Meal-induced oxidative stress and low-density lipoprotein oxidation in diabetes: The possible role of hyperglycemia

Ceriello, Antonio; Bortolotti, Nadia; Motz, Enrico; Pieri, Carlo; Marra, Michele; Tonutti, Laura; Lizzio, Sebastiano; Feletto, F.; Catone, Barbara; Taboga, C.

doi:10.1016/s0026-0495(99)90237-8

Cited by 176 publications

(115 citation statements)

References 35 publications

Supporting

Mentioning

108

Contrasting

Unclassified

Order By: Relevance

“…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: 99%

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

Assaloni

Ros

Quagliaro³

et al. 2005

Diabetologia

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

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

Assaloni

Ros

Quagliaro³

et al. 2005

Diabetologia

View full text Add to dashboard Cite

show abstract

“…The elevation of GGT could be expression of excess deposition of fat in liver (hepatic steatosis), and/or may reflect inflammation (Marchesini et al, 2001;Hotalamsligil, 2003;Malnick et al, 2003), both expressing the presence of oxidative stress and it plays a major role in pathological conditions such as inflammation, malignant diseases, aging, cardiovascular disease (Droge, 2002), and also in pathophysiology of diabetes (West, 2000;Haluzik and Nedvidkova, 2000;Rosen et al, 2001). A decrease in antioxidant capacity has been observed in the plasma of diabetic patients (Jones et al, 1988;Maxwell et al, 1997;Haluzik and Nedvidkova, 2000;Rosen et al, 2001), and evidence from numbers of experimental studies revealed that the formation of free radicals and presence of oxidative stress is a direct consequence of hyperglycemia (Diedrich et al, 1994;Graier et al, 1996;Ceriello et al 1999). So, we know that coffee contains many compounds, which may have potential to influence glucose metabolism process to prevent hyperglycemia and oxidative stress consequently.…”

Section: Discussionmentioning

confidence: 99%

Coffee consumption, serum γ-glutamyltransferase and risk of type II diabetes

Bidel

Silventoinen

et al. 2007

Eur J Clin Nutr

View full text Add to dashboard Cite

Objectives: To study the joint association of coffee consumption and serum g-glutamyltransferase (GGT) levels on the risk of developing type II diabetes. Design, setting and subjects: A total of 21 826 Finnish men and women who were 35-74 years of age and without any history of diabetes at baseline (years 1982, 1987, 1992 and 1997) were included in the present analyses. They were prospectively followed up for onset of type II diabetes (n ¼ 862 cases), death or until the end of the year 2002. Coffee consumption, serum GGT and other study parameters were determined at baseline using standardized measurements. Analyses were stratified by the serum GGT level classified into two classes using the 75th sex-specific percentiles as the cut point. Results: Coffee consumption was significantly and inversely associated with incident diabetes among both men and women. Serum GGT modified the association between coffee consumption and incident diabetes. Subjects in the high category of coffee consumption with the GGT level X75th percentile showed a significant inverse association for women, and for both sexes combined. The association was not significant in subjects with the GGT level p75th percentile. There was a significant interaction effect of GGT and coffee consumption on risk of type II diabetes in data of women (P ¼ 0.05) and in both sexes combined (P ¼ 0.02). Conclusions: Habitual coffee consumption is associated with lower incidence of type II diabetes particularly in those with higher baseline serum GGT levels.

show abstract

“…Diabetes has been associated with enhanced oxidative stress in several studies (Cominacini et al, 1994;Tsai et al, 1994; Beaudeux et al, Glycemic index in chronic disease LS Augustin et al 1995), although not in all (Jenkins et al, 1996;SanchezQuesada et al, 1996) and with reduced blood levels of antioxidants (Maxwell et al, 1997;Ceriello et al, 1998b). Recent findings suggest that metabolic processes following a meal may increase oxidative stress (Ceriello et al, 1999;Rao & Agarwal, 1999). A direct link has been found between postprandial glycemia and the induction of oxidative stress (Ceriello et al, 1998a(Ceriello et al, ,1999) that can be reversed by antioxidants (Paolisso et al, 1993(Paolisso et al, ,1994Sharma et al, 2000).…”

Section: Glycemic Index In Chronic Diseasementioning

confidence: 99%

“…Recent findings suggest that metabolic processes following a meal may increase oxidative stress (Ceriello et al, 1999;Rao & Agarwal, 1999). A direct link has been found between postprandial glycemia and the induction of oxidative stress (Ceriello et al, 1998a(Ceriello et al, ,1999) that can be reversed by antioxidants (Paolisso et al, 1993(Paolisso et al, ,1994Sharma et al, 2000). In this respect, possible mechanisms of action of low-GI diets include reduction of: (i) glucose toxicity, ie the effect of high glucose levels in depressing pancreatic function through free radical damage of pancreatic b cells; and (ii) glycosylation of proteins and key enzymes responsible for metabolic processes (advanced glycosylation end products -AGE, Paolisso et al, 1992;Ceriello, 2000).…”

Section: Glycemic Index In Chronic Diseasementioning

confidence: 99%

Glycemic index in chronic disease: a review

et al. 2002

View full text Add to dashboard Cite

Aim: The intent of this review is to critically analyze the scientific evidence on the role of the glycemic index in chronic Western disease and to discuss the utility of the glycemic index in the prevention and management of these disease states. Background: The glycemic index ranks foods based on their postprandial blood glucose response. Hyperinsulinemia and insulin resistance, as well as their determinants (eg high energy intake, obesity, lack of physical activity) have been implicated in the etiology of diabetes, coronary heart disease and cancer. Recently, among dietary factors, carbohydrates have attracted much attention as a significant culprit, however, different types of carbohydrate produce varying glycemic and insulinemic responses. Low glycemic index foods, characterized by slowly absorbed carbohydrates, have been shown in some studies to produce beneficial effects on glucose control, hyperinsulinemia, insulin resistance, blood lipids and satiety. Method: Studies on the short and long-term metabolic effects of diets with different glycemic indices will be presented and discussed. The review will focus primarily on clinical and epidemiological data, and will briefly discuss in vitro and animal studies related to possible mechanisms by which the glycemic index may influence chronic disease.

show abstract

Meal-induced oxidative stress and low-density lipoprotein oxidation in diabetes: The possible role of hyperglycemia

Cited by 176 publications

References 35 publications

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

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

Coffee consumption, serum γ-glutamyltransferase and risk of type II diabetes

Glycemic index in chronic disease: a review

Contact Info

Product

Resources

About