α-Dicarbonyls Increase in the Postprandial Period and Reflect the Degree of Hyperglycemia

Beisswenger, Paul J.; Howell, Scott K.; O’Dell, Rita M.; Wood, Mary E.; Touchette, Allison D.; Szwergold, Benjamin S.

doi:10.2337/diacare.24.4.726

Cited by 165 publications

(142 citation statements)

References 65 publications

(36 reference statements)

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“…This suggests involvement of additional oxidative mechanisms in its formation. In patients with type 1 diabetes, Beisswenger et al (31) observed an increase in 3DG within 2 h, whereas in our pilot study in patients with type 2 diabetes we did not observe a rise in 3DG after the first meal (21).…”

Section: Figure 2-relations Between Postprandial Changes Of the Oxidicontrasting

confidence: 40%

Fasting and Postprandial Glycoxidative and Lipoxidative Stress Are Increased in Women With Type 2 Diabetes

Schindhelm¹,

Alssema

Scheffer

et al. 2007

Diabetes Care

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OBJECTIVE -We studied acute changes in markers of glycoxidative and lipoxidative stress, including oxidized LDL, N ε -(carboxyethyl)-lysine (CEL), N ε -(carboxymethyl)-lysine (CML), and 3-deoxyglucosone (3DG), following two consecutive meals. RESEARCH DESIGN AND METHODS -Postmenopausal women (27 with normal glucose metabolism [NGM], 26 with type 2 diabetes) received two consecutive fat-rich meals and two consecutive carbohydrate-rich meals on two occasions. Glucose and triglyceride concentrations were measured at baseline and 1, 2, 4, 6, and 8 h following breakfast; lunch was given at 4 h. Oxidized LDL-to-LDL cholesterol ratio, CEL, CML, and 3DG were measured at baseline and at 8 h.RESULTS -Fasting oxidized LDL-to-LDL cholesterol ratio, 3DG, and CML were higher in women with type 2 diabetes compared with women with NGM and were comparable to the postprandial values at 8 h in NGM. Postprandial rises in the oxidized LDL-to-LDL cholesterol ratio and 3DG were similar in both groups. However, the oxidized LDL-to-LDL cholesterol ratio increased more after the fat-rich meals, whereas CML and 3DG increased more after the carbohydrate-rich meals. After the fat-rich meals, the increase in the oxidized LDL-to-LDL cholesterol ratio correlated with postprandial triglycerides, whereas the increase in 3DG was correlated with postprandial glucose.CONCLUSIONS -The acute changes in markers of glycoxidative and lipoxidative stress in both type 2 diabetes and NGM suggest that postabsorptive oxidative stress may partly underlie the association of postprandial derangements and cardiovascular risk. Diabetes Care 30:1789-1794, 2007P atients with type 2 diabetes have an increased risk of cardiovascular disease (CVD) (1), which can only partly be explained by classical CVD risk factors such as hypertension, high LDL cholesterol, low HDL cholesterol, and smoking (2). In postmenopausal women compared with men, the relative risk of CVD conferred by type 2 diabetes is even higher (3). Zilversmit (4) postulated in 1979 that disturbances in postprandial metabolism may contribute to the excess risk of CVD due to postprandial elevations of glucose and triglyceride-enriched lipoproteins (5,6).Oxidative stress is regarded as a common pathway by which many of the classical CVD risk factors and postprandial dysmetabolism may initiate and promote atherosclerosis (7). Indeed, elevated levels of oxidized LDL are associated with an increased risk for CVD (8). Prolonged exposure to a high-fat diet has been shown to result in an increase in plasma levels of oxidized LDL (9). Another mechanism that might link postprandial dysmetabolism and the risk of CVD in patients with type 2 diabetes includes the formation of advanced glycation end products (AGEs), which are related to micro-and macrovascular complications (10). Two of the most studied AGEs, N ε -(carboxyethyl)lysine (CEL) and N ε -(carboxymethyl)lysine (CML), can be formed on proteins by both glycoxidation and lipid peroxidation pathways. ␣-Dicarbonyl compounds such as 3-deoxyglucosone (3DG), glyoxal,...

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Section: Figure 2-relations Between Postprandial Changes Of the Oxidicontrasting

confidence: 40%

Fasting and Postprandial Glycoxidative and Lipoxidative Stress Are Increased in Women With Type 2 Diabetes

Schindhelm¹,

Alssema

Scheffer

et al. 2007

Diabetes Care

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“…However, the possibility that postprandial hyperglycaemia increases oxidative stress and inflammation in healthy subjects has previously been reported [12,13]. Furthermore, evidence showing that modulation of postprandial hyperglycaemia by diet or an insulin analogue in type 2 diabetes [25][26][27], and by pramlintide [28] in type 1 diabetes, is accompanied by a significant decrease of oxidative stress, while nuclear factor kappa B activation is decreased when controlling postprandial hyperglycaemia by acarbose [24], convincingly suggests that the effect of S21403 on postprandial oxidative stress and inflammation is related to its ability to reduce postprandial hyperglycaemia.…”

Section: Discussionmentioning

confidence: 98%

Effects of S21403 (mitiglinide) on postprandial generation of oxidative stress and inflammation in type 2 diabetic patients

Assaloni

Ros

Quagliaro³

et al. 2005

Diabetologia

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Aim/hypothesis: Evidence suggests that postprandial hyperglycaemia may be a cardiovascular risk factor in diabetes. Oxidative stress and inflammation are involved in the pathogenesis of diabetic complications and previous studies have shown increased oxidative stress and inflammation in the postprandial phase in diabetic patients. The aim of the present study was to evaluate whether controlling postprandial hyperglycaemia with S21403 (mitiglinide) is accompanied by a reduced generation of oxidative stress and inflammation. Subjects and methods: Forty type 2 diabetic patients participated in the study. Two different breakfast-tests were performed in each patient, with placebo or S21403. Plasma nitrotyrosine, plasma malondialdehyde (MDA), oxidised LDL (oxLDL), plasma total radical-trapping antioxidant parameter (TRAP), IL-6, IL-18, TNF-α, plasma glucose and insulin were measured. Results: After the administration of S21403, 40 mg, a rapid stimulation of insulin secretion was observed, accompanied by a reduction of postprandial hyperglycaemia. With S21403, a significant decrease of either nitrotyrosine, MDA and oxLDL levels, and a preservation of plasma TRAP compared with placebo was found. Significant decreases of IL-6, IL-18 and TNF-α were also observed with S21403 compared with placebo. Conclusions/interpretation: This study shows that controlling postprandial hyperglycaemia with S21403 significantly improves the cluster of oxidative stress and inflammation markers that are increased in the postprandial state in diabetic patients.

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“…The recruitment of diabetic patients for this study has been described previously [10] and patient characteristics are summarised in Table 1. Twenty-one type 1 diabetic patients, with normal creatinine clearance (although three patients had microalbuminuria) and no other microvascular complications, and 12 normal healthy control subjects were recruited.…”

Section: Subjectsmentioning

confidence: 99%

“…Urinary and plasma creatinine were determined by colorimetric assay (diagnostic kit 510; Sigma). Fasting plasma glucose (FPG), mean daily plasma glucose (24hG) and postprandial changes in plasma glucose (PPG) were assessed as described previously [10].…”

Section: Measurement Of Protein Glycation Oxidation and Nitration Admentioning

confidence: 99%

Degradation products of proteins damaged by glycation, oxidation and nitration in clinical type 1 diabetes

et al. 2005

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Aims/hypothesis: Hyperglycaemia in diabetes is associated with increased glycation, oxidative stress and nitrosative stress. Proteins modified consequently contain glycation, oxidation and nitration adduct residues, and undergo cellular proteolysis with release of corresponding free adducts. These free adducts leak into blood plasma for eventual renal excretion. The aim of this study was to perform a comprehensive quantitative analysis of protein glycation, oxidation and nitration adduct residues in plasma protein and haemoglobin as well as of free adducts in plasma and urine to quantify increased protein damage and flux of proteolytic degradation products in diabetes. Methods: Type 1 diabetic patients (n=21) and normal healthy control subjects (n=12) were studied. Venous blood samples, with heparin anticoagulant, and 24-h urine samples were taken. Samples were analysed for protein glycation, oxidation and nitration adducts by a quantitative comprehensive screening method using liquid chromatography with triple quadrupole mass spectrometric detection. Results: In type 1 diabetic patients, the concentrations of protein glycation, oxidation and nitration adduct residues increased up to three-fold in plasma protein and up to one-fold in haemoglobin, except for decreases in pentosidine and 3-nitrotyrosine residues in haemoglobin when compared with normal control subjects. In contrast, the concentrations of protein glycation and oxidation free adducts increased up to ten-fold in blood plasma, and urinary excretion increased up to 15-fold in diabetic patients. Conclusions/interpretation: We conclude that there are profound increases in proteolytic products of glycated and oxidised proteins in diabetic patients, concurrent with much lower increases in protein glycation and oxidation adduct residues.

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α-Dicarbonyls Increase in the Postprandial Period and Reflect the Degree of Hyperglycemia

Cited by 165 publications

References 65 publications

Fasting and Postprandial Glycoxidative and Lipoxidative Stress Are Increased in Women With Type 2 Diabetes

Fasting and Postprandial Glycoxidative and Lipoxidative Stress Are Increased in Women With Type 2 Diabetes

Effects of S21403 (mitiglinide) on postprandial generation of oxidative stress and inflammation in type 2 diabetic patients

Degradation products of proteins damaged by glycation, oxidation and nitration in clinical type 1 diabetes

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