The effect of atorvastatin on serum lipids,lipoproteins and NMR spectroscopy defined lipoprotein subclasses in type 2 diabetic patients with ischaemic heart disease

The effect of statin therapy on subclasses of LDL, VLDL and HDL lipoproteins is unclear. We compared changes in serum lipids, apolipoproteins and nuclear magnetic resonance (NMR) spectroscopy measured lipoprotein subclass concentration and average particle size over a minimum 6 months treatment period of atorvastatin 10 mg vs. placebo in 122 men and women. All subjects had type 2 diabetes and a modest dyslipidaemia (mean LDL-cholesterol 3.2 mmol/l and median triglycerides 1.8 mmol/l) and had a previous myocardial infarction. Compared with placebo, atorvastatin therapy was associated with a greater decrease in medium VLDL (median within person change -13.4 vs. -5.9 nmol/l, P<0.001 adjusted for baseline level), small VLDL (median change -17.8 vs. -8.1 nmol/l, P=0.002), large LDL (mean within person change -167.9 vs. -48.6 nmol/l, P<0.001) and medium LDL (median within person change -101.8 vs. -22.3 nmol/l, P=0.017). Atorvastatin therapy was also associated with a greater increase in large HDL than placebo (median change 1.40 vs. 0.80 micromol/l, P=0.02) and there was little change in small HDL so that average HDL particle size increased significantly with atorvastatin (P=0.04). In addition to reducing levels of (enzymatically measured) triglyceride, LDL-cholesterol and apolipoprotein B in diabetic patients, atorvastatin significantly reduces NMR measured medium and small VLDL and large and medium LDL, and increases large HDL.     

阿托伐他汀对老年2型糖尿病并高脂血症患者降脂疗效观察

目的 观察阿托伐他汀对老年2型糖尿病合并高脂血症患者降脂的疗效. 方法 研究对象每晚睡前服用阿托伐他汀片10 mg,疗程为12个月.治疗前及治疗后3、6、9、12个月分别测定血总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、谷丙转氨酶、谷草转氨酶、血糖、肌酐及颈总动脉、髂总动脉、股动脉的内膜中层厚度(IMT).结果阿托伐他汀治疗1年后,患者TC和LDL-C显著降低[(5.11±0.94)mmol/L至(4.46±0.98)mmol/L和(3.01±0.78)mmol/L至(2.55±0.83)mmol/L,均P<0.01],不同检测时间点LDL-C均达到治疗标准(<2.59 mmol/L),但TC只有在9个月时降至标准以下(<4.04 mmol/L).颈总动脉、髂总动脉和股动脉的IMT均呈减少的趋势,但差异无统计学意义,谷丙转氨酶、谷草转氨酶和肌酐无明显变化. 结论 阿托伐他汀对老年2型糖尿病合并高脂血症患者有明显降脂效果,不良反应小,并且具有保护血管内膜的作用.     

The effect of high dose simvastatin on, platelet size in patients with, type 2 diabetes mellitus

Statins reduce coronary heart disease risk by altering blood lipids and other mechanisms. One of the possible other mechanisms is through an effect on thrombosis. We assessed the effect of simvastatin 80 mg daily versus placebo given in a single blind crossover fashion on platelet size in response to standard ex vivo stimuli, a surrogate for platelet activation, in 12 subjects with type 2 diabetes and mixed dyslipidemia. Exposure to collagen, cold, and heat caused the expected changes in platelet volume. Contrary to our expectations, ex vivo platelet size during collagen and cold exposure increased by 2.6 and 1.7%, respectively (P < 0.05), during simvastatin treatment as opposed to the placebo period. We conclude that some of the effects of high dose simvastatin therapy on platelets may not necessarily be anti-atherogenic.     

Pro-apoptotic low-density lipoprotein subfractions in type II diabetes

OBJECTIVE: To test the hypothesis that differences in subfractions of circulating lipoproteins between diabetic and non-diabetic subjects exist and might contribute to the increased risk for atherosclerosis in type II diabetics. METHODS AND RESULTS: LDL isolated from diabetic (D) and control subjects (N) were separated by FPLC into five subfractions (L1-L5). The fractional distributions of N- and D-LDL were not different, but the most strongly retained subfractions of D-LDL (D-L5) were markedly more pro-apoptotic to bovine aortic endothelial cells in vitro than were the other subfractions in D- or N-LDL. D-L5 induced time- and concentration-dependent apoptosis that was inhibited by z-VAD-fmk. The most electronegative D-LDL subfractions contained substantial amounts of apoproteins AI, E and CIII, higher concentrations of non-esterified fatty acids and LpPLA2, and lower trinitrobenzenesulfonic acid (TNBSA) reactivities. Electronegative subfractions of D-LDL exhibited longer lag times and lower net increases in absorbance at 234 nm with Cu-catalyzed oxidation in vitro. CONCLUSIONS: The toxicities of electronegative subfractions of LDL from diabetic subjects to endothelial cells in vitro may be pivotal to vascular complications of diabetes in vivo, but the specific molecular alterations responsible for the toxicities of these subfractions of diabetic LDL are not known.     

Effect of ezetimibe/simvastatin compared with atorvastatin on lipoprotein subclasses in patients with type 2 diabetes and hypercholesterolaemia

Aim: To evaluate the effects of the usual starting and next higher doses of ezetimibe/simvastatin and atorvastatin on the cholesterol content of lipoprotein subclasses in patients with type 2 diabetes and hypercholesterolaemia. Methods: This post hoc analysis compared the effects of treatment with ezetimibe/simvastatin 10/20 mg vs. atorvastatin 10 and 20 mg/day and ezetimibe/simvastatin 10/40 mg/day vs. atorvastatin 40 mg/day on the cholesterol content of lipoprotein subclasses in the modified intent‐to‐treat (mITT) population (n = 1013) and in subgroups of patients with triglyceride (TG) levels <200 mg/dl (n = 600) and ≥200 mg/dl (2.6 mmol/l) (n = 413). Results: Ezetimibe/simvastatin significantly reduced low‐density lipoprotein cholesterol (LDL‐C) subclasses LDL₁‐C, LDL₂‐C and LDL₃‐C; real LDL‐C (LDL‐C^r); intermediate‐density lipoprotein cholesterol (IDL‐C), IDL₁‐C, IDL₂‐C; very low‐density lipoprotein cholesterol (VLDL‐C), VLDL₃‐C; and remnant‐like lipoprotein cholesterol (RLP‐C) from baseline more than atorvastatin at all dose comparisons (p < 0.01) in the mITT population. Significant improvements were also observed in high‐density lipoprotein cholesterol (HDL‐C) subclass HDL₃‐C at the ezetimibe/simvastatin 10/20 mg vs. atorvastatin 20 mg and highest dose comparisons (p < 0.001) and in VLDL_{1 + 2}‐C at the lowest and highest dose comparisons (p < 0.001). Changes in LDL₄‐C and LDL‐C subclass patterns (A, B and I) were comparable for both treatments. Generally, similar results were observed for patients with TG levels <200 and ≥200 mg/dl (2.3 mmol). For both treatments, notable differences between TG subgroups were that patients with elevated TGs had smaller reductions in LDL₂‐C, slightly smaller decreases in all IDL subclasses and greater decreases in all VLDL‐C subclasses than those with lower TG levels. Frequency of pattern B was also reduced more in patients with higher TGs for both treatments. Conclusions: Ezetimibe/simvastatin reduced the cholesterol content of most lipoprotein subclasses from baseline with generally similar efficacy in patients with low and high TGs. Despite the different mechanism of action of ezetimibe, the response to ezetimibe/simvastatin and atorvastatin treatment related to these lipoprotein subclasses was generally consistent with the overall effects of these therapies on the major lipid/lipoprotein classes. The clinical significance of these results awaits further study.     

Effect of sitagliptin therapy on postprandial lipoprotein levels in patients with type 2 diabetes

Aim: Recent studies indicate that type 2 diabetes is associated with an increased secretion of both hepatic and intestinal lipoproteins, leading to the accumulation of atherogenic triglyceride (TG)‐rich lipoproteins. Sitagliptin is a selective inhibitor of dipeptidyl peptidase‐4 that has been shown to reduce fasting and postprandial glucose levels in patients with type 2 diabetes presumably through incretin hormone‐mediated improvements in islet function. The objective of the present study is to examine the effects of treatment with sitagliptin on postprandial lipid and incretin hormone levels as well as glucose homeostasis in patients with type 2 diabetes. Methods: Thirty‐six subjects with type 2 diabetes (30 men/6 postmenopausal women with a mean age of 58.1 ± 6.4 years and a body mass index of 30.7 ± 4.9 kg/m²) were recruited in this double‐blind cross‐over study using sitagliptin 100 mg/day or placebo for a 6‐week period each, with a 4‐week washout period between the two phases. At the end of each phase of treatment, patients underwent an oral lipid tolerance test providing 35 g of fat per m² of body surface area and blood samples were taken over an 8‐h period. Results: Sitagliptin therapy significantly decreased the postprandial area under the curves (AUCs) for plasma apolipoprotein (apo)B (?5.1%, p = 0.002), apoB‐48 (?7.8%, p = 0.03), TG (?9.4%, p = 0.006), very low‐density lipoprotein (VLDL)‐cholesterol (?9.3%, p = 0.001), free fatty acids (FFAs) (?7.6%, p = 0.005) and glucose (?9.7%, p < 0.0001). Furthermore, the postprandial AUCs for plasma intact glucagon‐like peptide‐1 (+67.8%, p < 0.0001) and glucose‐dependent insulinotropic polypeptide (+67.3%, p < 0.0001) were significantly increased following treatment with sitagliptin, whereas the AUC for plasma glucagon was reduced by ?9.7% (p = 0.001) with no significant changes in the AUCs for plasma insulin and C‐peptide. Sitagliptin therapy also improved homeostasis model assessment (HOMA) index for insulin resistance (?14.6%, p = 0.01) and β‐cell function (+32.3%, p = 0.007). Conclusions: Treatment with sitagliptin for 6 weeks reduced postprandial plasma levels of TG‐rich lipoproteins of both intestinal and hepatic origin, most likely by increasing incretin hormone levels, reducing circulating plasma FFA concentrations and improving insulin sensitivity and β‐cell function.     

普罗布考联合阿托伐他汀对高密度脂蛋白亚型和甘油三酯水平的影响

目的探讨普罗布考联合阿托伐他汀对急性冠状动脉综合征合并2型糖尿病惠者HDL-C亚型和TG水平的影响。方法选取急性冠状动脉综合征合并2型糖尿病患者120例,随机分为治疗组和对照组各60例,治疗组给予普罗布考500 mg,2次/d;阿托伐他汀20 mg,1次/晚;对照组给予阿托伐他汀20 mg,1次/晚。2组均常规使用硝酸酯类和抗血小板药物。治疗前及治疗3个月后分别检测TG、TC、LDL-C、HDL-C、HDL_2、HDL_3。结果与治疗前比较,治疗3个月后,2组患者TG、TC、LDL-C均有下降(P<0.05),治疗组下降更为明显(P<0.01),治疗组患者HDL-C和HDL_2明显下降,HDL_3、HDL_3/HDL-C明显升高(P<0.05),对照组HDLC明显升高(P<0.05)。与对照组治疗后比较,治疗组TG、TC、LDL-C、HDL-C、HDL_2明显下降(P<0.05),HDL_3、HDL_3/HDL-C明显升高(P<0.05)。结论普罗布考联合阿托伐他汀治疗急性冠状动脉综合征合并2型糖尿病,可更好降低TG、TC、LDL-C,虽然同时HDL-C总量有所下降,但逆向转运TC能力更强的HDL_3却增加。     

Effects of high dose aleglitazar on renal function in patients with type 2 diabetes

Background

Aleglitazar is a new, balanced dual peroxisome proliferator-activated receptor (PPAR)α/γ agonist designed to optimize lipid and glycemic benefits and minimize PPAR-related adverse effects.

Methods

SESTA R was a 26-week, randomized, double-blind, multicenter study comparing the effects of a supratherapeutic dosage of aleglitazar (600 μg/day) with pioglitazone (45 mg/day) on change in measured GFR (mGFR) in 174 patients with type 2 diabetes and normal to mildly impaired renal function (estimated GFR [eGFR] 60 to 120 ml/min/1.73 m²).

Results

In 118 patients with evaluable GFR measurements, baseline mean (± SD) mGFR was 97.6 ± 17.5 ml/min/1.73 m² in the aleglitazar group and 101.9 ± 21.6 ml/min/1.73 m² in the pioglitazone group. Mean percent change from baseline mGFR was −16.9% (90% confidence interval −22.0 to −11.5) with aleglitazar and −4.6% (−10.15 to 1.35) with pioglitazone, a mean treatment difference of −13.0% (−19.0 to −6.5). The 17% decrease from baseline in mGFR was consistent with the 19% decrease in eGFR Modification of Diet in Renal Disease (MDRD) observed with aleglitazar, which reached a plateau after 4 weeks, with no further progression until treatment discontinuation. Following aleglitazar withdrawal, eGFR values returned to pretreatment levels within the 4-8-week follow-up, which suggests reversible hemodynamic changes in renal function.

Conclusions

Despite the increased incidence of expected, dose-dependent PPAR class side effects (e.g., peripheral edema, weight gain, and congestive heart failure) limiting further development of this supratherapeutic dosage of aleglitazar (600 μg/day), these data, together with the data from the dose-ranging SYNCHRONY study, suggest aleglitazar may be a potential new treatment for cardiovascular risk reduction in post-acute coronary syndrome patients at the therapeutic 150 μg daily dose.     

The effect of cimetidine and ranitidine on serum high density lipoprotein subfractions

Of the two major subfractions of high density lipoprotein (HDL), HDL2 cholesterol (HDL2-C) and not HDL3 cholesterol (HDL3-C) correlates negatively with coronary heart disease. To study the effect of cimetidine and ranitidine on HDL subfractions, 6 healthy males received cimetidine (600 mg bid) ranitidine (150 mg bid) and placebo (one tab bid) for 1 week each, in random order. Measurements of HDL cholesterol (HDL-C), HDL2-C, HDL3-C were made on day 7 of each week. Comparing cimetidine with placebo, HDL2-C/HDL-C, HDL2-C/total cholesterol and HDL2-C/HDL3-C increased significantly while HDL3-C/HDL-C decreased. There was no difference in HDL-C parameters between ranitidine and placebo. Cimetidine treatment results in redistribution of HDL subfractions in favour of HDL2. The mechanism is not H2-receptor antagonism as ranitidine had no such effect.     

The effect of cholestyramine on lipoprotein lipids in patients with primary type IIA hyperlipoproteinemia.

The effect of 3 months' treatment with cholestyramine on lipoprotein lipids was investigated in 12 patients. VLDL, LDL and HDL were separated by preparative ultracentrifugation. There was a significant decrease of serum cholesterol and phospholipids and an increase of serum triglycerides. All the VLDL-lipids increased by nearly 30%. The LDL-lipids decreased with a tendency for normalisation of their atypical lipid composition. The small but significant alterations of HDL triglycerides and cholesterol are correlated with the corresponding alterations of the other lipoproteins; the HDL-phospholipids were unchanged. The LDL/HDL-lipid ratios were decreased but not normalised. The 30% decrease of LDL-cholesterol is negatively correlated with an increase in all the VLDL-lipids.     

The effect of intensive dietary therapy on serum high density lipoprotein cholesterol in patients with type 2 (non-insulin-dependent) diabetes mellitus: A prospective study

Summary Intensive dietary therapy in 57 newly diagnosed Type 2 (non-insulin-dependent) diabetic patients led to an increase, compared with pre-treatment levels, in serum high density lipoprotein (HDL) cholesterol and the HDL/total cholesterol ratio after 3 and 6 months (0.05相似文献   

High-density lipoprotein subspecies between patients with type 1 diabetes and type 2 diabetes without / with intensive insulin therapy

The reduced levels of high-density lipoprotein (HDL) 2-cholesterol (C) in diabetes and other metabolic disorders associated with a high risk of cardiovascular disease are well established. Few studies, however, have compared the HDL subspecies in type 1 diabetes (T1D) with those in type 2 diabetes (T2D) with or without insulin. We examined HDL subspecies in 27 T1D with insulin, 33 T2D with insulin or insulin plus oral-anti-diabetic drugs (OADs), 36 T2D with OADs or diet/exercise, and 25 non-diabetic controls. Insulin was injected four times daily in a basal-bolus manner for both T1D and T2D. Plasma levels of C, apolipoprotein (apo) AI, and AII were determined in HDL2 and HDL3 by the single precipitation method. HDL-C levels were significantly higher in T1D and lower in T2D, compared with the controls. Insulin-treated T2D had higher HDL-C than non-insulin-treated T2D. T1D had higher HDL2-C and HDL2-apo AI levels than T2D. Insulin-treated T2D had higher HDL2-C and HDL2-apo AI levels than non-insulin-treated T2D. All of these differences were more pronounced for men than for women. HDL3 levels were comparable among controls,T1D and T2D. HDL2-C levels were inversely associated with BMI, HbA1c, triglyceride, small dense LDL-C, and LDL-C. Multiple regression analysis revealed that HDL2-C was independently associated with triglyceride, LDL-C, and intensive insulin therapy but not with HbA1c. In conclusion, these results suggest that intensive insulin therapy is associated with alterations of HDL subspecies, irrespective of the type of diabetes.     

The effect of atorvastatin on serum lipids and lipoproteins in patients with homozyous familial hypercholesterolemia undergoing LDL-apheresis therapy

The efficacy of atorvastatin, a new hydroxymethylglutaryl (HMG)-CoA reductase inhibitor, in reducing serum lipid levels, modifying lipoprotein composition, and suppressing cholesterol synthesis was evaluated in patients with homozygous familial hypercholesterolemia (homozygous FH) undergoing LDL-apheresis therapy. Atorvastatin was given in escalating doses (10, 20, and 40 mg/day) to nine patients with homozygous FH. Five of nine patients responded well to atorvastatin; four of these patients were receptor-defective and the remaining one was receptor-negative. The change in LDL-cholesterol in the receptor-defective patients averaged -20.6% compared to the baseline level at the highest dose of atorvastatin. Of five receptor-negative type patients, only one showed good response to atorvastatin therapy with a LDL-cholesterol reduction of 14.9%. Although the other four receptor-negative patients did not show a change in LDL-cholesterol, all of them exhibited a considerable increase in HDL-cholesterol. All patients showed reduced urinary excretion of mevalonic acid, suggesting that atorvastatin decreases LDL-cholesterol by inhibiting cholesterol biosynthesis even where LDL-receptor activity is not present. Atorvastatin also decreased serum triglycerides in both receptor-negative and defective patients, especially in the latter. As cholesterol level rebounds quickly after each apheresis procedure, a combination therapy using atorvastatin and apheresis may increase the efficacy of the apheresis treatment, improving cost-benefit effectiveness by reducing the frequency of the apheresis treatment.     

A renoprotective effect of low dose losartan in patients with type 2 diabetes

It has been reported that angiotensin II receptor blocker (ARB) improves proteinuria in diabetic patients. However, whether this is a direct effect of ARB or through lowering blood pressure is still controversial. The aim of this study is to determine the direct effect of ARB on diabetic nephropathy. Thirty-four type 2 diabetic patients with early kidney damage were divided into two groups: losartan group (n=17) and control group (n=17). In losartan group, low dose (25mg) of losartan was administered once daily for a year. Blood pressure at home, blood pressure at office and urinary albumin/creatinine ratio (UACR) were measured before and during the treatment. After a 1-year observation, the increment of UACR was significantly smaller in losartan group than that in control group [-23.8+/-13.7 mg/gCr vs. 15.9+/-13.2mg/gCr, mean+/-S.E.M., P=0.0114]. Mean blood pressure levels did not change before and during the observation period both in losartan group and control group, though only systolic blood pressure at home decreased slightly but significantly. There were no significant differences in the levels of HbA(1c), fasting plasma glucose, total cholesterol, triglyceride and body mass index between the two groups. The observed decrease in UACR in the losartan-treated group might be attributed to a direct renoprotective action in addition to a subtle decrease in systolic blood pressure at home.     

Vildagliptin therapy reduces postprandial intestinal triglyceride-rich lipoprotein particles in patients with type 2 diabetes

Aims/hypothesis We assessed the effects of vildagliptin, a novel dipeptidyl peptidase IV inhibitor, on postprandial lipid and lipoprotein metabolism in patients with type 2 diabetes.Subjects, materials and methods This was a single-centre, randomised, double-blind study in drug-naive patients with type 2 diabetes. Patients received vildagliptin (50 mg twice daily, n=15) or placebo (n=16) for 4 weeks. Triglyceride, cholesterol, lipoprotein, glucose, insulin, glucagon and glucagon-like peptide-1 (GLP-1) responses to a fat-rich mixed meal were determined for 8 h postprandially before and after 4 weeks of treatment.Results Relative to placebo, 4 weeks of treatment with vildagliptin decreased the AUC_0–8h for total trigyceride by 22±11% (p=0.037), the incremental AUC_0–8h (IAUC_0–8h) for total triglyceride by 85±47% (p=0.065), the AUC_0–8h for chylomicron triglyceride by 65±19% (p=0.001) and the IAUC_0–8h for chylomicron triglyceride by 91±28% (p=0.002). This was associated with a decrease in chylomicron apolipoprotein B-48 (AUC_0–8h, −1.0±0.5 mg l⁻¹ h, p=0.037) and chylomicron cholesterol (AUC_0–8h, −0.14±0.07 mmol l⁻¹ h, p=0.046). Consistent with previous studies, 4 weeks of treatment with vildagliptin also increased intact GLP-1, suppressed inappropriate glucagon secretion, decreased fasting and postprandial glucose, and decreased HbA_1c from a baseline of 6.7% (change, −0.4±0.1%, p<0.001), all relative to placebo.Conclusions/interpretation Treatment with vildagliptin for 4 weeks improves postprandial plasma triglyceride and apolipoprotein B-48-containing triglyceride-rich lipoprotein particle metabolism after a fat-rich meal. The mechanisms underlying the effects of this dipeptidyl peptidase IV inhibitor on postprandial lipid metabolism remain to be explored.     

Strong decrease of high sensitivity C-reactive protein with high-dose atorvastatin in patients with type 2 diabetes mellitus

OBJECTIVE: Statins are known to reduce CRP concentrations, but whether high doses are more effective is not known. METHODS: In a prospective double-blind multicenter study in 186 DM2 patients without manifest coronary artery disease and with dyslipidemia, the effect of a 30-week treatment with 10 and 80 mg atorvastatin or placebo on the reduction of hs-CRP levels was measured. RESULTS: Median CRP levels increased with 6.6% in the placebo group and were reduced by 15 and 47%, respectively, with atorvastatin 10 and 80 mg (P<0.001; significantly different from 10 mg atorvastatin and from placebo (P<0.001). Variation in IL-6 and plasma lipids associated for 21 and 8%, respectively, with variation in CRP levels (P<0.001 and P=0.01). Of patients with a baseline CRP level above an arbitrary threshold of 3.0 mg/l, 56% in the 80 mg atorvastatin group reached a level of less than 3.0 mg/l, versus 23% randomized to 10 mg atorvastatin (P<0.01) and 17% in the placebo group (P<0.005). CONCLUSIONS: In DM2 patients high dose atorvastatin induced a strong reduction in CRP levels. The decrease in CRP was mainly independent of effects on lipid lowering and changes in IL-6 levels. The pleiotropic effect of high-dose atorvastatin on inflammation could add to its cardioprotective effect in high-risk patients.     

Differential effect of atorvastatin and fenofibrate on plasma oxidized low-density lipoprotein, inflammation markers, and cell adhesion molecules in patients with type 2 diabetes mellitus

Type 2 diabetes mellitus is associated with elevated plasma triglyceride levels, low high-density lipoprotein cholesterol, and a high incidence of cardiovascular disease. Hydroxymethylglutaryl-coenzyme A reductase inhibitors and fibrates are frequently used in the treatment of diabetic dyslipidemia, but their specific impact on the inflammation processes involved in atherosclerosis remains to be fully characterized. The objective of this 2-group parallel study was to investigate the differential effects of a 6-week treatment with either atorvastatin 20 mg/d alone (n = 19) or micronized fenofibrate 200 mg/d alone (n = 19) on inflammation, cell adhesion, and oxidation markers in type 2 diabetes mellitus subjects with marked hypertriglyceridemia. In addition to the expected changes in lipid levels, atorvastatin decreased plasma levels of C-reactive protein (-26.9%, P = .004), soluble intercellular adhesion molecule 1 (-5.4%, P = .03), soluble vascular cell adhesion molecule 1 (-4.4%, P = .008), sE-selectin (-5.7%, P = .02), matrix metalloproteinase 9 (-39.6%, P = .04), secretory phospholipase A(2) (sPLA(2)) (-14.8%, P = .04), and oxidized low-density lipoprotein (-38.4%, P < .0001). On the other hand, fenofibrate had no significant effect on C-reactive protein levels and was associated with reduced plasma levels of sE-selectin only (-6.0%, P = .04) and increased plasma levels of sPLA(2) (+22.5%, P = .004). These results suggest that atorvastatin was potent to reduce inflammation, oxidation, and monocyte adhesion in type 2 diabetes mellitus subjects with marked hypertriglyceridemia, whereas fenofibrate decreased sE-selectin levels only and was associated with an elevation of sPLA(2) levels.