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• W2046217897 abstract "Microalbuminuria (MA) is an independent risk factor for atherosclerosis in patients with type 2 diabetes mellitus (T2DM). Postprandial lipemia is also associated with excess cardiovascular risk. However, the association between MA and postprandial lipemia in diabetes has not been investigated. A total of 64 patients with T2DM, 30 with and 34 without MA, were examined. Plasma total triglycerides (TGs), triglycerides contained in chylomicrons (CM-TG), and TGs in CM-deficient plasma were measured at baseline and every 2 h for 6 h after a mixed meal. Postheparin LPL and HL activities were also determined. Plasma levels of apolipoprotein A-V (apoA-V), apoC-II, and apoC-III were measured in the fasting state and 2 h postprandially. Patients with MA had higher postprandial total TG levels than those without MA (P < 0.001); this increase been attributed mainly to CM-TG. LPL activity and fasting concentrations of the measured apolipoproteins were not different between the studied groups, whereas HL activity was higher in the patients with MA. ApoC-II and apoC-III levels did not change postprandially in either study group, whereas apoA-V increased more in the patients with MA. These data demonstrate for the first time that MA is characterized by increased postprandial lipemia in patients with T2DM and may explain in part the excess cardiovascular risk in these patients. Microalbuminuria (MA) is an independent risk factor for atherosclerosis in patients with type 2 diabetes mellitus (T2DM). Postprandial lipemia is also associated with excess cardiovascular risk. However, the association between MA and postprandial lipemia in diabetes has not been investigated. A total of 64 patients with T2DM, 30 with and 34 without MA, were examined. Plasma total triglycerides (TGs), triglycerides contained in chylomicrons (CM-TG), and TGs in CM-deficient plasma were measured at baseline and every 2 h for 6 h after a mixed meal. Postheparin LPL and HL activities were also determined. Plasma levels of apolipoprotein A-V (apoA-V), apoC-II, and apoC-III were measured in the fasting state and 2 h postprandially. Patients with MA had higher postprandial total TG levels than those without MA (P < 0.001); this increase been attributed mainly to CM-TG. LPL activity and fasting concentrations of the measured apolipoproteins were not different between the studied groups, whereas HL activity was higher in the patients with MA. ApoC-II and apoC-III levels did not change postprandially in either study group, whereas apoA-V increased more in the patients with MA. These data demonstrate for the first time that MA is characterized by increased postprandial lipemia in patients with T2DM and may explain in part the excess cardiovascular risk in these patients. Macrovascular complications are the leading cause of morbidity and mortality in patients with type 2 diabetes mellitus (T2DM) (1Stamler J. Vaccaro O. Neaton J.D. Wentworth D. Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial..Diabetes Care. 1993; 16: 434-444Crossref PubMed Scopus (3566) Google Scholar). Microalbuminuria (MA) is common (prevalence rates of 10–48%) and is a well-established risk factor for macrovascular diseases in patients with T2DM (2Schmitz A. Vaeth M. Microalbuminuria: a major risk factor in non-insulin-dependent diabetes. A 10-year follow-up study of 503 patients..Diabet. Med. 1988; 5: 126-134Crossref PubMed Scopus (437) Google Scholar, 3Dinneen S.F. Gerstein H.C. The association of microalbuminuria and mortality in non-insulin-dependent diabetes mellitus. A systematic review of the literature..Arch. Intern. Med. 1997; 157: 1413-1418Crossref PubMed Scopus (0) Google Scholar). A number of abnormalities have been described in diabetic patients with MA, including high blood pressure, dyslipidemia, insulin resistance, endothelial dysfunction, left ventricular hypertrophy, hypercoagulation, and high plasma homocysteine as well as C-reactive protein levels (4MacIsaac R.J. Cooper M.E. Microalbuminuria and diabetic cardiovascular disease..Curr. Atheroscler. Rep. 2003; 5: 350-357Crossref PubMed Scopus (10) Google Scholar), all of which increase the cardiovascular risk in this group of patients.Diabetic dyslipidemia is common in T2DM and is characterized by high levels of fasting triglycerides (TGs), low HDL cholesterol levels, and predominance of small, dense LDL cholesterol particles (5Syvanne M. Taskinen M.R. Lipids and lipoproteins as coronary risk factors in non-insulin dependent diabetes mellitus..Lancet. 1997; 350 (Suppl. 1): 20-23Abstract Full Text Full Text PDF Google Scholar, 6Betteridge D.J. Diabetic dyslipidaemia..Eur. J. Clin. Invest. 1999; 29 (Suppl. 2): 12-16Crossref PubMed Scopus (42) Google Scholar). Moreover, the majority of patients with T2DM show high and prolonged postprandial lipemia after meals (7Katsilambros N. Postprandial triglyceridaemia..Diabet. Med. 1995; 12: 451-452Crossref PubMed Scopus (11) Google Scholar, 8De Man F.H. Cabezas M.C. Van Barlingen H.H. Erkelens D.W. de Bruin T.W. Triglyceride-rich lipoproteins in non-insulin-dependent diabetes mellitus: post-prandial metabolism and relation to premature atherosclerosis..Eur. J. Clin. Invest. 1996; 26: 89-108Crossref PubMed Scopus (108) Google Scholar, 9Ginsberg H.N. Zhang Y.L. Hernandez-Ono A. Regulation of plasma triglycerides in insulin resistance and diabetes..Arch. Med. Res. 2005; 36: 232-240Crossref PubMed Scopus (365) Google Scholar). Epidemiological data suggest that high plasma TG levels, both in the fasting state and postprandially, are associated with cardiovascular diseases in patients with diabetes (10Boquist S. Ruotolo G. Tang R. Bjorkegren J. Bond M.G. de Faire U. Karpe F. Hamsten A. Alimentary lipemia, postprandial triglyceride-rich lipoproteins, and common carotid intima-media thickness in healthy, middle-aged men..Circulation. 1999; 100: 723-728Crossref PubMed Scopus (216) Google Scholar, 11Fontbonne A. Eschwege E. Cambien F. Richard J.L. Ducimetiere P. Thibult N. Warnet J.M. Claude J.R. Rosselin G.E. Hypertriglyceridaemia as a risk factor of coronary heart disease mortality in subjects with impaired glucose tolerance or diabetes. Results from the 11-year follow-up of the Paris Prospective Study..Diabetologia. 1989; 32: 300-304Crossref PubMed Scopus (616) Google Scholar).LPL is the key enzyme involved in the metabolism of TG-rich lipoproteins (12Otarod J.K. Goldberg I.J. Lipoprotein lipase and its role in regulation of plasma lipoproteins and cardiac risk..Curr. Atheroscler. Rep. 2004; 6: 335-342Crossref PubMed Scopus (74) Google Scholar). However, literature data on the activity of LPL in patients with MA are not unanimous: some studies found decreased plasma LPL activity in microalbuminuric subjects (13Kashiwazaki K. Hirano T. Yoshino G. Kurokawa M. Tajima H. Adachi M. Decreased release of lipoprotein lipase is associated with vascular endothelial damage in NIDDM patients with microalbuminuria..Diabetes Care. 1998; 21: 2016-2020Crossref PubMed Scopus (35) Google Scholar), whereas others found no difference in LPL activity between normoalbuminuric and microalbuminuric subjects (14Groot P.H. van Stiphout W.A. Krauss X.H. Jansen H. van Tol A. van Ramshorst E. Chin-On S. Hofman A. Cresswell S.R. Havekes L. Multiple lipoprotein abnormalities in type 1 diabetic patients with renal disease..Diabetes. 1996; 45: 974-979Crossref PubMed Google Scholar, 15Kahri J. Groop P.H. Elliott T. Viberti G. Taskinen M.R. Plasma cholesterol ester transfer protein and its relationship to plasma lipoproteins and apolipoprotein A-I-containing lipoproteins in IDDM patients with microalbuminuria and clinical nephropathy..Diabetes Care. 1994; 17: 412-419Crossref PubMed Scopus (27) Google Scholar). Reduced LPL activity in patients with T2DM and MA may result in enhancement in postprandial lipemia. However, the potential association between MA and postprandial lipemia has not been investigated to date.Therefore, the main aim of this study was to examine the association between MA and postprandial lipemia in patients with T2DM. In addition, potential differences in LPL and HL activity, as well as in apolipoprotein A-V (apoA-V), apoC-II, and apoC-III involved in TG metabolism, between patients with and without MA were also investigated.METHODSSubjectsA total of 64 patients with T2DM were examined. Patients were recruited from the outpatient diabetes clinic of our hospital. Subjects with diseases that may cause dyslipidemia (macroalbuminuria, abnormal liver or thyroid function) and those treated with medications affecting plasma lipids (statins, fibrates, ezetimide), urinary albumin excretion (angiotensin-converting enzyme inhibitors, angiotensin receptor blockers), and LPL activity (heparin in the previous 3 months, glitazones) were excluded (16Nagashima K. Lopez C. Donovan D. Ngai C. Fontanez N. Bensadoun A. Fruchart-Najib J. Holleran S. Cohn J.S. Ramakrishnan R. et al.Effects of PPARγ agonist pioglitazone on lipoprotein metabolism in patients with type 2 diabetes mellitus..J. Clin. Invest. 2005; 115: 1323-1332Crossref PubMed Scopus (167) Google Scholar, 17Hirano T. Lipoprotein abnormalities in diabetic nephropathy..Kidney Int. 1999; 71: 22-24Abstract Full Text Full Text PDF Google Scholar). To avoid the potential effect of smoking on plasma lipid levels, current smokers were also excluded. Equal numbers of patients in the two groups had been treated with diuretics and β-adrenergic blockers, drugs that may affect lipid metabolism. The protocol was approved by the ethics committee of our hospital, and written informed consent was obtained from all participants. Subjects were divided into two groups according to the presence or absence of MA.Procedures and anthropometric measurementsEach subject attended the metabolic unit of our hospital twice in the morning after a 12–14 h fast. The antidiabetic medications were given at the end of the visits in the unit. In the first visit, a fasting blood sample was taken 15 min after contralateral intravenous administration of heparin (30 IU/kg body weight; Leo Pharmaceuticals, Weesp, The Netherlands) for the determination of LPL and HL activities. After ∼1 week from the first visit, patients received a standard mixed meal consisting of four slices of toast bread, 225 g of a low-fat cheese, and 40 g of butter (total energy, 783 kcal: 52.5% as fat, 20% as protein, and 27.5% as carbohydrates, mainly as complex carbohydrates). Patients were permitted to consume only water during the study.Blood was drawn in the fasting state and at 2, 4, and 6 h after the test meal for biochemical determinations. After proper preparation, plasma samples were stored in small aliquots at −80°C until assayed at the end of the study.Weight and height were measured using standard methods. Body mass index (BMI) and waist-to-hip ratio (WHR) were measured and calculated. Absence of at least two of the four peripheral pulses in the feet, a history of intermittent claudication, ischemic rest pain, gangrene, any previous revascularization procedure at the aorta or the leg arteries, and ankle brachial index < 0.9 were all considered indications of the presence of peripheral vascular disease. Coronary artery disease was determined by resting 12 lead electrocardiography, from hospital records of myocardial infarction, and from history of angina or coronary revascularization procedure. Cerebrovascular disease was assessed by history, clinical examination, and hospital records of stroke. Arterial blood pressure was measured in the sitting position on three occasions with an interval of 1 min between determinations. The average of the last two of the three measurements was taken as the final blood pressure value.Biochemical parametersLPL and HL activities were measured in fasting, postheparin plasma samples by fluorometric assay using the Confluolip kit [Progen, Heidelberg, Germany; intra-assay coefficient of variation (CV) = 3.5%, interassay CV = 3.8%]. Briefly, 2 μl of plasma was used as the source of LPL or HL and was mixed with 200 μl of freshly reconstituted substrate. The assay was performed for 15 min at 37°C, and LPL and HL activities were determined by the increase in fluorescence intensity measured in a fluorescence spectrometer at an excitation wavelength of 342 nm and an emission wavelength of 400 nm (18Beauchamp M.C. Letendre E. Renier G. Macrophage lipoprotein lipase expression is increased in patients with heterozygous familial hypercholesterolemia..J. Lipid Res. 2002; 43: 215-222Abstract Full Text Full Text PDF PubMed Google Scholar).Chylomicrons (CMs) were isolated from plasma by ultracentrifugation as described previously (19Tentolouris N. Kolia M. Tselepis A.D. Perea D. Kitsou E. Kyriaki D. Tambaki A.P. Karabina S.P. Sala C. Fragoulopoulos E. et al.Lack of effect of acute repaglinide administration on postprandial lipaemia in patients with type 2 diabetes mellitus..Exp. Clin. Endocrinol. Diabetes. 2003; 111: 370-373Crossref PubMed Scopus (7) Google Scholar). CMs floating to the top of the tube were carefully aspirated with a Pasteur pipette. One milliliter of CM-deficient plasma was also carefully collected from the bottom of the tube.Plasma apoA-V concentrations were measured at baseline and at the time of the peak concentration of plasma TGs (2 h after the test meal) by Linco Diagnostic Services (St. Charles, MO) using a dual-antibody apoA-V sandwich ELISA (20O'Brien P.J. Alborn W.E. Sloan J.H. Ulmer M. Boodhoo A. Knierman M.D. Schultze A.E. Konrad R.J. The novel apolipoprotein A5 is present in human serum, is associated with VLDL, HDL, and chylomicrons, and circulates at very low concentrations compared with other apolipoproteins..Clin. Chem. 2005; 51: 351-359Crossref PubMed Scopus (180) Google Scholar). ApoC-II and apoC-III were determined at the same time intervals by immunoturbidimetry with antisera from Kamiya Biomedical Co. (Seattle, WA) with commercially available kits and according to the manufacturer's instructions on an Olympus AU 640 automated analyzer (Diamond Diagnostics, Holliston, MA).Plasma total cholesterol and creatinine levels were determined on a Technicon RA-XT analyzer (Technicon, Ltd., Dublin, Ireland). HDL cholesterol levels were measured by the same method in the supernatant of CM-deficient plasma after precipitation of apoB-containing lipoproteins by adding heparin and manganese chloride. LDL cholesterol levels were estimated using the equation of Friedewald, Levy, and Fredrickson (21Friedewald W.T. Levy R.I. Fredrickson D.S. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge..Clin. Chem. 1972; 18: 499-502Crossref PubMed Scopus (63) Google Scholar). Triglycerides in the chylomicron fraction (CM-TG), in total plasma, and in CM-deficient plasma (non-CM-TG) were determined on a Technicon RA-XT analyzer. Plasma levels of FFAs were measured by enzymatic colorimetric assay (Bayer; Boehringer Mannheim). Serum glucose was measured by colorimetric method GOD-PERID (Bayer; Boehringer Mannheim). Glycosylated hemoglobin A1c was measured by HPLC (Roche Diagnostics, Mannheim, Germany) with a nondiabetic reference range of 4.1–6.0%. MA was diagnosed when albumin excretion rate (AER), measured by RIA (Pharmacia and Upjohn Diagnostics AB, Uppsala, Sweden), was 30–300 mg/24 h in at least two of three 24 h urine collections over a 3 month period. Serum insulin levels were determined by RIA (Biosure, Brussels, Belgium). Glomerular filtration rate was calculated according to the equation of Cockcroft and Gault (22Cockcroft D. Gault M.H. Prediction of creatinine clearance from serum creatinine..Nephron. 1976; 16: 31-41Crossref PubMed Scopus (12989) Google Scholar). The homeostasis model assessment equation was used to calculate insulin resistance (HOMA-IR) (23Matthews D.R. Hosker J.P. Rudenski A.S. Naylor B.A. Treacher D.F. Turner R.C. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man..Diabetologia. 1985; 28: 412-419Crossref PubMed Scopus (25098) Google Scholar). Blood for the determination of fibrinogen was collected in tubes containing trisodium citrate (0.105 M) anticoagulant. The blood samples were immediately placed on melted ice and centrifuged at 1,700 g for 10 min at 4°C within 15 min after blood collection. Fibrinogen determination was performed using the Clauss method on a Sta Compact (Diagnostica Stago, Asnieres-Sur-Seine, France; intra-assay CV = 2.64%, interassay CV = 2.82%).Statistical analysisStatistical analysis was performed using programs available in the SPSS 10.0 statistical package. Student's t-test was used to compare parameters between patients with and without MA, and a Chi-square test was used for categorical variables. When data were skewed, logarithmic transformations were performed to improve normality for statistical testing and back-transformed for presentation in tables. One-way ANCOVA was used to assess differences in the tested variables, adjusting for the effect of confounding factors. ANOVA for repeated measurements was performed to test the timing effect of the studied parameters after the test meal. The Greenhouse-Geisser adjustment was used when the sphericity assumptions were not fulfilled. Postprandial responses over the 6 h period were calculated as incremental area under the curve (AUC) using the trapezoid rule. The AUCs adjusted for baseline values were calculated by subtracting the fasting value from each postprandial value before area calculation. A paired Student's t-test was used for comparison of the differences of the values of the studied parameters in the postprandial and the baseline state. Comparisons in the values of the AUCs between subjects with and without MA were performed using the Mann-Whitney U-test. Correlations between the study parameters are expressed as Pearson's or Spearman's bivariate correlation coefficient (r). P < 0.05 (two-tailed) was considered statistically significant.RESULTSBaseline comparisonsTable 1 summarizes the characteristics of the studied patients with and without MA. The two groups were matched for sex and age. Duration of diabetes and diabetes control were similar in the two groups. Microalbuminuric patients had higher BMI, waist, and WHR than normoalbuminuric patients. More normoalbuminuric patients were treated with diet alone compared with microalbuminuric patients, but this difference was not statistically significant. Blood pressure was slightly higher in the microalbuminuric group. Concerning macroangiopathic complications, prevalence rates of coronary artery disease and peripheral vascular disease were similar in the two groups. Plasma insulin concentrations and HOMA-IR values were higher in the microalbuminuric group (P < 0.01).TABLE 1Demographic and clinical characteristics of the study subjects stratified according to MA statusCharacteristicsWithout MA (n = 34)With MA (n = 30)PMale/female, n (%)17 (50.0)/17 (50.0)17 (56.7)/13 (43.3)0.59Age (years)61.5 ± 7.663.0 ± 6.70.40Body mass index (kg/m2)28.4 ± 5.730.8 ± 5.60.09Waist (cm)99.5 ± 12.0108.8 ± 11.30.002Waist-hip ratio0.92 ± 0.060.96 ± 0.080.05Systolic blood pressure (mmHg)131.9 ± 16.8135.7 ± 14.60.34Diastolic blood pressure (mmHg)77.9 ± 8.179.8 ± 8.90.38Glomerular filtration rate (ml/min)85.8 ± 24.596.4 ± 45.70.28Duration of diabetes (years)10.0 (1.0–18.3)10.5 (3.0–17.0)0.93Glycosylated hemoglobin A1c (%)7.4 ± 1.27.8 ± 1.20.18Treatment for diabetes, n (%) Diet alone6 (17.6)1 (3.3) Antidiabetic tablets19 (55.9)22 (73.3) Insulin9 (26.5)7 (23.3)0.1424 h urine albumin (mg/24 h)7.6 (1.8–11.5)68.8 (46.5–94.1)<0.001Insulin (pmol/l)47.9 (22.1–73.6)104.9 (79.8–114.6)<0.001Homeostasis model assessment equation insulin resistance index2.5 (1.3–4.2)6.1 (4.5–7.8)0.001Retinopathy, n (%) No24 (70.6)23 (76.7) Background7 (20.6)6 (20.0) Proliferative3 (8.8)1 (3.3)0.65Hypertension, n (%)11 (32.4)9 (30.0)0.83Coronary artery disease, n (%)3 (8.8)2 (6.7)0.74Peripheral vascular disease, n (%)1 (2.9)2 (6.7)0.48Use of β-adrenergic blockers, n (%)6 (17.6)3 (10.0)0.38Use of diuretics, n (%)7 (20.6)5 (16.7)0.68MA, microalbuminuria. Data are shown as means ± SD, n (%), or median (interquartile range). Open table in a new tab At baseline, plasma concentrations of glucose, total cholesterol, HDL cholesterol, LDL cholesterol, FFAs, total TGs, CM-TG, and non-CM-TG were not different between patients with and without MA (Table 2 , Fig. 1 ). However, patients with MA had higher plasma fibrinogen levels (Table 2).TABLE 2Fasting and postprandial profiles of the measured parameters in patients with (+) and without (−) MAParameterFasting2 h4 h6 hPP*Glucose (mmol/l)MA−8.82 ± 3.1612.89 ± 5.2511.63 ± 4.629.86 ± 3.99<0.00010.30MA+9.28 ± 2.9715.69 ± 4.9812.37 ± 5.229.89 ± 4.68<0.0001Insulin (pmol/l)MA−57.5 ± 62.8236.4 ± 138.8159.46 ± 120.281.40 ± 62.2<0.00010.03MA+105.7 ± 45.7409.5 ± 380.8256.48 ± 218.4114.52 ± 73.40.005Total cholesterol (mmol/l)MA−4.95 ± 0.844.89 ± 0.824.87 ± 0.804.92 ± 0.830.180.69MA+5.02 ± 0.845.01 ± 0.794.91 ± 0.865.02 ± 0.840.23Total TGs (mmol/l)MA−1.25 ± 0.611.47 ± 0.611.46 ± 0.611.46 ± 0.61<0.001<0.001MA+1.27 ± 0.511.96 ± 0.591.88 ± 0.721.48 ± 0.84<0.001CM-TG (mmol/l)MA−0.44 ± 0.310.64 ± 0.310.63 ± 0.360.51 ± 0.16<0.001<0.001MA+0.44 ± 0.241.08 ± 0.461.01 ± 0.430.64 ± 0.19<0.001Non-CM-TG (mmol/l)MA−0.81 ± 0.210.83 ± 0.210.83 ± 0.190.79 ± 0.170.040.36MA+0.83 ± 0.190.89 ± 0.240.86 ± 0.210.83 ± 0.220.001HDL cholesterol (mmol/l)MA−1.00 ± 0.171.00 ± 0.171.01 ± 0.181.00 ± 0.350.300.22MA+0.95 ± 0.220.94 ± 0.230.95 ± 0.230.95 ± 0.440.74LDL cholesterol (mmol/l)MA−3.58 ± 0.893.32 ± 0.693.21 ± 0.773.31 ± 0.900.0080.29MA+3.47 ± 0.663.00 ± 0.703.02 ± 0.843.18 ± 0.74<0.0001ApoA-V (ng/ml)MA−128.5 ± 49.8145.8 ± 48.3——0.060.01MA+132.0 ± 78.6168.1 ± 80.8<0.001ApoC-II (mg/dl)MA−3.41 ± 1.683.11 ± 1.64——0.180.58MA+3.77 ± 1.603.69 ± 1.560.56ApoC-III (mg/dl)MA−9.43 ± 2.948.75 ± 2.54——0.080.14MA+9.63 ± 3.159.60 ± 2.860.91Fibrinogen (g/l)MA−1.98 ± 0.561.97 ± 0.551.89 ± 0.521.96 ± 0.550.350.20MA+2.32 ± 0. 642.28 ± 0.712.26 ± 0.642.24 ± 0.710.36FFA (mmol/l)MA−0.293 ± 0.1500.188 ± 0.9140.161 ± 0.0990.186 ± 0.108<0.00010.26MA+0.327 ± 0.1380.208 ± 0.1220.192 ± 0.1130.215 ± 0.102<0.0001ApoA-V, apolipoprotein A-V; CM, chylomicron; CM-TG, triglycerides in chylomicron fraction; TG, triglyceride. Data are means ± SD. P indicates the result of ANOVA for repeated measurements within each group (P value for the effect of time); P* indicates the result of ANOVA for repeated measurements between the two groups (MA− vs. MA+) (time × group interaction). Open table in a new tab Postheparin LPL activity values (mean ± SEM) were not different between patients with and without MA (180.1 ± 24.3 vs. 165.6 ± 25.4 pmol/ml/h; P = 0.29). Postheparin HL activity values were higher in microalbuminuric than in normoalbuminuric patients (161.7 ± 21.0 vs. 88.2 ± 17.2 pmol/ml/h; P = 0.006). The ratio of HL to LPL activity values was also higher in patients with MA (0.89 ± 0.05 vs. 0.53 ± 0.04; P = 0.04).Fasting plasma apoA-V concentrations were not significantly different between patients with and without MA (P = 0.84). The same was valid for the plasma levels of apoC-II (P = 0.41) and apoC-III (P = 0.80) (Table 2) as well as the apoC-II/apoC-III ratio (0.39 ± 0.15 vs. 0.36 ± 0.12; P = 0.32).Comparisons in the postprandial stateAfter the meal, plasma glucose, insulin, total TGs, CM-TG, and non-CM-TG increased significantly compared with baseline values in both normoalbuminuric and microalbuminuric subjects; the increase was significantly higher in the microalbuminuric than in the normoalbuminuric group in all of these variables, except for glucose and non-CM-TG (Table 2, Fig. 1). On the contrary, plasma levels of LDL cholesterol as well as of FFAs decreased after the meal compared with baseline values; however, this decrease was not significantly different between the studied groups. Plasma concentrations of total cholesterol, HDL cholesterol, and fibrinogen did not change significantly from baseline after the meal in either study group (Table 2).Plasma apoA-V concentrations increased 2 h after the test meal compared with baseline values in the microalbuminuric patients (P < 0.001), whereas there was a trend towards an increase in the normoalbuminuric patients (P = 0.06) (Table 2). The percentage increase from the baseline was significantly higher in patients with MA than in those without MA [median value (interquartile range), 36.5% (18.6, 72.1) vs. 6.0% (−10.2, 31.5), respectively; P = 0.003]. On the contrary, plasma levels of apoC-II and apoC-III did not change significantly 2 h after the test meal compared with the baseline values in either study group; moreover, no significant differences were observed between patients with and without MA (Table 2).The incremental AUCs of total TGs and CM-TG were significantly higher in the patients with MA compared with those without MA (both P < 0.001) (Fig. 1). These differences remained significant (P < 0.001 for both AUCs of total TGs and CM-TG) even after adjustment for BMI, waist circumference, WHR, and HOMA-IR. The incremental AUC of non-CM-TG was higher in the microalbuminuric group, but this difference was not statistically significant (Fig. 1).Additionally, we looked for differences in AERs and postprandial lipemia between study subjects stratified according to the presence (n = 50) or absence (n = 14) of metabolic syndrome (MS) using the ATP III criteria (24Expert Panel. 2001. Executive summary of the third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). J. Am. Med. Assoc.285: 2486–2497.Google Scholar). Analysis showed that patients with MS had higher [median value (interquartile range)] AERs [49.1 (11.3, 82.5) vs. 27.0 (11.2, 50.0) mg/24 h; P = 0.01], AUC of total TGs [1.38 (0.72, 2.35) vs. 0.73 (0.27, 1.36) mmol/h/l; P = 0.004], and AUC of CM-TG [1.17 (0.60, 2.14) vs. 0.54 (0.17, 1.30) mmol/h/l; P = 0.02)]. The AUC of non-CM-TG was not different between the two groups [0.13 (−0.03, 0.24) vs. 0.04 (−0.09, 0.17) mmol/h/l; P = 0.14].Bivariate correlations and multivariate analysisIn the total study population, AER correlated significantly with the incremental AUCs of total TGs (r = 0.48, P = 0.002) and CM-TG (r = 0.43, P = 0.006) but not with the incremental AUC of non-CM-TG (r = 0.14, P = 0.38). LPL activity values did not correlate significantly with the values of the fasting total TGs, CM-TG, and non-CM-TG or with the incremental AUCs after the test meal of these same parameters. HL activity values showed a significant negative association with the values of the fasting non-CM-TG (r = −0.33, P = 0.03) but not with those of the fasting total TGs and CM-TG or with the values of the incremental AUCs of total TG, CM-TG, and non-CM-TG. In the fasting state, plasma apoC-II levels correlated significantly with fasting total TG (r = 0.49, P < 0.001), CM-TG (r = 0.26, P = 0.04), and non-CM-TG (r = 0.31, P = 0.01). Plasma apoC-III levels also correlated significantly with total TG (r = 0.61, P < 0.001), CM-TG (r = 0.51, P < 0.001) and non-CM-TG (r = 0.50, P < 0.001). However, fasting levels of apoC-II and apoC-III did not correlate significantly with the lipase activities or the postprandial AUCs of total TGs, CM-TG, and non-CM-TG. Furthermore, HOMA-IR correlated significantly with the incremental AUC of total TGs (r = 0.32, P = 0.01) and CM-TG (r = 0.28, P = 0.03); however, these relationships did not remain significant after controlling for the effect of MA. No significant associations were found between HOMA-IR and the incremental AUCs of non-CM-TG, LPL activity, and HL activity values.Multivariate linear regression analysis in the total sample population, after adjustment for MA status or AER, waist circumference, HOMA-IR, and MS status, demonstrated that the AUC of total TGs was independently and significantly associated only with the presence of MA [standardized regression coefficient (β) = 0.51, P < 0.001] and the degree of MA (β = 0.50, P < 0.001); the same was valid for the AUC of CM-TG (β = 0.51, P < 0.001 and β = 0.42, P = 0.02, respectively). The same analysis showed a suggestive association between the AUC of non-CM-TG and the degree of MA (β = 0.33, P = 0.07).DISCUSSIONThe novel finding of this study is that normotriglyceridemic patients with T2DM and MA have an almost 3-fold higher postprandial triglyceridemia than patients without MA after ingestion of a mixed test meal.Exaggerated postprandial lipemia is related to proatherogenic conditions, and clinical studies provide evidence that exposure to postprandial lipoproteins is associated with cardiovascular diseases (10Boquist S. Ruotolo G. Tang R. Bjorkegren J. Bond M.G. de Faire U. Karpe F. Hamsten A. Alimentary lipemia, postprandial triglyceride-rich lipoproteins, and common carotid intima-media thickness in healthy, middle-aged men..Circulation. 1999; 100: 723-728Crossref PubMed Scopus (216) Google Scholar, 11Fontbonne A. Eschwege E. Cambien F. Richard J.L. Ducimetiere P. Thibult N. Warnet J.M. Claude J.R. Rosselin G.E. Hypertriglyceridaemia as a risk factor of coronary heart disease mortality in subjects with impaired glucose tolerance or diabetes. Results from the 11-year follow-up of the Paris Prospective Study..Diabetologia. 1989; 32: 300-304Crossref PubMed Scopus (616) Google Scholar). A variety of in vitro and clinical studies suggest that postprandial CM and VLDL are associated with adverse effects on vascular endothelium (8De Man F.H. Cabezas M.C. Van Barlingen H.H. Erkelens D.W. de Bruin T.W. Triglyceride-rich lipoproteins in non-insulin-dependent diab" @default.
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• W2046217897 title "High postprandial triglyceridemia in patients with type 2 diabetes and microalbuminuria" @default.
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