Relationships between plasma measures of oxidative stress and metabolic control in NIDDM

Nourooz‐Zadeh, Jaffar; Rahimi, A.; Tajaddini-Sarmadi, Javad; Tritschler, Hans; Rösen, P.; Halliwell, Barry; Betteridge, D. J.

doi:10.1007/s001250050729

Cited by 262 publications

(132 citation statements)

References 47 publications

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“…Our results are consistent with those of other studies on antioxidant status of diabetic patients (Collier et al 1990;Altomare et al 1992;Gallou et al 1993). Antioxidant molecule, GSH, significantly decreased as shown in other studies (Giugliano et al 1996;Nourooz-Zadeh et al 1997). Sundaram et al (1996) confirm the relationship between the period of illness and GSH depletion.…”

Section: Discussionsupporting

confidence: 93%

Lipid Peroxidation and Resistance to Oxidation in Patients with Type 2 Diabetes Mellitus

Paşaoğlu

Sancak

Bukan

2004

Tohoku J. Exp. Med.

100

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We investigated lipid peroxidation, resistance of plasma and red blood cells to oxidation, and antioxidant defense system in erythrocytes and sera in patients with type 2 diabetes mellitus. One group included newly diagnosed 20 patients and the other included 20 patients treated with oral antidiabetic agents (OAD). Twenty healthy subjects served as controls. Serum and red blood cell malondialdehyde (MDA), glutathione (GSH), resistance to oxidation, and plasma thiol (total -SH) levels were measured. In addition, glycated hemoglobin, serum fructosamine, uric acid, total protein, total cholesterol, triglyceride and glucose levels were determined. Although newly diagnosed patients had higher serum and erythrocyte MDA levels than those of controls, the highest levels of MDA were determined in patients treated with OAD. MDA levels after exposing to oxidation increased in OAD group more than in newly diagnosed patients. Total -SH and erythrocyte GSH levels of the both diabetic groups were lower than controls. These results show that serum and erythrocyte lipid peroxidation was increased in diabetic patients. The sera of the patients showed a decreased resistance against oxidation. We therefore suggest that the effect of increased free radicals may be prevented by antioxidant systems in early stages of type 2 diabetes but in advanced stages this relationship is impaired owing to decreased antioxidant activity. Decreased red blood cell GSH and serum total -SH levels may be due to a compensation mechanism of the antioxidants. diabetes mellitus; lipid peroxidation; antioxidants

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Section: Discussionsupporting

confidence: 93%

Lipid Peroxidation and Resistance to Oxidation in Patients with Type 2 Diabetes Mellitus

Paşaoğlu

Sancak

Bukan

2004

Tohoku J. Exp. Med.

100

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“…This can be explained by the fact that HbA 1c is a "mean" evaluation of glycemic control and reflects, only in part, glycemic fluctuations, such as postprandial hyperglycemia or disglycemia states, which may induce a pro-oxidative status and may play a significant role in the pathogenesis of diabetic complications (10,11,25). In fact, a recent prospective study by Berg et al (26) showed that intensive insulin treatment can reduce the increased ROOH levels in type 1 diabetic patients.…”

Section: Results -As Shown Inmentioning

confidence: 99%

“…There is currently great interest in the potential role of increased oxidative stress in the development of diabetic complications (8,9). In patients with diabetes, oxidative stress seems to be caused by both increased production of plasma reactive oxygen species and reduction of antioxidant defenses (10), with a consequent increase in lipid peroxidation (11,12) and oxidized LDLs, which are more atherogenic than native LDLs (13). Some authors observed increased oxidative stress in early stages of type 1 diabetes in children and adolescents (14) Recently, we demonstrated in patients with well-controlled type 1 diabetes that total plasma antioxidant capacity (TRAP) was significantly lower and that two different markers of lipid peroxidation, such as conjugated dienes (CDs) and lipid hydroperoxides (ROOHs), were significantly augmented (15).…”

mentioning

confidence: 99%

Early Increase of Oxidative Stress and Reduced Antioxidant Defenses in Patients With Uncomplicated Type 1 Diabetes

et al. 2002

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OBJECTIVE -Diabetes increases the risk of coronary heart disease (CHD) to a greater extent in women than in men. We investigated whether type 1 diabetic patients with short duration of disease and without complications have an altered oxidative status and whether there are differences between men and women.RESEARCH DESIGN AND METHODS -We investigated oxidative status in 29 control subjects and 37 patients with uncomplicated type 1 diabetes with duration of 6 Ϯ 3 years.RESULTS -Compared with control subjects, type 1 diabetic patients had lower total plasma antioxidant capacity (TRAP) (720.3 Ϯ 111.2 vs. 972.5 Ϯ 97.7 mol/l in men, P Ͻ 0.001; 579.8 Ϯ 95.4 vs. 930.1 Ϯ 84.2 in women, P Ͻ 0.001), higher lipid hydroperoxide (ROOH) levels (6.4 Ϯ 2.2 vs. 2.0 Ϯ 0.7 mol/l in men, P Ͻ 0.001; 8.1 Ϯ 1.9 vs. 2.2 Ϯ 0.6 in women, P Ͻ 0.001), higher total conjugated diene (CD) levels (0.037 Ϯ 0.003 vs. 0.033 Ϯ 0.002 A.U. in men, P Ͻ 0.001), lower 246-nm CD levels (0.0032.Ϯ 0.0010 vs. 0.0070 Ϯ 0.0012 A.U. in men, P Ͻ 0.001; 0.0022 Ϯ 0.0011 vs. 0.0072 Ϯ 0.0014 A.U. in women, P Ͻ 0.001), and higher 232-nm CD levels (0.0348 Ϯ 0.0041 vs. 0.0257 Ϯ 0.0022 A.U. in men, P Ͻ 0.001; 0.0346 Ϯ 0.0031 vs. 0.0246 Ϯ 0.0074 A.U. in women, P Ͻ 0.001). Compared with diabetic men, diabetic women had lower TRAP (P Ͻ 0.01), higher ROOH levels (P Ͻ 0.01), and lower 246-nm CD levels (P Ͻ 0.05). Plasma concentration of uric acid was significantly lower in patients with type 1 diabetes than in control subjects (3.3 Ϯ 0.3 vs. 4.3 Ϯ 0.2 mg/dl; P ϭ 0.009) with a significant difference between women and men with type 1 diabetes (2.6 Ϯ 0.3 vs. 3.9 Ϯ 0.3, respectively; P ϭ 0.009).CONCLUSIONS -Our findings suggest that reduced antioxidant activity and increased oxidative stress occur early after the diagnosis of type 1 diabetes, especially in women, and this might explain, at least in part, the increased susceptibility of diabetic women to cardiovascular complications.

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“…come mainly from clinical studies that correlated oxidative stress variables with the metabolic control of patients [2,3]. Other studies reported potential metabolic effects of pharmacological doses of various antioxidative agents given to healthy volunteers or to diabetic subjects [4±6].…”

mentioning

confidence: 99%

Lipoic acid protects against oxidative stress induced impairment in insulin stimulation of protein kinase B and glucose transport in 3T3-L1 adipocytes

et al. 1999

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Oxidative stress has been recently implicated in the pathogenesis of various diseases. Consequently, the potential therapeutic or preventive effects of antioxidative agents has been raised [1]. Both poorly controlled Type I (insulin-dependent) diabetes mellitus as well as Type II (non-insulin-dependent) diabetes mellitus are characterized by reduced capacity of peripheral tissues (i. e. skeletal muscle and adipose tissue) to respond to the metabolic effects of insulin. The causes and cellular mechanisms responsible for this abnormality are still not fully understood despite intense investigative effort. Several lines of evidence suggest that increased oxidative stress occurs in diabetes and could have a role in the development or deterioration of peripheral insulin resistance. These Diabetologia (1999) Abstract Aims/hypothesis. Oxidative stress has been shown to impair insulin-stimulated glucose transporter 4 translocation in 3T3-L1 adipocytes. This study explores the potential of the antioxidant lipoic acid to protect the cells against the induction of insulin resistance when given before exposure to oxidative stress. Methods. 3T3-LI were exposed for 16 h to lipoic acid after which cells were exposed for 2 h to continuous production of H 2 O 2 by adding glucose oxidase to the culture medium. Results. These conditions resulted in a 50±70 % reduction in insulin-stimulated glucose transport activity associated with a decrease in reduced glutathione content from 37.4 ± 3.1 to 26.4 ± 4.9 nmol/mg protein, (p < 0.005). Lipoic acid pretreatment increased insulin-stimulated glucose transport following oxidative stress, reaching 84.8 ± 4.4 % of the control, associated with an increase in reduced glutathione content. Oxidation impaired the 4.89 ± 0.36-fold insulin-stimulated increase in glucose transporter 4 content in plasma membrane lawns of control cells. Lipoic acid pretreatment was, however, associated with preserved insulin-induced glucose transporter 4 translocation in cells exposed to oxidation, yielding 80 % of its content in controls. Although tyrosine phosphorylation patterns were not affected by lipoic acid pretreatment, insulin-stimulated protein kinase B/Akt serine 473 phosphorylation and activity were considerably impaired by oxidation but protected by lipoic acid pretreatment. A protective effect was not observed with either troglitazone, its isolated vitamin E moiety, or with vitamin C. Conclusion/interpretation. This study shows the ability of lipoic acid to provide partial protection against the impaired insulin-stimulated glucose transporter 4 translocation and protein kinase B/Akt activation induced by oxidative stress, potentially by its capacity to maintain intracellular redox state. [Diabetologia (1999) 42: 949±957]

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Relationships between plasma measures of oxidative stress and metabolic control in NIDDM

Cited by 262 publications

References 47 publications

Lipid Peroxidation and Resistance to Oxidation in Patients with Type 2 Diabetes Mellitus

Lipid Peroxidation and Resistance to Oxidation in Patients with Type 2 Diabetes Mellitus

Early Increase of Oxidative Stress and Reduced Antioxidant Defenses in Patients With Uncomplicated Type 1 Diabetes

Lipoic acid protects against oxidative stress induced impairment in insulin stimulation of protein kinase B and glucose transport in 3T3-L1 adipocytes

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