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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of coronary artery (CAD) disease in the Indian urban population is comparable to British population. Dietary intakes, antioxidant vitamins, prevalence of risk factors and CAD, were studied in a random sample of 152 adult urban subjects between 26-65 years of age (80 males, 72 females) from Peerzada street, Moradabad and compared with Indian immigrants to U.K. and a British comparison group. There was no significant relation with vitamin A. Smoking and diabetes were the confounding factors. Plasma antioxidant vitamin C (21.6 +/- 3.3 vs 42.5 +/- 4.5 mumol/L), vitamin E (15.2 +/- 2.8 vs 21.4 +/- 3.2 mumol/L) and beta-carotene (0.33 +/- 0.6 vs 0.55 +/- 0.08 mumol/L) were significantly lowered and lipid peroxides higher (2.82 +/- 0.22 vs 1.3 +/- 0.20 nmol/ml) in patients with CAD compared to subjects without any risk factors. The relation between low plasma level of vitamin C and E levels and carotene remained independently and inversely related after adjustment for smoking, diabetes and other risk factors. Regression analysis showed that after adjustment. Odd's ratio for carotene (1.82, 95% C.I. 0.50 to 3.72), vitamin C (2.23, 95% C.I. 1.14 to 5.26) and vitamin E (2.35, 95% C.I. 1.29 to 5.30) were significantly related to CAD. Underlying these changes, dietary intake of vitamin A, E, C and beta-carotene was significantly less in patients with CAD. Vitamin C and beta-carotene intake were less in smokers and diabetes. Compared with British population, the Indian urbans consumed less total and saturated fat and cholesterol and more polyunsaturated fat and complex carbohydrates. The plasma total and low density lipoprotein cholesterol levels were less in Indian urbans compared to Britons and so were mean body weight, body mass index and waist-hip ratio. Plasma insulin levels were comparable. The fatty acid composition of the diet, blood lipids, central obesity and insulin levels do not appear to account for high rates of CAD among Indians. The findings suggest that urban population in India may benefit from eating diets rich in antioxidant vitamin C, E and beta-carotene.
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PMID:Diet, antioxidant vitamins, oxidative stress and risk of coronary artery disease: the Peerzada Prospective Study. 783 64

Abnormal plasma ascorbic acid (AA) and dehydroascorbic acid (DHAA) levels observed in diabetes may be correlated to a deficiency in the recycling of AA. Ascorbic acid and DHAA levels are altered in diabetic liver in the present study. In addition, a coupling of the hexose monophosphate (HMP) shunt by way of NADPH to glutathione reductase and subsequent DHAA reduction is demonstrated. Ascorbic acid production was assayed directly and by way of the HMPS pathway. Results indicate that AA production from DHAA via the HMPS pathway occurs, and is significantly decreased in diabetic liver. Glucose-6-phosphate dehydrogenase (G6PDH) activity is shown to be decreased in diabetic liver. Since G6PDH is essential in providing NADPH for the reduction of glutathione required for subsequent DHAA reduction, its decreased activity is consistent with altered levels of AA and DHAA observed in diabetic tissues.
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PMID:Enzymatic basis for altered ascorbic acid and dehydroascorbic acid levels in diabetes. 846 10

Increased generation of reactive oxygen species, coupled with impaired endogenous scavenging mechanisms, plays a prominent role in the aetiology of neurovascular abnormalities in experimental diabetes mellitus. We examined the efficacy of the natural anti-oxidants vitamins C, E and beta-carotene in preventing nerve conduction and nutritive blood flow deficits in streptozotocin-diabetic rats. One month of diabetes caused a 19.1% reduction in sciatic motor conduction velocity (p < 0.001). This was approximately prevented 80-90% by high-dose (1000 mg.kg-1.day-1) vitamin E and beta-carotene treatments (p < 0.001). Vitamin C had lesser effects; the maximum protection found for motor conduction velocity was 36% using a dose of 150 mg.kg-1.day-1 (p < 0.001). High dose (500 mg.kg-1.day-1 (p < 0.001). High dose (500 mg.kg-1.day-1) vitamin C had a lesser effect on conduction than intermediate doses. Joint vitamin C and lower dose (500 mg.kg-1.day-1) vitamin E treatment had a predominantly additive preventive effect against nerve dysfunction. Resistance to hypoxic conduction failure for sciatic nerve in vitro was markedly increased by diabetes and this remained relatively unaffected by treatment. Sciatic nutritive endoneurial blood flow, measured using microelectrode polarography and hydrogen clearance, was reduced 46.1% by 1 month of diabetes (p < 0.001). This was prevented to the extent of 87%, 36% and 98% by vitamins E, C and beta-carotene, respectively (p < 0.01). These data emphasize the role of oxidative stress in the development of early neurovascular changes in experimental diabetes and show that naturally available scavengers have a neuroprotective action.
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PMID:Effects of natural free radical scavengers on peripheral nerve and neurovascular function in diabetic rats. 858 37

Increased lipid peroxidation and reduced antioxidant status may contribute to the development of complications in diabetes. The aim of this study was to assess the effects of dietary treatment of noninsulin-dependent diabetes on these parameters. Twenty patients with newly diagnosed noninsulin-dependent diabetes were recruited along with 20 age, sex, and smoking-status-matched control subjects. Dietary intake was assessed by food frequency questionnaire and 24-h dietary recall and blood collected for biochemical analyses before and 2 months after dietary treatment was initiated. Carbohydrate, fat, and protein intake fell in patients following dietary advice. Among micronutrients, intakes of vitamins C, E, and A, carotene, selenium, copper, zinc, and iron were similar in patients and controls. Vitamin C intake in patients rose following dietary advice (44.6 +/- 11.7 vs. 49.5 +/- 5.5 mg/d, p < .05), while there was no change in intake of other micronutrients. Fasting plasma glucose in diabetic subjects fell from 13.6 +/- 1.1 mmol/l at recruitment to 9.7 +/- 1.1 mmol/l after diet (p < .01), and this was accompanied by a fall in hemoglobin Alc from 7.44 +/- 0.67% to 5.91 +/- 0.57% (p < .01). Serum malondialdehyde was higher in patients than controls at T0 (2.39 +/- 0.55 mumol/l vs. 1.48 +/- 0.33; p < .01), and fell following diet to 1.42 mumol/l (p < 0.01). Ascorbate was lower in patients than controls (1.27 +/- 2.9 mumol/k vs. 41.4 +/- 9.3; p < .01) at baseline and rose after diet to 27.8 +/- 6.4 (p < .01). beta-Carotene also rose after diet in patients (0.13 +/- 0.04 mumol/l vs. 0.17 +/- 0.04; p < 0.05), as did lipid corrected alpha-tocopherol (4.39 +/- 1.09 mumol/mmol cholesterol vs. 5.16 +/- 1.18; p < .05). Reduced lipid peroxidation and improved antioxidant status may be one mechanism by which dietary treatment contributes to the prevention of diabetic complications.
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PMID:The effect of dietary treatment on lipid peroxidation and antioxidant status in newly diagnosed noninsulin dependent diabetes. 889 76

This paper reviews the scientific evidence regarding the vitamin C status of people with diabetes mellitus and whether they might have increased dietary vitamin C requirements. English language articles published from 1935 to the present that either compare ascorbic acid concentrations of persons with and without diabetes mellitus or assess the impact of vitamin C supplementation on various health outcomes among persons with diabetes mellitus were examined. Most studies have found people with diabetes mellitus to have at least 30% lower circulating ascorbic acid concentrations than people without diabetes mellitus. Vitamin C supplementation had little impact on blood glucose concentrations, but was found to lower cellular sorbitol concentrations and to reduce capillary fragility. Much of the past research in this area has been methodologically weak. To further understand the relation of ascorbic acid and diabetes mellitus, randomized clinical trials of ascorbic acid supplementation should be a high priority for research.
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PMID:Does diabetes mellitus increase the requirement for vitamin C? 891 39

The effect of vitamin C supplementation on hepatic cytochrome P450 expression was investigated in streptozotocin (STZ) diabetic male Wistar Albino rats. STZ-treated rats displayed the usual characteristics of diabetes including; hyperphagia, polydipsia, decreased body weight gain and also the increased expression and activity of hepatic CYP1A, 2B, 2E and 4A proteins. Vitamin C administration in drinking water (2% w/v) was associated with significant decreases in the levels of hyperglycaemia (P < 0.05), glycosylated haemoglobin (P < 0.05), hyperlipidaemia (P < 0.001), and hyperketonaemia (P < 0.001) associated with STZ-diabetes. Vitamin C-treatment selectively reduced the activity and expression of CYP2E proteins (P < 0.001). These effects on CYP2E expression may be mediated by the reduced levels of circulating ketone bodies, however, a direct effect on CYP2E expression in diabetes cannot be discounted.
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PMID:Effect of vitamin C supplementation on hepatic cytochrome P450 mixed-function oxidase activity in streptozotocin-diabetic rats. 900 94

Alloxan diabetic rats supplemented with vitamin C (ascorbic acid) orally in drinking water had increased plasma and liver ascorbic acid as compared to unsupplemented diabetic rats. The levels of liver reduced glutathione also increased in vitamin C supplemented diabetic rats as compared to non-supplemented diabetic rats. Vitamin C supplementation did not have any effect in reducing increased liver lipid peroxidation in diabetic rats. The results of the present study suggest that diabetes results in decreased levels of protective antioxidant species and vitamin C is effective to some extent in maintaining levels of plasma and liver ascorbic acid and liver reduced glutathione.
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PMID:Effect of vitamin C supplementation on oxidative stress in experimental diabetes. 933 71

A brief description of the phenomenon of nonenzymatic glycosylation will be presented, some examples given from the literature and then a brief summary of the results of laboratory research conducted in this area by myself and coworkers since 1981. Excessive glycosylation causes undesirable changes in proteins. Such glycosylation also occurs to collagen in oral tissue. In a study on induced experimental diabetes in rats we observed a defective platelet aggregation curve for gingival collagen. Glycosylation of proteins is known to result in functional defects, for example hemoglobin acquires an increased affinity for oxygen. Glycosylation of rat and bovine lens crystallins has been reported as being an important genesis of cataracts in diabetes. Increased glycosylation of submandibular collagen has been shown to occur in diabetes. However collagen from normal subjects has also been found to show an age related advanced glycosylation end product pigment. Increased platelet membrane protein glycosylation has been reported and the hyperaggregation typically observed in these cases thought to be due to glycosylation. The presence of red cell membrane proteins has also been reported and the impairment of red cell function in diabetes has been reported in cases of excessive glycosylation. According to some investigators cataract formation is prevented by some specific drug which inhibits the glycosylation of lens crystallins. Vitamin C has lowering effects on nonenzymatic glycation. Dentists should take into account the possibility of glycosylation of oral proteins such as collagen in cases of impaired gingiva tooth connection.
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PMID:Nonenzymatic glycosylation of tissue and blood proteins. 956 11

The tissue concentration of lipid hydroperoxides, which was determined by a specific method involving chemical derivatization and HPLC, increased significantly in the heart, liver, kidney and muscle of diabetic rats 8 weeks after the intraperitoneal injection of streptozotocin compared with that of the control group. These results demonstrate that an enhanced oxidative stress is caused in these tissues by diabetes. Vitamin C concentrations of the brain, heart, lung, liver, kidney and plasma of the diabetic rats decreased significantly after 8 weeks compared with those of the control group. Vitamin E concentrations of the brain, heart, liver, kidney, muscle and plasma of the diabetic rats increased significantly after 4 weeks compared with the control group. After 8 weeks, an elevation in vitamin E concentration was observed in the heart, liver, muscle and plasma of the diabetic rats.
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PMID:Change in tissue concentrations of lipid hydroperoxides, vitamin C and vitamin E in rats with streptozotocin-induced diabetes. 991 99

Ascorbic acid, or vitamin C, has been reported to lower erythrocyte sorbitol concentrations, and present studies were performed to determine the mechanism of this effect. Incubation of erythrocytes with increasing concentrations of glucose (5-40 mM) progressively increased erythrocyte sorbitol contents, reflecting increased flux through aldose reductase. At extracellular concentrations of 90 microM, both ascorbic acid and its oxidized form, dehydroascorbate, decreased intracellular sorbitol by 25 and 45%, respectively. This inhibition was not dependent on the extracellular glucose concentration, or on erythrocyte contents of free NADPH or GSH. To test for a direct effect of ascorbate on aldose reductase, erythrocyte hemolysates were prepared and supplemented with 100 microM NADPH. Hemolysates reduced glucose to sorbitol in a dose-dependent manner that was inhibited with a Ki of 120 microM by the aldose reductase inhibitor tetramethylene glutaric acid. Above 100 microM, ascorbic acid also lowered hemolysate sorbitol generation by about 30%. Studies with ascorbic acid derivatives showed that the reducing capacity of ascorbic acid was not required for inhibition of sorbitol production from glucose in erythrocyte hemolysates. These results show that high, but physiologic, concentrations of ascorbic acid can directly inhibit erythrocyte aldose reductase, and provide a rationale for the use of oral vitamin C supplements in diabetes.
Diabetes Res Clin Pract 1999 Jan
PMID:Inhibition of aldose reductase in human erythrocytes by vitamin C. 1019 83


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