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Query: UMLS:C0011849 (
diabetes
)
277,896
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Physiological functions of skeletal muscle are compromised in
diabetes
. This may involve free radical mechanisms and may be reversed by antioxidants. We have studied effects of vitamin C on twitch tension, resting membrane potential (RMP) and miniature endplate potentials (MEPPs) frequencies in dorsiflexor muscle of diabetic murine. Forty mice were divided randomly into 2 groups (n = 20 each). One group served as control and the other was injected once with streptozotocin (STZ) solution (60 mg/kg, i.p.) to induce
diabetes
. The animals were then divided further into two subgroups (n = 10 each).
Vitamin C
(200 mg/kg, i.p.) was administered daily to one control and one diabetic group for three weeks prior to recording day. Experiments were conducted four weeks following
diabetes
induction. Isometric twitch tension (evoked directly by muscle stimulation and indirectly by nerve stimulation) was measured in urethane anesthetized (2 mg/g, i.p.) mice via a transducer connected to computer system. Utilizing intracellular recording method, resting membrane potential RMP and MEPPs frequencies were also measured. Compared to control, diabetic mice showed reduced twitch tension (4.2 +/- 0.5 g control versus 2.6 +/- 0.2 g diabetic) and demonstrated delayed half time of decay. Diabetic flexor muscle also displayed significant reduction in MEPPs frequencies with no changes in RMP.
Vitamin C
reversed tension reduction in diabetic mice (from 2.6 +/- 0.2 g to 3.9 +/- 0.3 g), impacted delayed half time of decay and increased MEPPs frequencies.
Vitamin C
improves
diabetes
-induced nerve and muscle dysfunction possibly via a free radical scavenging mechanism.
...
PMID:The impact of vitamin C on diabetes induced alterations at murine neuromuscular junction. 1210 89
Oxidative stress plays an important role in the chronic complications of insulin-dependent
diabetes mellitus
(IDDM). Hyperketonemia, as well as hyperglycemia, is involved in the generation of oxygen-free radicals. We have studied the degree of oxidative stress in six patients before, during, and after correction of diabetic ketoacidosis (DKA) by determining the plasma ratios of C20 and C18 fatty acids to C16 fatty acids in the cholesteryl esters of the lipoproteins as well as in the plasma concentrations of the antioxidant vitamins A, C, and E. Lipid peroxidation was slightly increased prior to treatment. However, the C20/C16 ratio at 120 h was significantly decreased in comparison to the ratio at pretreatment (P<.025), at 6-8 h (P<.005), and at 24 h (P<.025). The C18/16 ratio at 120 h was also decreased in comparison to the ratio at 6-8 h (P<.025), indicating an increase in lipid peroxidation after correction of DKA. Vitamin A was below normal at pretreatment and was increased at 120 h (P<.05).
Vitamin C
was normal at pretreatment and decreased to low normal at 24 h (P<.005). Vitamin E was normal at pretreatment and decreased to below normal at 24 and 120 h, although the changes were not statistically significant. These data demonstrate that there is an increase in lipid peroxidation after the correction of DKA and therefore support the position that administering antioxidant vitamins during the treatment of DKA could be beneficial in minimizing oxidative stress and possibly both the acute and chronic complications of IDDM.
J
Diabetes
Complications
PMID:Lipid peroxidation and antioxidant vitamins prior to, during, and after correction of diabetic ketoacidosis. 1212 88
Vitamin C
exists in two major forms. The charged form, ascorbic acid (AA), is taken up into cells via sodium-dependent facilitated transport. The uncharged form, dehydroascorbate (DHA), enters cells via glucose transporters (GLUT) and is then converted back to AA within these cells. Cell types such as certain endothelial and epithelial cells as well as neurons that are particularly prone to damage during
diabetes
tend to be those that appear to be dependent on GLUT transport of DHA rather than sodium-dependent AA uptake. We hypothesize that diabetic neuropathies, nephropathies and retinopathies develop in part by exclusion of DHA uptake by GLUT transporters when blood glucose levels rise above normal. AA plays a central role in the antioxidant defense system. Exclusion of DHA from cells by hyperglycemia would deprive the cells of the central antioxidant, worsening the hyperglycemia-induced oxidative stress level. Moreover, AA participates in many cellular oxidation-reduction reactions including hydroxylation of polypeptide lysine and proline residues and dopamine that are required for collagen production and metabolism and storage of catecholamines in neurons. Increase in the oxidative stress level and metabolic perturbations can be expected in any tissue or cell type that relies exclusively or mainly on GLUT for co-transport of glucose and DHA including neurons, epithelial cells, and vascular tissues. On the other hand, since DHA represents a significant proportion of total serum ascorbate, by increasing total plasma ascorbate concentrations during hyperglycemia, it should be possible to correct the increase in the oxidative stress level and metabolic perturbations, thereby sparing diabetic patients many of their complications.
...
PMID:Are diabetic neuropathy, retinopathy and nephropathy caused by hyperglycemic exclusion of dehydroascorbate uptake by glucose transporters? 1218 23
The present study was designed to evaluate the oxidative stress-related parameters in alloxan-induced
diabetes
in rabbits. After 3, 6, 12 and 24 weeks of hyperglycaemia the enzymatic and non-enzymatic factors were measured in heart tissue of diabetic and control groups. Superoxide dismutase and glutathione peroxidase activities and the contents of total sulfhydryl compounds significantly increased at all time intervals. Catalase activity increased initially (after 3 and 6 weeks), decreased after 12 weeks and increased again at the 24th week of the experiment. Glutathione reductase activity increased initially (at 3rd week), decreased below control level after 6 and 12 weeks, then increased again.
Ascorbic acid
concentration decreased after 3 and 6 weeks, and increased at the 12th and 24th weeks. The level of lipid peroxidation products was reduced after 3, 6 and 12 weeks of the experiment. After 24 weeks it was significantly elevated. These data suggest that hyperglycaemia induces oxidative stress in the heart but the defense mechanisms in the heart tissue are fairly efficacious against oxidative injury.
...
PMID:Changes in antioxidant status of heart muscle tissue in experimental diabetes in rabbits. 1236 95
Experimental evidence suggests that acute parenteral administration of high-dose ascorbic acid has beneficial vascular effects in type 2 diabetes. We studied the hemodynamic effects of chronic oral supplementation in this condition. Thirty patients, 45 to 70 years of age, with type 2 diabetes, were randomly assigned in a double-blind manner to receive 500 mg ascorbic acid daily by mouth or placebo. Patients were studied at baseline and after 4 weeks of assigned treatment. The central aortic augmentation index (AgIx) and the time to wave reflection (Tr) were derived from radial artery pulse wave analysis data. AgIx and Tr were used as measures of systemic arterial stiffness and aortic stiffness, respectively.
Ascorbic acid
decreased brachial systolic blood pressure from 142.1+/-12.6 (SD) to 132.3+/-12.1 mm Hg (difference [95% CI] 9.9 [4.7, 15.0]; P<0.01), brachial diastolic pressure from 83.9+/-4.8 to 79.5+/-6.0 mm Hg (4.4 [1.8, 7.0]; P<0.01), and AgIx from 26.8+/-5.5% to 22.5+/-6.8% (4.3 [1.5, 7.1]; P<0.01). Tr increased from 137.1+/-12.6 to 143.4+/-9.2 ms (-6.3 [-10.1, -2.5]; P<0.01). Placebo had no hemodynamic effects, and this difference between treatments was significant (P<0.01 for blood pressure and Tr, P=0.03 for AgIx). We have therefore shown that after 1 month, oral ascorbic acid lowered arterial blood pressure and improved arterial stiffness in patients with type 2 diabetes. As strict control of blood pressure reduces cardiovascular risk in
diabetes
, ascorbic acid supplementation may potentially be a useful and inexpensive adjunctive therapy. Larger and longer studies now need to be performed.
...
PMID:Ascorbic acid reduces blood pressure and arterial stiffness in type 2 diabetes. 1246 57
Aegle marmelos Corr. (Rutaceae) is widely used in Indian Ayurvedic medicine for the treatment of
diabetes mellitus
. The hypoglycaemic effect of the water extract of the fruits of Aegle marmelos was examined in streptozotocin-induced diabetic Wistar rats. Oral administration of the water extract (125 and 250mgkg(-1)) twice a day for 4 weeks resulted in significant reductions in blood glucose, plasma thiobarbituric acid reactive substances, hydroperoxides, ceruloplasmin and alpha-tocopherol and a significant elevation in plasma reduced glutathione and
Vitamin C
in diabetic rats. The effect of the extract at a dose of 250mgkg(-1) was more effective than glibenclamide in restoring the values of these parameters. The results of this study clearly shows the hypoglycaemic activity of the fruit extract.
...
PMID:Hypoglycaemic effect of water extracts of Aegle marmelos fruits in streptozotocin diabetic rats. 1286 Mar 9
During myocardial infarction (MI), high levels of circulating procoagulant microparticles (MP) shed from endothelial cells and platelets diffuse prothrombotic and proinflammatory potentials crucial for the coronary prognosis. In addition to conventional treatments, we evaluated whether vitamin C treatment could modify circulating levels of procoagulant MP. Upon admission, 61 patients with MI were prospectively randomized for immediate additional vitamin C treatment. Circulating MP were quantified by functional prothrombinase assay before and after 5 days of vitamin C administration (1 g day-1). The cellular origin of MP was also assessed. In vitamin C-treated patients, the reduction in platelet-derived MP was 10% higher (P = 0.01). In patients with
diabetes mellitus
, dyslipidemia or more than two cardiovascular risk factors, vitamin C decreased endothelial and platelet-derived MP levels by approximately 70% and 13%, respectively. This early effect on circulating platelet and endothelial-derived MP, testifies to the importance of oxidative stress during MI.
Vitamin C
could prove beneficial for the outcome of patients at higher thrombotic risk.
...
PMID:Protective effects of vitamin C on endothelium damage and platelet activation during myocardial infarction in patients with sustained generation of circulating microparticles. 1287 55
To examine the effect of vitamin C on blood flow in diabetic dental pulp, the animal model of streptozotocin (STZ)-induced diabetic rats (i.v. injection of STZ 55 mg/kg BW) was used. Male Sprague-Dawley rats weighing 200-250 g were divided into 3 groups: non-
diabetes
(CON),
diabetes
(STZ), and
diabetes
supplemented by vitamin C (STZ+Vit C).
Vitamin C
was supplemented by drinking water (1 g/l). At 12 weeks (wks) and 24 wks after the STZ injection, the laser Doppler flow-meter (Model ALF 21, USA) was used to measure pulpal blood flow (PBF) while the animals were anesthetized with sodium pentobarbital (50 mg/kg BW). The experimental results showed that at 12 and 24 wks after the STZ injection, hyperglycemia hypertension and loss of body weight were significantly developed. Simultaneously, decreased plasma vitamin C level was demonstrated significantly in STZ rats. The reduction of pulpal blood flow (PBF) in the lower incisors was observed in STZ rats at both monitored time points. Interestingly, the supplementation of vitamin C for 24 wks restored PBF. In conclusion, the present study demonstrated that long-term supplementation of vitamin C, a natural antioxidant, could markedly prevent the diabetic-induced reduction in PBF.
...
PMID:The effect of long-term supplementation of vitamin C on pulpal blood flow in streptozotocin-induced diabetic rats. 1472 56
In the present study, kidney superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) activities, vitamin C and lipid peroxidation levels were investigated in diabetic rats.
Diabetes
was induced in rats by streptozotocin and the treated rats received 1 g/l vitamin C with 0.5 mM CoCl2 in drinking water at 2-week intervals for 6 weeks. Kidney SOD, GSH-Px, CAT activities and lipid peroxidation levels were significantly increased in diabetic rats at the end of the 2nd, 4th and 6th weeks (p < 0.05), whereas vitamin C level was decreased significantly (p < 0.05) at the end of the 6th week compared to those of controls.
Vitamin C
with cobalt treatment of diabetic rats resulted in partial restoration of SOD and CAT activities, thiobarbituric acid reactant substances and vitamin C levels at all times studied, whereas treatment did not change GSH-Px activity. These results suggest that vitamin C with cobalt effectively normalized hyperglycemia (at the end of the 6th week) but could not completely restore the altered endogenous defence systems in diabetic rat kidney.
Diabetes
Nutr Metab 2003 Aug
PMID:In vivo effect of vitamin C with cobalt on oxidative stress in experimental diabetic rat kidney. 1476 69
The glycation of proteins alters both their structure and function. These changes have been linked to diabetic disorders and aging. The glycation of hemoglobin is also used as a diagnostic tool; the extent of glycation being a reflection of blood glucose averaged over a two to three month period. Accurate measures of average blood sugar (e.g., glycohemoglobin (GHb)) are important in clinical management of
diabetes
, pregnancy, cancer, etc.
Ascorbic acid
(AA) can react with proteins, including hemoglobin, and possibly interfere with GHb measurements. Past reports on the impact of AA on in vivo glycation have been equivocal. We studied GHb in subjects supplementing up to 20 g AA daily and found that for each 30 micromol/L increase in plasma AA, GHb was reduced by approximately 0.1. These results suggest that high AA intake can depress glycation, reduce GHb and lead to a clinically relevant underestimation of average blood sugar. Because AA is the most commonly consumed dietary supplement, awareness of an AA-associated bias in GHb is imperative. Of even broader significance is the possibility of AA-mediated inhibition of glycation in all proteins and the implications for aging. Moreover, AA could contribute through several other mechanisms to slowing of human aging (e.g., antioxidant properties, acceleration of pentose phosphate pathway, replacement of structural proteins).
...
PMID:Ascorbic acid, glycation, glycohemoglobin and aging. 1496 39
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