Association Between Postprandial Remnant-like Particle Triglyceride (RLP-TG) Levels and Carotid Intima-Media Thickness (IMT) in Japanese Patients with Type 2 Diabetes: Assessment by Meal Tolerance Tests (MTT)

Utsunomiya University, Totigi, Tochigi, Japan
Endocrine (Impact Factor: 3.88). 11/2005; 28(2):157-63. DOI: 10.1385/ENDO:28:2:157
Source: PubMed


Our study evaluated the relationship between the pathologic changes associated with atherosclerosis, as primarily represented by postprandial remnant-like lipoproteins and carotid intima-media thickness (IMT), in type 2 diabetic patients. Meal tolerance tests (MTT) were performed in 68 patients with type 2 diabetes. The subjects were divided by pre-meal and 2-h postprandial triglyceride (TG) levels into the normotriglyceridemia (NTG) group; the postprandial hypertriglyceridemia (PHTG) group; and the fasting hypertriglyceridemia (FHTG) group. HOMA-R values were significantly higher in the FHTG group than in the NTG group, with the plasma pre-heparin LPL mass and serum adiponectin levels in the FHTG and PHTG groups significantly lower than in the NTG group. One- and two hour postprandial RLP-TG levels were significantly higher in the PHTG group than in the NTG group, while there was no significant difference in postprandial glucose levels between the two groups. The IMT values were significantly higher in both the FHTG and PHTG groups than in the NTG group. Logistics regression analysis of the 1- and 2-h RLP-TG values using IMT as an induced variable showed the odds ratio for high IMT values to be 5.17 (p < 0.05) for the 1-h RLP-TG values and 3.01 (p = 0.105) for the 2-h RLP-TG values. Our study results suggest that delayed TG metabolism leading to the retention of remnants in type 2 diabetic patients appears to be closely associated with atherosclerosis, and that postprandial hyperlipidemia is an independent risk factor for the early onset of atherosclerosis.

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    • "Thus we suppose that the increase of lipidic charge in postprandial test could induce a significant hypertriglyceridemia during meal absorption and higher probability to measure a bicarbinated water effect. Moreover a strong association has been reported between postprandial triglyceridemia and early atherosclerosis markers [6,7,28] which suppose that fasting triglyceridemia is tightly dependent on the postprandial lipemia. Indeed, as soon as 1979, Zilversmit proposed that atherosclerosis was a postprandial phenomenon [29]. "
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    ABSTRACT: During postprandial state, TG concentration is increasing and HDL cholesterol decreasing, leading to a transitory pro-atherosclerotic profile. Previous studies have reported that bicarbonate water improve postprandial lipemia. The objective of this study was to analyze the effect of a strongly bicarbonated mineral water on lipoprotein levels during fasting and postprandial state. A controlled, randomised, double-blind cross-over design was conducted in 12 moderately hypercholesterolemic subjects after a daily ingestion of 1.25 L of mineral (SY) or low mineral water during eight weeks separated by a one week wash-out period. Blood samples were collected in first visit to the hospital (V1) before water consumption (referent or SY) and in a second visit (V2) after eight week water consumption period. The effect of the consumed water was studied in fasting and in postprandial state during ingestion of a meal and 0.5 L of water. No difference was observed between SY and referent water consumption for measured parameters at fasting and postprandial state. Comparison of data between V1 and V2 after SY consumption showed a significant decrease in triglyceridemia (23%), VLDL TG(31%) and tendency to a decrease of VLDL cholesterol (p = 0.066) at fasting state. Whatever the consumed water during postprandial state, the measurement of total areas under curves did not show a significant difference. Although this study did not show any difference between the two waters, we showed a decrease of basal TG and VLDLTG when subjects consumed SY. In discussion section, we discussed the unexpected absence of effect of high mineralized water on postprandial lipemia.
    Full-text · Article · Jul 2013 · Lipids in Health and Disease
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    • "In order to investigate TG intolerance caused by a variety of factors including heterozygous LPL-deficiency [60], insulin resistance, noninsulin-dependent diabetes mellitus (NIDDM) [61], and ApoE isoforms [62] we determined ApoE genotypes, and HL and LPL activities. "
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    ABSTRACT: The relationship between CETP and postprandial hyperlipemia is still unclear. We verified the effects of varying activities of plasma CETP on postprandial lipemia and precocious atherosclerosis in asymptomatic adult women. Twenty-eight women, selected from a healthy population sample (n = 148) were classified according to three CETP levels, all statistically different: CETP deficiency (CETPd ≤ 4.5%, n = 8), high activity (CETPi ≥ 23.8, n = 6) and controls (CTL, CETP ≥ 4.6% and ≤ 23.7%, n = 14). After a 12 h fast they underwent an oral fat tolerance test (40 g of fat/m² of body surface area) for 8 hours. TG, TG-rich-lipoproteins (TRL), cholesterol and TRL-TG measurements (AUC, AUIC, AR, RR and late peaks) and comparisons were performed on all time points. Lipases and phospholipids transfer protein (PLTP) were determined. Correlation between carotid atherosclerosis (c-IMT) and postprandial parameters was determined. CETP TaqIB and I405V and ApoE-ε3/ε2/ε4 polymorphisms were examined. To elucidate the regulation of increased lipemia in CETPd a multiple linear regression analysis was performed. In the CETPi and CTL groups, CETP activity was respectively 9 and 5.3 higher compared to the CETPd group. Concentrations of all HDL fractions and ApoA-I were higher in the CETPd group and clearance was delayed, as demonstrated by modified lipemia parameters (AUC, AUIC, RR, AR and late peaks and meal response patterns). LPL or HL deficiencies were not observed. No genetic determinants of CETP deficiency or of postprandial lipemia were found. Correlations with c-IMT in the CETPd group indicated postprandial pro-atherogenic associations. In CETPd the regression multivariate analysis (model A) showed that CETP was largely and negatively predicted by VLDL-C lipemia (R² = 92%) and much less by TG, LDL-C, ApoAI, phospholipids and non-HDL-C. CETP (model B) influenced mainly the increment in ApoB-100 containing lipoproteins (R² = 85% negatively) and phospholipids (R² = 13%), at the 6(th)h point. The moderate CETP deficiency phenotype included a paradoxically high HDL-C and its sub fractions (as earlier described), positive associations with c-IMT, a postprandial VLDL-C increment predicting negatively CETP activity and CETP activity regulating inversely the increment in ApoB100-containing lipoproteins. We hypothesize that the enrichment of TG content in triglyceride-rich ApoB-containing lipoproteins and in TG rich remnants increases lipoproteins' competition to active lipolysis sites,reducing their catabolism and resulting on postprandial lipemia with atherogenic consequences.
    Full-text · Article · May 2011 · Lipids in Health and Disease
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    • "In 21-year follow-up in the young Finns study which started in 1980 in children then ages 3 to 18 years, type IIB dyslipidemia was related to CIMT [21]. Mori et al [35] have reported a significant association between postprandial TG levels and CIMT in Japanese patients with type 2 diabetes mellitus. Shoji et al [36] reported that small dense LDL was the best marker of carotid IMT, along with TG. "
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    ABSTRACT: To assess relationships between pediatric lipids and subsequent cardiovascular disease (CVD) in the fourth to fifth decades, we conducted 22- to 31-year follow-up studies (1998-2003) in former schoolchildren first studied in 1973-1976. The follow-up included 53% of eligible former subjects. We compared pediatric and adult body mass (in kilograms per square meter) and lipids in 19 cases with at least 1 CVD event and in 789 CVD event-free subjects. Mean +/- SD age was 12.3 +/- 3.3 years at entry and 38.5 +/- 3.8 years at follow-up. Mean age at the first CVD event was 37.1 +/- 4.9 years. The major novel finding of our study was that childhood triglycerides (TG) were consistently and independently associated with young adult CVD. The distributions of both childhood and adult TG were shifted to higher levels in the cases than controls. Of the 19 cases, 7 (37%) had childhood TG greater than the pediatric 95th percentile (153 mg/dL); and 6 of these 7 had high TG (>/=150 mg/dL) at adult follow-up. Overall, 61% of cases had high TG as adults. After adjusting for age, sex, and race, by analysis of variance, cases had higher TG levels both in childhood and in young adulthood. A bootstrapping method and the Cox proportional hazard analysis were used to predict CVD in the cohort with explanatory variables sex; race; childhood body mass index, low-density lipoprotein, log high-density lipoprotein cholesterol, and log TG; and adult cigarette smoking and type 2 diabetes mellitus. Childhood TG level was a significant, independent explanatory variable for young adult CVD hazard (hazard ratio, 5.35; 95% confidence interval, 1.69-20.0 for each 1-unit increase in natural logarithm scale) along with adult type 2 diabetes mellitus (hazard ratio, 19.4; 95% confidence interval, 4.24-114.2). Pediatric hypertriglyceridemia appears to be a significant, independent, potentially reversible correlate of young adult CVD.
    Full-text · Article · Jun 2009 · Metabolism: clinical and experimental
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