title: Hyperglycemic Stress and Carbon Stress in Diabetic Glucotoxicity.
abstract: Diabetes and its complications are caused by chronic glucotoxicity driven by persistent hyperglycemia. In this article, we review the mechanisms of diabetic glucotoxicity by focusing mainly on hyperglycemic stress and carbon stress. Mechanisms of hyperglycemic stress include reductive stress or pseudohypoxic stress caused by redox imbalance between NADH and NAD(+) driven by activation of both the polyol pathway and poly ADP ribose polymerase; the hexosamine pathway; the advanced glycation end products pathway; the protein kinase C activation pathway; and the enediol formation pathway. Mechanisms of carbon stress include excess production of acetyl-CoA that can over-acetylate a proteome and excess production of fumarate that can over-succinate a proteome; both of which can increase glucotoxicity in diabetes. For hyperglycemia stress, we also discuss the possible role of mitochondrial complex I in diabetes as this complex, in charge of NAD(+) regeneration, can make more reactive oxygen species (ROS) in the presence of excess NADH. For carbon stress, we also discuss the role of sirtuins in diabetes as they are deacetylases that can reverse protein acetylation thereby attenuating diabetic glucotoxicity and improving glucose metabolism. It is our belief that targeting some of the stress pathways discussed in this article may provide new therapeutic strategies for treatment of diabetes and its complications.
authors.affiliation: 1 Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA; 2 Department of Biochemistry and Molecular Biology, Gannan Medical University, Ganzhou, Jiangxi province, China, 341000.
authors.forename: Xiaoting
authors.initials: X
authors.lastname: Luo
authors.affiliation: 1 Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
authors.forename: Jinzi
authors.initials: J
authors.lastname: Wu
authors.affiliation: 1 Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA; 3 College of Life Sciences and Technology, Xinjiang University, Urumqi, Xinjiang, China, 830046.
authors.forename: Siqun
authors.initials: S
authors.lastname: Jing
authors.affiliation: 1 Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
authors.forename: Liang-Jun
authors.initials: LJ
authors.lastname: Yan
keywords: carbon stress; diabetes; glucotoxicity; hyperglycemic stress; pseudohypoxia; reactive oxygen species; redox imbalance
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