Microvascular Complications of Impaired Glucose Tolerance
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Figures
- FIG. 1.
Disruption of vascular NO signaling and direct metabolic injury contribute to IGT complications. NO synthesized by eNOS mediates large- and small-vessel vasodilation and promotes endothelial thrombolysis. Transient or sustained hyperglycemia depletes NADPH and increases formation of ROS. ROS directly damage endothelial and other target organ cells and alter utilization of NO from vasoregulatory tasks to detoxification of ROS. AGEs increase ROS formation and cause direct metabolic injury. These synergistic insults promote small-tissue ischemia, large-vessel atherogenesis and thrombogenesis, and contribute to complications in IGT.
- FIG. 2.
Adipocyte lipolysis, release of FFAs, and changes in adipocytokines in response in states of insulin resistance and obesity contribute to both acute changes in vasoreactivity and chronic endothelial injury. Increased circulating FFAs reinforce insulin resistance and increase gluconeogenesis in the liver, accelerating hyperglycemia and feeding into the hyperglycemic effects described in Fig. 1. Fatty acid peroxidaton directly increases ROS, and FFAs contribute to endothelial injury. Insulin resistance increases adipocyte release of tumor necrosis factor-α (TNF-α), which acts through the sphingolipid ceramide to damage endothelial cells. Adiponectin secretion is reduced, with inhibition of its vasoprotectve effect.
Tables
- TABLE 1
1997 ADA criteria (4) for IFG, IGT, and diabetes
Condition Fasting plasma glucose (mg/dl) Test and values 2-h OGTT (mg/dl) HbA1c (%) Normal ≤109 ≤139 NA IFG 110–125 NA NA IGT NA 140–199 NA Diabetes ≥126 ≥200 Variable -
IFG is preferred to IGT by the ADA because of its greater convenience, but IFG and IGT are regarded as equivalent. The ADA recommends against use of HbA1c as a diagnostic test for diabetes. HbA1c threshold for diabetes is variable, but typically between 6.1 and 7.0%. No HbA1c values are recognized as equivalent to IGT or IFG.
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- Article
- Abstract
- Recognition and natural history of IGT.
- Microvascular complications of IGT: neuropathy, retinopathy, and renal microproteinuria.
- Pathogenesis of IGT complications: general considerations.
- Hyperglycemia inhibits nitric oxide-mediated vasodilation.
- Insulin resistance.
- FFAs and adipocytokines induce endothelial injury.
- Other metabolic effects of hyperglycemia.
- Treatment and areas for future study.
- Acknowledgments
- Footnotes
- REFERENCES
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