Hyperglycemic Pseudohypoxia and Diabetic Complications

Author:

Williamson Joseph R1,Chang Katherine1,Frangos Myrto1,Hasan Khalid S1,Ido Yasuo1,Kawamura Takahiko1,Nyengaard Jens R1,Den Enden Maria van1,Kilo Charles1,Tilton Ronald G1

Affiliation:

1. Departments of Pathology, Pediatrics, and Internal Medicine, Washington University School of Medicine St. Louis, Missouri Department of Internal Medicine, Chubu Rosai Hospital Nagoya, Japan Stereological Research Lab, Aarhus University Aarhus, Denmark Department of Internal Medicine, Middelheim Hospital Antwerp, Belgium

Abstract

Vasodilation and increased blood flow are characteristic early vascular responses to acute hyperglycemia and tissue hypoxia. In hypoxic tissues these vascular changes are linked to metabolic imbalances associated with impaired oxidation of NADH to NAD+ and the resulting increased ratio of NADH/NAD+. In hyperglycemic tissues these vascular changes also are linked to an increased ratio of NADH/NAD+, in this case because of an increased rate of reduction of NAD+ to NADH. Several lines of evidence support the likelihood that the increased cytosolic ratio of free NADH/NAD+ caused by hyperglycemia, referred to as pseudohypoxia because tissue partial pressure oxygen is normal, is a characteristic feature of poorly controlled diabetes that mimics the effects of true hypoxia on vascular and neural function and plays an important role in the pathogenesis of diabetic complications. These effects of hypoxia and hyperglycemia-induced pseudohypoxia on vascular and neural function are mediated by a branching cascade of imbalances in lipid metabolism, increased production of superoxide anion, and possibly increased nitric oxide formation.

Publisher

American Diabetes Association

Subject

Endocrinology, Diabetes and Metabolism,Internal Medicine

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