, independent of LDL-cholesterol values (16Lee S-J. Campos H. Moye L.A. Sacks F.M. LDL containing apolipoprotein CIII is an independent risk factor for coronary events in diabetic patients.Arterioscler. Thromb. Vasc. Biol. 2003; 23: 853-858Google Scholar, 17Lee S-J. Sacks F.M. Effect of pravastatin on intermediate-density and low-density lipoproteins containing apolipoprotein CIII in patients with diabetes mellitus.Am. J. Cardiol. 2003; 92: 121-124Google Scholar). ApoC-III, by inhibiting the hydrolysis of triglycerides in VLDL, causes hypertriglyceridemia, but it is not clear why it should increase the atherogenicity of LDL. However, in a detailed study, Olin-Lewis et al. (18Olin-Lewis K. Krauss R.M. Belle M. La Blanche P.J. Barrett P.H.R. Wight T.N. Chait A. ApoC-III content of apoB-containing lipoproteins is associated with binding to the vascular proteoglycan biglycan.J. Lipid Res. 2002; 43: 1969-1977Google Scholar) showed that the affinity of LDL subclasses for the PG biglycan increased with decreasing particle diameter, and this trend was associated with increasing apoC-III content and greater positive charge. Furthermore, these investigators found that depletion of apoC-III reduced the affinity for the PG biglycan and that enrichment with apoC-III increased the association. The low content of phospholipids and free cholesterol in sdLDL is associated with changes in the exposure of segments of the apoB-100 that modify its affinity for the apoB/E receptor (1Chan L. Apolipoprotein B, the major protein component of triglyceride-rich and low-density lipoproteins.J. Biol. Chem. 1992; 267: 25621-25624Google Scholar, 3Gustafsson M. Borén J. Mechanisms of lipoprotein retention by the extracellular matrix.Curr. Opin. Lipidol. 2004; 15: 505-514Google Scholar, 15Khalil M.F. Wagner W.D. Goldberg I.J. Molecular interactions leading to lipoprotein retention and the initiation of atherosclerosis.Arterioscler. Thromb. Vasc. Biol. 2004; 24: 2211-2218Google Scholar, 19Capell W. Zambon A. Austin M. Brunzell J. Hokanson J. Compositional differences of LDL particles in normal subjects with LDL subclass phenotype A and LDL subclass phenotype B.Arterioscler. Thromb. Vasc. Biol. 1996; 16: 1040-1046Google Scholar, 20Olsson U. Camejo G. Hurt-Camejo E. Elfsber K. Wiklund O. Bondjers G. Possible functional interactions of apolipoprotein B-100 segments that associate with cell proteoglycans and the apoB/E receptor.Arterioscler. Thromb. Vasc. Biol. 1997; 17: 149-155Google Scholar). Such changes can also contribute to the increased affinity of sdLDL for PGs, because sequences 3359–3369 (B site) and in PG also in receptor binding (1Chan L. Apolipoprotein B, the major protein component of triglyceride-rich and low-density lipoproteins.J. Biol. Chem. 1992; 267: 25621-25624Google Scholar, 20Olsson U. Camejo G. Hurt-Camejo E. Elfsber K. Wiklund O. Bondjers G. Possible functional interactions of apolipoprotein B-100 segments that associate with cell proteoglycans and the apoB/E receptor.Arterioscler. Thromb. Vasc. Biol. 1997; 17: 149-155Google Scholar, J. I. W. K. S. of the low density lipoprotein in apolipoprotein and the of its binding by the in 1998; Scholar). LDL from human apoB-100 and human that the in surface phospholipids the affinity for PGs, by increasing the exposure of the A M. Borén J. Mechanisms of lipoprotein retention by the extracellular matrix.Curr. Opin. Lipidol. 2004; 15: 505-514Google Scholar). In the present in a study, subclasses of LDL of density from with the metabolic syndrome, LDL particles B and subclinical atherosclerosis in the of exchangeable apolipoproteins compared with those in healthy In a of with type 2 diabetes and subclinical atherosclerosis and healthy the hypothesis that was in the In addition, evaluated the of exchangeable apolipoproteins of plasma LDL with affinity for subjects in this were from a of Fagerberg B. J. atherosclerosis and inflammation in with diabetes and diabetes.Diabetes Care. 2004; 27: Scholar). In the study, subjects with sdLDL B subclinical atherosclerosis in the carotid as by but were compared with and healthy controls with risk associated with the metabolic syndrome to the with the of an of insulin resistance for the C. of metabolic of the and Association on to Thromb. Vasc. Biol. 2004; 24: Scholar). subjects clinical of cardiovascular disease and subclinical as by in the carotid or femoral (11Hulthe J. Bokemark L. Wikstrand J. Fagerberg B. The metabolic syndrome, LDL particle size, and atherosclerosis: the Atherosclerosis and Insulin Resistance (AIR) study.Arterioscler. Thromb. Vasc. Biol. 2000; 20: 2140-2147Google Scholar). was as or more than to The between and 2 was in and quantitative were in the when the classification was not to the I. M. G. Wikstrand J. of in the carotid and of a Scholar). The of these subjects are in of the subjects with B the for the metabolic of subjects in healthy controls and patients with phenotype B and serum 2 in a In the study, patients with type 2 diabetes from the patients in the Atherosclerosis and Insulin Resistance (AIR) were compared with and healthy controls with risk of the metabolic syndrome, as defined by the with the of as of insulin resistance subjects were from the at (11Hulthe J. Bokemark L. Wikstrand J. Fagerberg B. The metabolic syndrome, LDL particle size, and atherosclerosis: the Atherosclerosis and Insulin Resistance (AIR) study.Arterioscler. Thromb. Vasc. Biol. 2000; 20: 2140-2147Google Scholar, Fagerberg B. J. atherosclerosis and inflammation in with diabetes and diabetes.Diabetes Care. 2004; 27: Scholar). of the patients were with subjects were on and subjects were on the included diabetic of subjects in healthy controls and patients with type 2 of patients on in the carotid and and on in the femoral of patients on in the carotid and and on in the femoral of patients on in the carotid and and on in the femoral in a The LDL phenotype of was by as (11Hulthe J. Bokemark L. Wikstrand J. Fagerberg B. The metabolic syndrome, LDL particle size, and atherosclerosis: the Atherosclerosis and Insulin Resistance (AIR) study.Arterioscler. Thromb. Vasc. Biol. 2000; 20: 2140-2147Google Scholar, C. S. Krauss Association of low-density lipoprotein particles with the of coronary disease in and Med. 1996; Scholar, R.M. of subclasses of plasma low density lipoproteins in normal Lipid Res. 23: Scholar). The at the and the patients to The LDL density subclasses were isolated from serum by ultracentrifugation in gradients of containing and with of deuterium oxide as C. M. M. G. K. C. G. Camejo G. in deuterium oxide a for of binding and to Lipid Res. Scholar). were by of the of the LDL subclasses the for protein content of LDL was the to the with as the was in LDL by a an apoB cholesterol was The densities of the and of the gradients were by C. M. M. G. K. C. G. Camejo G. in deuterium oxide a for of binding and to Lipid Res. Scholar). of the LDL subclasses were evaluated by as by Krauss and R.M. of subclasses of plasma low density lipoproteins in normal Lipid Res. 23: Scholar). In the LDL and from subjects were by the surface-enhanced laser is a more and approach for protein in compared with the types of protein and protein were with the of and were a to of a protein of LDL was with of binding and the was to the and for The were with of binding for to binding and with of types of were and A of or with containing was to to The were in a protein The was the in the and a of the protein protein were for of in The was at of LDL were and by in of containing and for and by the The and was as The was for to the and was and the was at for of were and of were and by the by for subsequent identification of protein with The of the was with in at for 2 at for at in of and on protein to the by subsequent the on the were and by as K. P. of depletion for in proteomic of serum Scholar). the were by and the were with and increase in and and were carried out in a The were with 2 of and a The were to the of of with and a of was on an mass in and was mass and was positive at a of of with the the were from the a the The was with an the immunoblotting the was of serum LDL to was as with modifications versican isolated from intima G. F. López F. and of a proteoglycan from human Scholar, Bondjers G. Camejo G. L. Wiklund O. of LDL to a human arterial proteoglycan of J. Scholar, O. Bondjers G. I. Camejo G. between LDL and arterial proteoglycans in to serum levels and of 1996; Scholar). In of serum was to of containing 2 and was also to a containing A versican. The were at for and for at at the was with of and the was The was in of B containing and of the were for cholesterol and for of the exchangeable apolipoproteins associated with the LDL from serum by the the in the content of apoC-III in was the apolipoprotein was in to the and at of serum LDL to of the was as of the differences between controls and patients was with and was were evaluated with the in of serum from a with the B phenotype and a healthy are in LDLs isolated with this are in of protein content, and from lipoproteins from the plasma with gradients C. M. M. G. K. C. G. Camejo G. in deuterium oxide a for of binding and to Lipid Res. Scholar). Furthermore, are more to free with the the LDL is at physiological and and can by and the proteomic approach the for or The apoB were by for the proteomic of were to the subsequent analyses in with this LDLs with densities of the LDL subclass from subjects in in to that of the of Krauss R.M. Lipids and lipoproteins in patients with type 2 diabetes.Diabetes Care. 2004; 27: 1496-1504Google Scholar). LDLs with densities of to the of of Krauss R.M. Lipids and lipoproteins in patients with type 2 diabetes.Diabetes Care. 2004; 27: 1496-1504Google Scholar) was the class in of the subjects with the B phenotype in In the study, of the controls showed a at and of the patients with type 2 diabetes showed a at that the density as with the LDL the and the high prevalence of sdLDL in both types of patients (11Hulthe J. Bokemark L. Wikstrand J. Fagerberg B. The metabolic syndrome, LDL particle size, and atherosclerosis: the Atherosclerosis and Insulin Resistance (AIR) study.Arterioscler. Thromb. Vasc. Biol. 2000; 20: 2140-2147Google Scholar). to the LDL subclasses were on the and protein by of sdLDLs from patients and controls in 2 on the protein the sdLDLs from the patients higher of the with of and compared with those of the The were as apoC-III with and and subsequent identification of their matched by The was by The differences in mass of the that of C. M. A. M. P. J. J. J. A apolipoprotein C-III associated with in a of Lipid Res. 1997; Scholar). of patients and controls from 2 on the protein The at and were more in the sdLDLs of controls than in those of were as with and and subsequent identification by immunoblotting The of of of the mass between and the identification and of and apoE in the LDL and apoE were in the of the sdLDLs of controls compared with those of patients not protein of sdLDLs of from healthy controls and from diabetic patients on protein as was as a The with of and were reduced in sdLDLs in patients compared with controls the content of the apolipoproteins by in the sdLDLs for apoB-100 content in both The sdLDLs from the patients higher content of apoC-III compared with the dense from the matched controls in the other the patients showed a content of apoC-I, apoA-I, and apoE in its sdLDL class than the In the sdLDLs of patients with type 2 diabetes also more apoC-III and of apoC-I, apoA-I, and apoE than the dense of the matched controls In the there was a higher content in the sdLDLs than in the buoyant particles of apoC-III and In the there was also a higher content in the sdLDLs than in the buoyant LDLs of apoC-III but not of The differences found between the exchangeable apolipoproteins in the buoyant LDLs of controls and patients in the for apoB-100 content were not as as those found in apolipoproteins in sdLDLs of patients with LDL phenotype B and matched controls in both small, dense LDL. are in by the surface-enhanced laser and by apolipoprotein B-100 content of sdLDLs in patients and controls from both in are in of the differences in apolipoprotein content between the dense LDL class and the from controls was evaluated with the in a small, dense LDL. are in by the surface-enhanced laser and by apolipoprotein B-100 content of sdLDLs in patients and controls from both in are in of the differences in apolipoprotein content between the dense LDL class and the from controls was evaluated with the of serum with arterial versican as causes the of LDL Bondjers G. Camejo G. L. Wiklund O. of LDL to a human arterial proteoglycan of J. Scholar, O. Bondjers G. I. Camejo G. between LDL and arterial proteoglycans in to serum levels and of 1996; Scholar, G. U. Wiklund O. F. Bondjers G. and modulate of complexes between LDL and arterial proteoglycans in Scholar, U. Camejo G. Bondjers G. Molecular that the association of low density lipoprotein apoB-100 with Scholar). for the apoB-100 the of LDL-cholesterol of the from 2 was higher than from as apoB for patients for Furthermore, analyses of the complexes that the LDL from patients and more and than the complexes from differences were The of the complexes from controls and patients with type 2 diabetes are in In with these found a significant correlation between the apoC-III content of sdLDLs from patients in 2 and the of LDL-cholesterol by the PG from serum was significant correlation between the apoC-III content in sdLDLs of controls and the LDL-cholesterol by the arterial versican the of apoC-III on the association of LDL in serum with the content of apoC-III in controls and patients with type 2 diabetes was increased by human apoC-III. these were to with the The in that increasing apoC-III, the of LDL-cholesterol from the increased but this was not the for the that in the of apoC-III is a more of the association of LDL with versican than in of cholesterol in from healthy controls and patients with type 2 diabetes increasing the content of apoC-III in the The values are The patients in the the B LDL insulin resistance and to a compared with controls of the matched controls showed the B phenotype. this LDL to and the and of the for lipoprotein and apolipoprotein The for lipoprotein subclass the of the distribution of exchangeable and apolipoproteins to the LDL particles in that with ultracentrifugation at high salt K. H. Campos E. Alaupovic P. of for human lipoproteins containing lipoprotein Scholar, L. and of lipoproteins by Enzymol. Scholar). Furthermore, the proteomic approach quantitative and identification of apolipoproteins with an of The that the sdLDL subclass with densities of in patients with subclinical atherosclerosis and with the B phenotype is enriched in apoC-III and depleted of apoC-I, apoA-I, and apoE compared with the in healthy The patients in the 2 with type 2 diabetes and the B phenotype and subclinical atherosclerosis also a content of apoC-III in the sdLDL than the of the sdLDL from these patients showed a content of apoC-I, apoA-I, and apoE plasma apoC-III and that associated with LDL are strong of coronary especially in and by the metabolic syndrome A. G. M. K. S. G. Apolipoprotein a strong of coronary risk in and a of the metabolic syndrome in both 2003; Scholar). Furthermore, in patients with type 2 diabetes and coronary those in the of LDL with the apoC-III have a higher risk of coronary events than those in the with the apoC-III content (16Lee S-J. Campos H. Moye L.A. Sacks F.M. LDL containing apolipoprotein CIII is an independent risk factor for coronary events in diabetic patients.Arterioscler. Thromb. Vasc. Biol. 2003; 23: 853-858Google Scholar). sdLDL particles are the of large, triglyceride-rich and that its apoC-III content is to its of and C. M. A. J. distribution of apolipoprotein C-III and its to the presence in plasma of triglyceride-rich 2001; Scholar, Barrett P.H.R. Apolipoprotein B-100 in with plasma apolipoprotein C-III 2002; Scholar). a by dense LDLs can in patients with the metabolic syndrome and type 2 diabetes, those The leading to the reduced content of apoC-I, apoA-I, and apoE that also found the sdLDL subclass of patients with the metabolic syndrome or type 2 diabetes to is that this the reduced of these apolipoproteins in the plasma of these patients and a reduced of the sdLDL particle to as to for apoE in D. Apolipoprotein C-III of apolipoprotein from of particle Lipid Res. Scholar). plasma was in 2 for the diabetic patients and and the of was reduced in patients compared with controls these the is not clear why sdLDL is more atherogenic than buoyant but its high affinity for arterial increase its retention in the an step in atherogenesis (2Camejo G. Hurt-Camejo E. Wiklund O. Bondjers G. Association of lipoproteins with arterial proteoglycans: pathological significance.Atherosclerosis. 1998; 139: 205-222Google Scholar, 3Gustafsson M. Borén J. Mechanisms of lipoprotein retention by the extracellular matrix.Curr. Opin. Lipidol. 2004; 15: 505-514Google Scholar, 4Tannock L.R. Chait A. Lipoprotein-matrix interactions in macrovascular disease in diabetes.Front. Biosci. 2004; 9: 1728-1742Google Scholar, E. Camejo G. Rosengren B. López F. Wiklund O. Bondjers G. Differential uptake of proteoglycan-selected subfractions of low density lipoprotein by human macrophages.J. Lipid Res. 1990; 31: 1387-1398Google Scholar, E. S. L. P. Camejo G. P. Rosengren B. J. J. P. et levels of small, low density lipoproteins with high affinity for arterial in patients with of to this atherogenic 2001; Scholar). In patients with clinical of atherosclerosis and with the atherogenic lipoprotein phenotype associated with insulin a higher affinity of LDL for arterial than in controls with the Bondjers G. Camejo G. L. Wiklund O. of LDL to a human arterial proteoglycan of J. Scholar, G. H. F. The of low density lipoproteins with arterial proteoglycans: an risk Scholar, B. M. C. J. of plasma and on the between low density lipoprotein with human arterial 1996; Scholar, J. M. J. C. of and low-density lipoproteins with human arterial Thromb. Vasc. Biol. 1997; 17: Scholar). In the present study, a significant correlation between the content of apoC-III in sdLDL and the affinity of the LDL in serum for arterial versican Furthermore, patients showed an enrichment of apoC-III in the isolated particles with these may in the arterial to their Furthermore, the by Olin-Lewis et al. (18Olin-Lewis K. Krauss R.M. Belle M. La Blanche P.J. Barrett P.H.R. Wight T.N. Chait A. ApoC-III content of apoB-containing lipoproteins is associated with binding to the vascular proteoglycan biglycan.J. Lipid Res. 2002; 43: 1969-1977Google Scholar) that there is a significant correlation between LDL and affinity for the PG biglycan and that the of apoC-III to apoB is an to this that the apoC-III content is a more factor for the with versican in the and LDL from patients with diabetes than in healthy However, to the of these differences and it to a detailed of the of isolated LDL subclasses from patients and controls with versican. some the that the of the sdLDL with arterial in patients with diabetes that may the between the B phenotype and arterial disease. The major of is that were in a it is not to However, the studied, with subjects with high and low risk of cardiovascular was from a and the may of subjects with these risk that In that the is with the metabolic syndrome and patients with type 2 diabetes, the B and subclinical atherosclerosis have high levels of sdLDL in apoC-III that increase its with the arterial intima and its in oxidative and enzymatic In addition, these sdLDL particles to on apoA-I, an apolipoprotein that to LDL in the arterial atherogenic modifications L. M. A. High density lipoproteins at the of diabetes inflammation and cardiovascular Opin. Lipidol. 2004; 15: Scholar). that this class of sdLDL in the association of increased apoC-III in LDL with the augmented risk of cardiovascular disease in insulin resistance and type 2 diabetes (16Lee S-J. Campos H. Moye L.A. Sacks F.M. LDL containing apolipoprotein CIII is an independent risk factor for coronary events in diabetic patients.Arterioscler. Thromb. Vasc. Biol. 2003; 23: 853-858Google Scholar, 17Lee S-J. Sacks F.M. Effect of pravastatin on intermediate-density and low-density lipoproteins containing apolipoprotein CIII in patients with diabetes mellitus.Am. J. Cardiol. 2003; 92: 121-124Google Scholar).
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