Abstract |
In the last two decades, diabetes mellitus has reached epidemic proportions in the United States. Most of the recent increase in prevalence of diabetes involves type 2 disease and is a result of an alarming increase in prevalence of obesity, although type 1 diabetes may also be on the rise. Advances in treatment have essentially eliminated ketoacidosis as a cause of death and led to better glycemic control than ever before. Consequently, diabetics now live a longer life, allowing many of them to develop the chronic complications of the disease. Here we review the evidence that a maladaptive response to hyperglycemia contributes to diabetic neuropathy, a major microvascular complication. We postulate that the same response may also be the culprit for the other chronic complications of diabetes.
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Authors | Lawrence Chan, Tomoya Terashima, Mineko Fujimiya, Hideto Kojima |
Journal | Transactions of the American Clinical and Climatological Association
(Trans Am Clin Climatol Assoc)
Vol. 117
Pg. 341-51; discussion 351-2
( 2006)
ISSN: 0065-7778 [Print] United States |
PMID | 18528485
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
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Topics |
- Animals
- Bone Marrow Cells
(metabolism)
- Diabetes Complications
(etiology, metabolism)
- Diabetes Mellitus, Type 1
(therapy)
- Diabetic Neuropathies
(etiology, metabolism)
- Genetic Therapy
- Humans
- Hyperglycemia
(metabolism)
- Proinsulin
(biosynthesis)
- Tissue Distribution
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