The cellular and molecular mechanisms of diabetic complications

G. L. King, M. Brownlee

Research output: Contribution to journalArticle

238 Citations (Scopus)

Abstract

In this article, the cellular and molecular mechanisms of diabetic complications have been reviewed. Hyperglycemia-induced mechanisms that may induce vascular dysfunction in specific sites of diabetic microvascular damage include increased polyol pathway flux, altered cellular redox state, increased formation of diacylglycerol and the subsequent activation of specific PKC isoforms, and accelerated nonenzymatic formation of advanced glycation endproducts. Several of these mechanisms may be responsible for the potentially damaging overproduction of reactive oxygen species observed with hyperglycemia. Each of these mechanisms may contribute to the known pathophysiologic features of diabetic complications by a number of mechanisms, including the upregulation of cytokines and growth factors. Diabetic macrovascular disease may arise more from insulin resistance than from hyperglycemia, and the authors speculate that this may reflect a selective loss of insulin-dependent vascular homeostasis.

Original languageEnglish (US)
Pages (from-to)255-270
Number of pages16
JournalEndocrinology and Metabolism Clinics of North America
Volume25
Issue number2
DOIs
StatePublished - 1996
Externally publishedYes

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Diabetes Complications
Hyperglycemia
Insulin
Blood Vessels
Diglycerides
Reactive Oxygen Species
Intercellular Signaling Peptides and Proteins
Protein Isoforms
Chemical activation
Cytokines
Fluxes
Oxidation-Reduction
Insulin Resistance
Homeostasis
Up-Regulation
polyol

ASJC Scopus subject areas

  • Endocrinology
  • Biochemistry

Cite this

The cellular and molecular mechanisms of diabetic complications. / King, G. L.; Brownlee, M.

In: Endocrinology and Metabolism Clinics of North America, Vol. 25, No. 2, 1996, p. 255-270.

Research output: Contribution to journalArticle

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