The role of antioxidants and other agents in alleviating hyperglycemia mediated oxidative stress and injury in liver

Abstract

Several antioxidants and agents having similar antioxidant effects are known to exert beneficial effects in ameliorating the injurious effects of hyperglycemia on liver in different diabetic in vitro and in vivo models. The review deals with some of the agents which have been shown to exert protective effects on liver against hyperglycemic insult and the various mechanisms involved. The different classes of agents which protect the diabetic liver or decrease the severity of hyperglycemia mediated injury include flavonoids, catechins, and other polyphenolic compounds, curcumin and its derivatives, certain vitamins, hormones and drugs, trace elements, prototypical antioxidants and amino acids. Some of the pronounced changes mediated by the antioxidants in liver exposed to hyperglycemia include decreased oxidative stress, and alterations in carbohydrate and lipid metabolism. Other mechanisms through which the agents ameliorate hyperglycemia mediated liver injury include decrease in oxidative DNA and protein damage, restoration of mitochondrial structural and functional integrity, decrease in inflammation and improved insulin signaling. Thus, antioxidants may prove to be an important mode of defense in maintaining normal hepatic functions in diabetes.

A catechin-enriched green tea extract prevents glucose-induced survival reduction in Caenorhabditis elegans through sir-2.1 and uba-1 dependent hormesis

“…With regard to the latter, green tea catechins were demonstrated to decrease glucose levels and to increase glucose tolerance in insulinresistant mice [25]. EGCG attenuated dexamethasone and TNF-α promoted ROS generation and increased glucose uptake ability in this study [25], congruent with concepts that catechins are mainly acting through their antioxidative properties [26,27]. However, there are also reports suggesting that other mechanisms, including direct interactions with plasma membrane proteins, regulation of signal transduction pathways or mitochondrial function, might be more important in order to exert many of its beneficial biological actions [28].…”

Arsenic induces diabetic effects through beta-cell dysfunction and increased gluconeogenesis in mice

“…These results are consistent with previous researches2526, indicating that iAs can increase the hepatic toxicity. In db/db control mice, these genes were also up-regulated in liver and adipocyte, indicating that diabetes can also cause oxidative damage and inflammation2728. iAs exposure further increased oxidative damage and inflammation, and worsened hepatotoxicity in diabetic individual.…”

Effects of the Aqueous Extracts of Rhodamnia cinerea on Metabolic indices and Sorbitol-Related Complications in Type 2 Diabetic Rats

“…Similarly, the ability of the extract to regulate oxidative stress in these tissues may have played a role in the regulation of sorbitol. It has been demonstrated that increased oxidative stress propagates the buildup of sorbitol and other complications in Type 2 diabetes (Dey & Lakshmanan 2013;Rahimi et al 2005) and the results from this study showed that the untreated diabetic control group had lower antioxidant capacities in the lens, kidney and nerve (Table 2), while the R. cinerea-treated groups had improved antioxidant capacities, although only those of the kidney were significant different (p<0.05).…”