Glycosylation inhibitors, PKC inhibitors and related interventions against complications

Aino Soro-Paavonen, Mark Cooper

Research output: Chapter in Book/Report/Conference proceedingChapter (Book)Researchpeer-review

Abstract

Chronic hyperglycaemia predisposes the diabetic patient to a markedly increased risk of end-organ complications in the eyes, kidneys, peripheral nerves and the vasculature. The most effective way to reduce the risk of diabetic complications is intensive insulin treatment leading to optimal glycaemic control [1,2]. However, excellent control of hyperglycaemia is achieved in less than 25% of type 1 diabetic patients [3]. Glucose-mediated vascular damage has been reported to occur via four major mechanisms including activation of the intracellular signal transductor, protein kinase C (PKC), increased polyol pathway accumulation, enhanced hexosamine pathway flux and increased formation of advanced glycation end-products (AGEs) [4]. All these processes are activated by mitochondrial superoxide production [4].

Original languageEnglish
Title of host publicationPharmacotherapy of Diabetes
Subtitle of host publicationNew Developments: Improving Life and Prognosis for Diabetic Patients
PublisherHumana Press
Pages219-228
Number of pages10
ISBN (Print)9780387697369
DOIs
Publication statusPublished - 1 Dec 2007
Externally publishedYes

Keywords

  • advanced glycation end-product
  • diabetic complications
  • Hyperglycaemia
  • protein kinase C
  • receptor for advanced glycation end-product

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