Ascorbic acid metabolism in diabetes mellitus (original) (raw)
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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.
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...
The effect of ascorbate supplementation on oxidative stress in the streptozotocin diabetic rat
Free Radical Biology and Medicine, 1992
An increase in oxidative stress may contribute to the development of diabetic complications. The key aqueousphase chain-breaking antioxidant ascorbate is known to be deficient in diabetes, and we have therefore investigated the effects of ascorbate supplementation on oxidative stress in the streptozotocin diabetic rat. Markers of lipid peroxidation (malondialdehyde [MDA] and diene conjugates) were increased in plasma and erythrocytes of untreated diabetic animals, and levels of the antioxidants ascorbate and retinol were reduced. Plasma tocopherol was unchanged. Insulin treatment normalized MDA and ascorbate levels, although ascorbate metabolism remained disturbed, as indicated by increased levels of dehydroascorbate. High-dose ascorbate supplementation in the absence of insulin treatment restored plasma ascorbate to normal and increased plasma retinol and tocopherol levels. However, MDA and diene conjugate levels remained unchanged, possibly as a result of increased iron availability. High-dose ascorbate supplementation should be approached with caution in diabetes, as ascorbate may exert both antioxidant and prooxidant effects in vivo.
The effect of ascorbic acid supplementation on brain oxidative events in experimental diabetes
2010
Increased oxidant stress plays an important role in the etiopathogenesis of chronic complications of diabetes. This study aimed to examine the effects of ascorbic acid (vitamin C, AA) supplementation on the oxidant and antioxidant processes in the brain of diabetic rats. Wistar albino rats were divided into four groups: group 1 (control), group 2 (ascorbic acid, AA, vitamin C), group 3 (diabetes), and group 4 (diabetes ? AA). The rats were treated with a single dose of streptozotocin (45 mg/kg, intraperitoneal) to induce diabetes. After 48 h, the rats whose fasting blood glucose levels exceeded 200 mg/100 mL were included in the diabetes groups. The rats in the AA and diabetes ? AA groups were treated with AA (20 mg/kg/day), administered intragastrically for 21 days. At the end of the experiment, malondialdehyde (MDA), glutathione (GSH), AA, and total nitric oxide (NOx) levels in the liver tissues were determined. Analysis of variance (ANOVA) and Mann-Whitney U tests were used for statistical analyses. Whereas the MDA levels increased in the diabetes group, the NOx levels decreased. The NOx levels increased in the diabetes ? AA group compared with the control subjects. There were no significant differences in the diabetes ? AA group in terms of GSH levels.
Glucose inhibits cellular ascorbic acid uptake by fibroblasts
Cell Biology International Reports, 1985
It has been suggested earlier that the local deficiency of ascorbic acid in tissues could be responsible for development of various angiopathies in diabetes. Hyperglycemia is one of the factors which could contribute considerably to the development of local the effect of glucose on uptake of L-u ,crbic acid deficieny. Therefore, C ascorbic acid by fibroblasts was studied in vitro. The data clearly show that ascorbic acid uptake is inhibited-instantly by glucose in a concentration dependent fashion. The results support the contention that local ascorbic acid deficiency in tissues could be a natural consequence of hyperglycemia of whatever cause. The rate of ascorbic acid uptake under various conditions suggests that additional supplements of ascorbic acid might be helpful to individuals in averting deleterious effects of hyperglycemia on tissue ascorbic acid supply.
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.
Mini-Reviews in Medicinal Chemistry, 2012
Ascorbic acid is a low molecular weight antioxidant well known as anti-scorbut acting vitamin C in humans, primates and guinea pigs. This review summarizes basic data about ascorbic acid in its physiological action point of view. It is divided into biochemistry of ascorbic acid synthesis, mechanism of antioxidant action and participation in anabolism, pharmacokinetics and excretion, exogenous ascorbic acid immunomodulatory effect and participation in infectious diseases, impact on irradiation and intoxication pathogenesis, and supplementary demands. The primary intention was to consider ascorbic acid not only as an antioxidant but also as a chemical compound affecting multiple pathways with a potential beneficial impact in many diseases and processes in human body.
Gluconeogenesis from ascorbic acid: ascorbate recycling in isolated murine hepatocytes
FEBS Letters, 1996
Ascorbic acid synthesis and breakdown were investigated in isolated hepatocytes prepared from fasted mice. Stimulation of gluconeogenesis by alanine or xylitol led to ascorbate synthesis. On the other hand, ascorbate or dehydroascorbate addition resulted in concentration-dependent glucose production and elevation of the pentose phosphate pathway intermediate xylulose 5-phosphate. Stimulation of ascorbate oxidation and/or the inhibition of dehydroascorbate reduction increased glucose formation. Inhibition of the pentose phosphate pathway decreased glucose production from dehydroascorbate with increased accumulation of xylulose 5-phosphate. These results suggest that ascorbate can be recycled by a novel way involving intermediates of the pentose phosphate pathway, gluconeogenesis and hexuronic acid pathway.