1999
DOI: 10.1016/s0026-0495(99)90237-8
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Meal-induced oxidative stress and low-density lipoprotein oxidation in diabetes: The possible role of hyperglycemia

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Cited by 175 publications
(113 citation statements)
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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: 99%
“…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%
“…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%
“…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%