Plasma vitamin C affects glucose homeostasis in healthy subjects and in non-insulin-dependent diabetics

Paolisso, Giuseppe; D’Amore, Anna; Balbi, V.; Volpe, C. Della; Galzerano, Domenico; Giugliano, Dario; Sgambato, S; Varricchio, M; D'Onofrio, F

doi:10.1152/ajpendo.1994.266.2.e261

Cited by 88 publications

(65 citation statements)

References 18 publications

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“…Increased cellular injury in these mouse models is prevented by SOD mimetics, confirming the direct role of SOD2 in enhancing disease phenotypes (Patel, 2003;Ali et al, 2004). Such evidence has led to heightened interest in the clinical application of antioxidants for neurological disorders, including DN (Paolisso et al, 1994;Natarajan et al, 2002;Henriksen, 2006;Coverley and Baxter, 1997). One caveat is that the SOD2 +/− mice also display evidence of cardiovascular insufficiency (Ohashi et al, 2006;Strassburger et al, 2005).…”

Section: Discussionmentioning

confidence: 77%

SOD2 protects neurons from injury in cell culture and animal models of diabetic neuropathy

Vincent

Russell

Sullivan

et al. 2007

Experimental Neurology

105

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Hyperglycemia-induced oxidative stress is an inciting event in the development of diabetic complications including diabetic neuropathy. Our observations of significant oxidative stress and morphological abnormalities in mitochondria led us to examine manganese superoxide dismutase (SOD2), the enzyme responsible for mitochondrial detoxification of oxygen radicals. We demonstrate that over expression of SOD2 decreases superoxide (O 2 •− ) in cultured primary dorsal root ganglion (DRG) neurons and subsequently blocks caspase-3 activation and cellular injury. Under expression of SOD2 in dissociated DRG cultures from adult SOD2 +/− mice results in increased levels of O 2 •− , activation of caspase-3 cleavage and decreased neurite outgrowth under basal conditions that are exacerbated by hyperglycemia. These profound changes in sensory neurons led us to explore the effects of decreased SOD2 on the development of diabetic neuropathy (DN) in mice. DN was assessed in SOD2 +/− C57BL/6J mice and their SOD2 +/+ litter mates following streptozotocin (STZ) treatment. These animals, while hyperglycemic, do not display any signs of DN. DN was observed in the C57BL/6Jdb/db mouse, and decreased expression of SOD2 in these animals increased DN. Our data suggest that SOD2 activity is an important cellular modifier of neuronal oxidative defense against hyperglycemic injury.

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Section: Discussionmentioning

confidence: 77%

SOD2 protects neurons from injury in cell culture and animal models of diabetic neuropathy

Vincent

Russell

Sullivan

et al. 2007

Experimental Neurology

105

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“…The antioxidative capacity of this compound has been reported [27,28] and may have a role in its insulin sensitizing action. Vitamin C is a clinically used antioxidant that is water soluble and has potential effects on peripheral glucose utilization [6,29]. Thus, the potential protective effects of troglitazone, its isolated vitamin E moiety and of vitamin C against insulin resistance induced by oxidative stress were evaluated.…”

Section: Resultsmentioning

confidence: 99%

Lipoic acid protects against oxidative stress induced impairment in insulin stimulation of protein kinase B and glucose transport in 3T3-L1 adipocytes

et al. 1999

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Oxidative stress has been recently implicated in the pathogenesis of various diseases. Consequently, the potential therapeutic or preventive effects of antioxidative agents has been raised [1]. Both poorly controlled Type I (insulin-dependent) diabetes mellitus as well as Type II (non-insulin-dependent) diabetes mellitus are characterized by reduced capacity of peripheral tissues (i. e. skeletal muscle and adipose tissue) to respond to the metabolic effects of insulin. The causes and cellular mechanisms responsible for this abnormality are still not fully understood despite intense investigative effort. Several lines of evidence suggest that increased oxidative stress occurs in diabetes and could have a role in the development or deterioration of peripheral insulin resistance. These Diabetologia (1999) Abstract Aims/hypothesis. Oxidative stress has been shown to impair insulin-stimulated glucose transporter 4 translocation in 3T3-L1 adipocytes. This study explores the potential of the antioxidant lipoic acid to protect the cells against the induction of insulin resistance when given before exposure to oxidative stress. Methods. 3T3-LI were exposed for 16 h to lipoic acid after which cells were exposed for 2 h to continuous production of H 2 O 2 by adding glucose oxidase to the culture medium. Results. These conditions resulted in a 50±70 % reduction in insulin-stimulated glucose transport activity associated with a decrease in reduced glutathione content from 37.4 ± 3.1 to 26.4 ± 4.9 nmol/mg protein, (p < 0.005). Lipoic acid pretreatment increased insulin-stimulated glucose transport following oxidative stress, reaching 84.8 ± 4.4 % of the control, associated with an increase in reduced glutathione content. Oxidation impaired the 4.89 ± 0.36-fold insulin-stimulated increase in glucose transporter 4 content in plasma membrane lawns of control cells. Lipoic acid pretreatment was, however, associated with preserved insulin-induced glucose transporter 4 translocation in cells exposed to oxidation, yielding 80 % of its content in controls. Although tyrosine phosphorylation patterns were not affected by lipoic acid pretreatment, insulin-stimulated protein kinase B/Akt serine 473 phosphorylation and activity were considerably impaired by oxidation but protected by lipoic acid pretreatment. A protective effect was not observed with either troglitazone, its isolated vitamin E moiety, or with vitamin C. Conclusion/interpretation. This study shows the ability of lipoic acid to provide partial protection against the impaired insulin-stimulated glucose transporter 4 translocation and protein kinase B/Akt activation induced by oxidative stress, potentially by its capacity to maintain intracellular redox state. [Diabetologia (1999) 42: 949±957]

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“…However, it diminishes the microalbuminuria, erythrocyte sorbitol levels and plays a chief role in ameliorating insulin resistance of diabetic patients due to its antioxidant function [25,26].…”

Section: Vitamin Cmentioning

confidence: 99%

A Review on Role of Antioxidants in Diabetes

Rajendiran

Packirisamy

Giribabu³

2018

Asian J Pharm Clin Res

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Diabetes mellitus is a chronic metabolic disease. Oxidative stress plays a major part in the pathogenesis of diabetes. Supplementation with antioxidants and the medicinal plants which possess antioxidants activity have been reported their hypoglycemic activity. The antioxidants are used to treat and reduce the complication of diabetes mellitus. The diet supplementations of antioxidants vitamins are beneficial in the treatment of diabetes. This review article was summarizing the role of antioxidants in diabetes mellitus.

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Plasma vitamin C affects glucose homeostasis in healthy subjects and in non-insulin-dependent diabetics

Cited by 88 publications

References 18 publications

SOD2 protects neurons from injury in cell culture and animal models of diabetic neuropathy

SOD2 protects neurons from injury in cell culture and animal models of diabetic neuropathy

Lipoic acid protects against oxidative stress induced impairment in insulin stimulation of protein kinase B and glucose transport in 3T3-L1 adipocytes

A Review on Role of Antioxidants in Diabetes

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