Glucose inhibits cellular ascorbic acid uptake by fibroblasts (original) (raw)
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Ascorbic acid metabolism in diabetes mellitus
Metabolism, 1981
In contrast to normal subjects diabetic patients had very low plasma ascorbic acid and significantly high (p < 0.001) dehydroascorbic acid irrespective of age. sex, duration of the disease, type of treatment. and glycemic control. However, there was no significant difference between the mean leukocyte ascorbate concentrations of the two populations. The in vitro rates of dehydroascorbate reduction in the hemolysate and the erythrocyte reduced glutathione levels and the glucose-6-phosphate dehydrogenase activities, which regulate the dehydroascorbate reduction, were similar in normal and diabetic subjects. The turnover of ascorbic acid was higher in the diabetics than that in the normal volunteers. Experiments with diabetic rats indicated that the increased turnover of ascorbic acid was probably due to increased oxidation of ascorbate to dehydroascorbete in tissue mitochondria. Ascorbic acid supplementation at a dose of 500 mg per day for a brief period of 15 days resulted in an increase in the plasma ascorbate level temporarily, but it did not lower the blood glucose level of the diabetic patients.
Ascorbic acid prevents vascular dysfunction induced by oral glucose load in healthy subjects
European Journal of Internal Medicine, 2012
Objectives: To examine the effects of oral glucose load on forearm circulatory regulation before and after ascorbic acid administration in healthy subjects. Design: Microcirculation study with laser Doppler was performed at the hand in basal conditions, after ischemia and after acetylcholine and nitroprusside; strain gauge plethysmography was performed at basal and after ischemia. The tests were repeated in the same sequence 2 hour after oral administration of glucose (75 g). The subjects were randomised for administration of ascorbic acid (1 g bid) or placebo (sodium bicarbonate 1 g bid) for 10 days. After that, the tests were repeated before and after a new oral glucose load. Blood pressure and heart rate were monitored. Results: Macrocirculatory flux, pressure values and heart rate were unvaried throughout the study. The glucose load caused a reduction in the hyperemic peak flow with laser Doppler and plethysmography; it reduced flux recovery time and hyperemic curve area after ischemia; acetylcholine elicited a minor increase in flux with laser Doppler. The response to nitroprusside was unvaried after glucose load as compared to basal conditions. Treatment with ascorbic acid prevented the decrease in hyperemia after glucose, detected with laser Doppler and plethysmography. Ascorbic acid prevented the decreased response to acetylcholine after glucose, the response to nitroprusside was unaffected by ascorbic acid. Results after placebo were unvaried. Conclusions: Oral glucose load impairs endothelium dependent dilation and hyperaemia at microcirculation, probably via oxidative stress; ascorbic acid can prevent it.
Diabetologia, 1991
Abnormalities of ascorbic acid metabolism have been reported in experimentally-induced diabetes and in diabetic patients. Ascorbate is a powerful antioxidant, a cofactor in collagen biosynthesis, and affects platelet activation, prostaglandin synthesis and the polyol pathway. This suggests a possible close interrelationship between ascorbic acid metabolism and pathways known to be influenced by diabetes. We determined serum ascorbic acid and its metabolite, dehydroascorbic acid, as indices of antioxidant status, and the ratio, dehydroascorbate/ascorbate, as an index of oxidative stress, in 20 matched diabetic patients with and 20 without microangiopathy and in 22 age-matched control subjects. Each study subject then took ascorbic acid, 1 g daily orally, for six weeks with repeat measurements taken at three and six weeks. At baseline, patients with microangiopathy had lower ascorbic acid concentrations than those without microangiopathy and control subjects (42.1+19.3 vs 55.6 _+ 20.0, p < 0.01, vs 82.9 _+ 30.9 gmol/1, p < 0.001) and elevated dehydroascorbate/ascorbate ratios (0.87+0.46 vs 0.61 + 0.26, p < 0.01, vs 0.38 + 0.14, p < 0.001). At three weeks, ascorbate concentrations rose in all groups (p < 0.0001) and was maintained in control subjects (151.5 + 56.3 ~tmol/1), but fell in both diabetic groups by six weeks (p<0.01). Dehydroascorbate/ascorbate ratios fell in all groups at three weeks (p < 0.0001) but rose again in the diabetic groups by six weeks (p < 0.001) and was unchanged in the control subjects. Dehydroascorbate concentrations rose significantly from baseline in all groups by six weeks of ascorbic acid supplementation (p < 0.05). No significant changes were observed in fructosamine concentrations in any group during the study. Diabetes mellitus is associated with a major disturbance of ascorbic acid metabolism which is only partially corrected by ascorbate supplementation.
The biochemical, physiological and therapeutic roles of ascorbic acid
African Journal of Biotechnology, 2010
Ascorbic acid is an important micronutrient necessary for a significant number of metabolic reactions in humans and other primates. It is a strong reducing agent involved in reduction reaction and it is structurally related to glucose. Experimental and epidemiological studies have documented the biochemical, physiological and therapeutic roles of ascorbic acid. It is an essential water-soluble antioxidant vitamin derived from exogenous source; thus its role in human health is worthy to be considered particularly because of the current global economic trend. The biochemical, physiological and therapeutic roles of ascorbic acid is reviewed, providing further insights into the role of ascorbic acid in biological functions.
Transfer of ascorbic acid across the vascular endothelium: mechanism and self-regulation
AJP: Cell Physiology, 2009
To determine how ascorbic acid moves from the bloodstream into tissues, we assessed transfer of the vitamin across the barrier generated by EA.hy926 endothelial cells when these were cultured on semipermeable filter supports. Ascorbate transfer from the luminal to the abluminal compartment was time dependent, inhibited by anion channel blockers and by activation of protein kinase A, but was increased by thrombin. Ascorbate transfer occurred by a paracellular route, since it did not correlate with intracellular ascorbate contents and was not rectified or saturable. Nonetheless, intracellular ascorbate inhibited the transfer of both ascorbate and radiolabeled inulin across the endothelial barrier. The increase in barrier function due to ascorbate was dependent on its intracellular concentration, significant by 15 min of incubation, prevented by the cytoskeletal inhibitor colchicine, associated with F-actin stress fiber formation, and not due to collagen deposition. These results show ...
Serum Ascorbic Acid Level In Type 2 Diabetes Mellitus
2017
Introduction: Ascorbic acid (Vitamin C) is an important scavenger of oxygen derived free radicals, structurally similar to glucose, which can replace it in many chemical reactions and thus is effective for prevention of nonenzymatic glycosylation of protein and helps in the regeneration of α-tocopherol and prevents LDL oxidation thereby reducing cardiovascular risk. Aims and Objectives: To estimate Haemoglobin A1c (HbA1c), Triglycerides (TG) and Vitamin C levels in type 2 diabetes mellitus patients and compare it with that of healthy individuals. Materials and methods: A cross sectional study done in the department of Biochemistry in collaboration with Department of Medicine, Regional Institute of Medical Sciences, Imphal, Manipur from September 2011 to August 2013 included eighty confirmed cases of type 2 diabetes mellitus (T2DM) patients and forty age and sex matched healthy controls. Vitamin C and Triglyceride levels were estimated colorimetrically while HbA1c was measured by Fas...
Ascorbic acid synthesis is stimulated by enhanced glycogenolysis in murine liver
FEBS Letters, 1994
Ascorbic acid synthesis was stimulated by glucagon, dibutyryl cyclic AMP, as well as phenylephrine, vasopressin or okadaic acid, in hepatocytes prepared from fed mice. However, no such effect was observed in glycogen-depleted cells from starved animals, either in the presence or absence of glucose. The rate of ascorbate synthesis showed close correlation with the glucose release by hepatocytes. In mice the injection of glucagon increased plasma ascorbate concentration fifteenfold, and caused a sixfold elevation of the ascorbate content of the liver. These results show that hepatic ascorbate synthesis is dependent on glycogenolysis, and indicate a regulatory role of ascorbate released by the liver.
Diabetes/Metabolism Research and Reviews, 2003
Background Defective leukocyte-endothelial interactions are observed in experimental diabetes and may reduce the capacity to mount an adequate inflammatory response. The present study investigated the effect of ascorbic acid, an inhibitor of free radical and glycated protein formation as well as an aldose reductase inhibitor, on leukocyte-endothelial interaction in alloxan-diabetic rats.
Ascorbic and Dehydroascorbic Acid-Connections to Type 1 Diabetes
The etiology of Type 1 diabetes (T1D) is unknown. While especially Band D-vitamins have been to some extent studied in relation to development of Type 1 diabetes, Vitamin C has been ignored despite its important effects as an antioxidant protecting against oxidative stress, its influence on the immune function including autoimmunity, and the possible direct effects on the pancreatic beta cells. Recently the demonstration of increased dehydroascorbic acid before the development of autoantibodies in serum of children with genetic risk for T1D has drawn some attention to the ascorbic and dehydroascorbic acids, which decades ago have been linked to effects on the pancreatic beta cells. As long as there is no safe, efficacious and practical way of preventing Type 1 diabetes there are reasons to resume the interest for vitamins, including Vitamin C.