Peroxidative stress in diabetic blood vessels. Reversal by pancreatic islet transplantation

Pieper, Galen M.; Jordan, Milan; Dondlinger, L. A.; Adams, Mark B.; Roza, Allan M.

doi:10.2337/diabetes.44.8.884

Cited by 42 publications

(27 citation statements)

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“…Vascular reactivity to noradrenaline in the transplanted group remained unaltered, and was not significantly different to the controls. This is in agreement with the only other transplant study which has directly investigated the responses of rat blood vessels to contractile and relaxant agents (Pieper et al, 1995).…”

Section: Discussionsupporting

confidence: 78%

The effect of insulin treatment and of islet transplantation on the resistance artery function in the STZ‐induced diabetic rat

Heygate

Davies

Holmes

et al. 1996

British J Pharmacology

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1 This study was designed to investigate the influence of insulin treatment and islet transplantation on the smooth muscle contractility and endothelium-dependent and independent relaxation of resistance arteries in the chemically induced streptozotocin (STZ) diabetic rat after 6-8 weeks, and 12-14 weeks of diabetes, compared to non-diabetic age-matched controls. 2 The morphology, and contractile responses to high potassium physiological salt solution (KPSS), KPSS containing 10-M noradrenaline (NAK), and concentration-response curves to noradrenaline (NA) of mesenteric resistance arteries were recorded, along with the endothelium-dependent relaxation responses to acetylcholine (ACh) and bradykinin (BK), and endothelium-independent relaxation to sodium nitroprusside (SNP). Concentration-response curves were then repeated in the presence of a nitric oxide synthase inhibitor, NG-nitro-L-arginine (L-NOARG). 3 Insulin-treated diabetic rats in the 12 week study demonstrated enhanced vascular contractility to KPSS, NAK and NA, compared to age-matched non-diabetic controls. 4 Incubation with L-NOARG resulted in both a significant increase in maximum contractile response, and sensitivity (pD2) to NA in the untreated diabetic group (6 weeks). A significant shift in sensitivity was also seen in the insulin-treated diabetic group. In the 12 week study, incubation with L-NOARG resulted in an increased maximum contractile response and sensitivity to NA in the insulin-treated diabetics. An increase in sensitivity was also observed in the untreated diabetic group. 5 Endothelium-dependent relaxation to ACh was significantly augmented in the untreated diabetics (6-weeks), compared to the control group. In the 12-week study, relaxation to both ACh and BK was not significantly different in any of the experimental groups when compared to the sham-operated nondiabetic controls. 6 Incubation with L-NOARG resulted in a significant attenuation of the maximum relaxation response to ACh and BK in all of the experimental groups, in the 6-and the 12-week study. 7 There was no significant difference in the maximum relaxation response or sensitivity to sodium nitroprusside between the diabetic groups and their age-matched controls in either the 6-week or the 12-week study. 8 The results of this study suggest an enhanced release of nitric oxide in the early stages of diabetes, which is more evident in the untreated diabetic rats than the insulin treated, and appears to normalize as the duration of diabetes progresses. This study also shows that the alteration in vascular reactivity of the resistance arteries can be restored to within normal limits by the transplantation of islets of Langerhans, and that islet transplantation is an effective strategy in the correction of the metabolic abnormalities associated with insulin-dependent diabetes.

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Section: Discussionsupporting

confidence: 78%

The effect of insulin treatment and of islet transplantation on the resistance artery function in the STZ‐induced diabetic rat

Heygate

Davies

Holmes

et al. 1996

British J Pharmacology

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“…Thus, Amadori albumin can be associated with diabetic nephropathy, and it can be localised in retinal capillaries from diabetic patients [38]. Furthermore, all these studies are also consistent with the idea that oxidative stress observed in patients or diabetic animals is directly related to the metabolic control of the disease [33,34,35,36,37,38,46,47,48].…”

Section: Discussionsupporting

confidence: 71%

Early and intermediate Amadori glycosylation adducts, oxidative stress, and endothelial dysfunction in the streptozotocin-induced diabetic rats vasculature

et al. 2003

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Aims/hypothesis. In a model of streptozotocin-induced Type 1 diabetes mellitus in rats of 9 weeks duration, we analysed time associations between the development of hyperglycaemia, early and intermediate glycosylation Amadori adducts, or AGE compared with enhancement of oxidative stress and endothelial dysfunction.Methods. Endothelial function was tested at several stages of streptozotocin-induced diabetes and after treatment with insulin, resulting in different concentrations of blood glucose, glycosylated haemoglobin (an Amadori adduct), and AGE. Other animals were studied antagonising the formation of AGE with aminoguanidine. Results. Relaxation in response to acetylcholine (1 nmol/l to 10 µmol/l) was tested in isolated segments from aorta or mesenteric microvessels. Impairment of endothelium-dependent relaxations occurred after 2 weeks of untreated diabetes. Preincubation of vessels affected with 100 U/ml superoxide dismutase improved the relaxations to acetylcholine, along the time-course of the endothelial impairment. This indicates the participation of reactive oxygen species on diabetic endothelial dysfunction. The impairment of endothelium-dependent relaxations was recovered after 3 more weeks of insulin treatment. Aminoguanidine treatment did not modify this pattern of development. The time course of the rise and disappearance of endothelial dysfunction showed a higher correlation with glycosylated haemoglobin concentrations than with blood glucose or serum AGE. Conclusion/interpretation. Enhancement of early and intermediate Amadori adducts of protein glycosylation was the factor showing a better relation with the development of endothelium impairment. These results are consistent with a role for these products in the development of diabetic vasculopathy. [Diabetologia (2003) 46:556-566] Keywords Diabetes mellitus, endothelial dysfunction, nitric oxide, superoxide anions, hyperglycaemia, Amadori adducts, advanced glycosylation end-products. Endothelial dysfunction seems to be a key factor in the development of diabetic vascular complications. The impairment of endothelium-dependent vasodilatations is an early event occurring in diabetic patients [1,2,3] and animal diabetic models [4,5,6, 7]. Enhanced oxidative stress in diabetes mellitus has been also shown [8,9], which can be detected by peroxidation products [10] or by increased generation of reactive oxygen species (ROS), mainly superoxide anions [11]. Indeed, enhanced oxidative stress is proposed to be a major cause of diabetic endothelial dysfunction [12,13].There is also increasing evidence that diabetic endothelial dysfunction and oxidative stress are a conse-

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“…The pancreatic levels of lipid peroxides significantly decreased within 48 hr, and the low levels were maintained for 2 weeks. According to the report of Pieper et al (6), in streptozotocin-induced diabetes, a distal metabolite to hydrogen peroxide (e.g., hydroxyl radicals) may be an important mediator of tissue damage. We repeated the experiments in which the catalase activ ities were measured together with the lipid peroxide levels 2 weeks and 7 weeks after streptozotocin injection (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…In diabetes, catalase, in particular, is important to scavenge hydrogen peroxides that may be generated under diabetic conditions. Pieper et al (6) have reported a significant increase in catalase activity, but not superoxide dismutase and glutathione peroxidase in dia betic vasculature. They have concluded that hydrogen peroxide is a major determinant of diabetic tissue damage.…”

mentioning

confidence: 99%

Lipid Peroxidation in the Pancreas and Other Organs in Streptozotocin Diabetic Rats

Tatsuki

Satoh

Yamamoto

et al. 1997

Japanese Journal of Pharmacology

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Peroxidative stress in diabetic blood vessels. Reversal by pancreatic islet transplantation

Cited by 42 publications

References 0 publications

The effect of insulin treatment and of islet transplantation on the resistance artery function in the STZ‐induced diabetic rat

The effect of insulin treatment and of islet transplantation on the resistance artery function in the STZ‐induced diabetic rat

Early and intermediate Amadori glycosylation adducts, oxidative stress, and endothelial dysfunction in the streptozotocin-induced diabetic rats vasculature

Lipid Peroxidation in the Pancreas and Other Organs in Streptozotocin Diabetic Rats

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