Association of postprandial hypertriglyceridemia and carotid intima-media thickness in patients with type 2 diabetes.

Abstract

OBJECTIVE -Serum triglyceride levels are important in the development of atherosclerosis. Although triglyceride levels are generally increased in the postprandial periods, the association between postprandial triglyceride (pTG) levels and atherosclerosis has not been investigated in diabetic patients. To investigate the role of pTG levels in atherosclerosis, we examined the correlation between pTG levels and carotid intimal-medial thickness (IMT).RESEARCH DESIGN AND METHODS -Carotid IMT was measured by ultrasonography in 61 patients with type 2 diabetes. Plasma glucose (PG), insulin, total cholesterol, triglycerides, and HDL cholesterol levels were measured after overnight fasting and 4 h after a meal.RESULTS -Carotid IMT of the patients with fasting hypertriglyceridemia was greater than that of the patients with normal fasting triglyceride (fTG) levels (0.85 ± 0.12 vs. 0.76 ± 0.14 mm; P = 0.02). The carotid IMT was increased in the patients with pTG levels Ͼ2.27 mmol/l. The normo-normo (NN) and normo-hyper (NH) groups consisted of patients with normal fTG levels but with pTG levels Ͻ2.27 and Ͼ2.27 mmol/l, respectively. Patients with both hypertriglyceridemia and pTG levels Ͼ2.27 mmol/l formed the hyper-hyper (HH) group. Carotid IMT was significantly increased in the NH (0.86 ± 0.13 mm) and HH (0.85 ± 0.12 mm) groups compared with the NN group (0.73 ± 0.13 mm; P Ͻ 0.01). Although postprandial PG, pTG, and fasting LDL cholesterol levels were all independently correlated with carotid IMT, pTG levels had the strongest statistical influence (P = 0.002).CONCLUSIONS -Postprandial hypertriglyceridemia despite normal fTG levels may be an independent risk factor for early atherosclerosis in type 2 diabetes.

Glycated and Oxidized Protein Degradation Products Are Indicators of Fasting and Postprandial Hyperglycemia in Diabetes

“…CML probably emerged as an indicator sensitive to PPG because oxidative stress enhanced in the postprandial period increased the rate of degradation of fructosyl-lysine to CML. Although we observed a strong relationship between urinary levels of dityrosine and mean glucose levels, the limited data on oxidative stress in this study, including measurement of 3-NT, dityrosine, and MetSO, did not confirm this hypothesis, although many other independent studies have shown that postprandial hyperglycemia and hyperlipidemia enhances oxidative stress (27)(28)(29)(30)(31). These findings are in contrast to the relative insensitivity of the Amadori product, represented by fructosyl-lysine residues of Hb or A1C (N␣-fructosyl-valine ϩ fructosyl-lysine residues), which were not significantly decreased by lispro treatment (Table 3 and [21]).…”

“…In recent studies we have found that postprandial methylglyoxal levels are significantly decreased by treatment with nateglinide in type 2 diabetes (37), suggesting that decreases in methylglyoxalderived AGEs may also occur with other treatments targeting postprandial glycemia. Since postprandial increases in ␣,␤-dicarbonyls and their associated AGEs can lead to direct cellular damage, decreasing their levels with lispro as well as decreasing postprandial oxidative lipemia and oxidative stress (27)(28)(29)31,38) could potentially lead to a reduction in longterm vascular complications.…”

Evidence for an Independent and Cumulative Effect of Postprandial Hypertriglyceridemia and Hyperglycemia on Endothelial Dysfunction and Oxidative Stress Generation

“…Postprandial hypertriglyceridemia may represent an independent predictor of CVD in nondiabetic patients 2 and may be a predictor of carotid intima-media thickness in patients with type 2 diabetes. 22 However, recent studies support the hypothesis that postprandial hyperglycemia also is a risk factor for CVD. 23 The concept that postprandial hypertriglyceridemia and hyperglycemia may be important factors for the development of CVD is supported by evidence that both induce endothelial dysfunction, 6 -9 whereas there is a broad consensus that abnormalities of endothelium-dependent arterial relaxation are an early marker of atherosclerosis 4 and may predict CVD.…”

Differential effect of pioglitazone (PGZ) and rosiglitazone (RGZ) on postprandial glucose and lipid metabolism in patients with type 2 diabetes mellitus: a prospective, randomized crossover study

“…Importantly, a number of studies have shown that postprandial lipaemia is linked to endothelial dysfunction and generation of oxidative stress in patients with T2Dm [13,14], that are well-established factors in the pathogenesis of atherosclerosis. In addition, a correlation between carotid intima-medial thickness and postprandial hypertriglyceridaemia has been shown despite normal fasting TGs [15]. Thus, the characteristics of postprandial lipid metabolism may be relevant for the development of atherosclerosis in patients with T2Dm.…”