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Controversies in Treating Diabetes pp 233–249Cite as

Unifying Hypothesis of Diabetic Complications

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Part of the book series: Contemporary Endocrinology ((COE))

Summary

Over the past four decades, several molecular mechanisms have been implicated in glucose-mediated vascular damage: increased flux through the polyol pathway, accumulation of advanced glycation endproduct precursors, activation of protein kinase C isoforms, and increased hexosamine pathway activity. Each of these mechanisms has been studied independently of the others, and there has been no apparent common element linking them. Recent discoveries have made clear that all of these seemingly unrelated mechanisms arise from a single, hyperglycemia-induced process: the overproduction of reactive oxygen species by the mitochondrial electron transport chain.

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Authors
  1. Takeshi Matsumura MD
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  2. Michael Brownlee MD
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Editors and Affiliations

  1. Division of Endocrinology, Diabetes, and Bone Disease, Department of Medicine, Mount Sinai School of Medicine, New York, NY

    Derek LeRoith MD PhD

  2. Diabetes Research Institute Department of Medicine, Eastern Virginia Medical School The Leonard Strelitz Diabetes Institutes, Norfolk, VA

    Aaron I. Vinik MD PhD FCP FACP

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© 2008 Humana Press

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MD, T.M., MD, M.B. (2008). Unifying Hypothesis of Diabetic Complications. In: LeRoith, D., Vinik, A.I. (eds) Controversies in Treating Diabetes. Contemporary Endocrinology. Humana Press. https://doi.org/10.1007/978-1-59745-572-5_12

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  • DOI: https://doi.org/10.1007/978-1-59745-572-5_12

  • Publisher Name: Humana Press

  • Print ISBN: 978-1-58829-708-2

  • Online ISBN: 978-1-59745-572-5

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