Advanced glycation end products in diabetic complications

Michael Brownlee

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Advanced glycation end products accumulate as a function of the level of chronic hyperglycemia via generation of reactive dicarbonyl intermediates. Inside cells, advanced glycation end products accumulate rapidly and cause altered function of intracellular proteins. Outside cells, advanced glycation end products accumulate over longer periods of time, interfering with normal extracellular matrix interactions and causing advanced glycation end product receptor-mediated pathologic changes in gene expression. In animal models, pharmacologic inhibition of advanced glycation end product formation prevents diabetic complications in the retina, glomerulus, peripheral nerve, and artery. Efficacy results from a study in type I diabetic patients with overt nephropathy are anticipated in the third quarter of 1998.

Original languageEnglish (US)
Pages (from-to)291-297
Number of pages7
JournalCurrent Opinion in Endocrinology and Diabetes
Volume3
Issue number4
StatePublished - 1996

Fingerprint

Advanced Glycosylation End Products
Diabetes Complications
Peripheral Nerves
Hyperglycemia
Extracellular Matrix
Retina
Animal Models
Arteries
Gene Expression
Proteins

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Internal Medicine

Cite this

Advanced glycation end products in diabetic complications. / Brownlee, Michael.

In: Current Opinion in Endocrinology and Diabetes, Vol. 3, No. 4, 1996, p. 291-297.

Research output: Contribution to journalArticle

@article{697b3df711b74eb196206d2ee5b10171,
title = "Advanced glycation end products in diabetic complications",
abstract = "Advanced glycation end products accumulate as a function of the level of chronic hyperglycemia via generation of reactive dicarbonyl intermediates. Inside cells, advanced glycation end products accumulate rapidly and cause altered function of intracellular proteins. Outside cells, advanced glycation end products accumulate over longer periods of time, interfering with normal extracellular matrix interactions and causing advanced glycation end product receptor-mediated pathologic changes in gene expression. In animal models, pharmacologic inhibition of advanced glycation end product formation prevents diabetic complications in the retina, glomerulus, peripheral nerve, and artery. Efficacy results from a study in type I diabetic patients with overt nephropathy are anticipated in the third quarter of 1998.",
author = "Michael Brownlee",
year = "1996",
language = "English (US)",
volume = "3",
pages = "291--297",
journal = "Current Opinion in Endocrinology, Diabetes and Obesity",
issn = "1752-296X",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

TY - JOUR

T1 - Advanced glycation end products in diabetic complications

AU - Brownlee, Michael

PY - 1996

Y1 - 1996

N2 - Advanced glycation end products accumulate as a function of the level of chronic hyperglycemia via generation of reactive dicarbonyl intermediates. Inside cells, advanced glycation end products accumulate rapidly and cause altered function of intracellular proteins. Outside cells, advanced glycation end products accumulate over longer periods of time, interfering with normal extracellular matrix interactions and causing advanced glycation end product receptor-mediated pathologic changes in gene expression. In animal models, pharmacologic inhibition of advanced glycation end product formation prevents diabetic complications in the retina, glomerulus, peripheral nerve, and artery. Efficacy results from a study in type I diabetic patients with overt nephropathy are anticipated in the third quarter of 1998.

AB - Advanced glycation end products accumulate as a function of the level of chronic hyperglycemia via generation of reactive dicarbonyl intermediates. Inside cells, advanced glycation end products accumulate rapidly and cause altered function of intracellular proteins. Outside cells, advanced glycation end products accumulate over longer periods of time, interfering with normal extracellular matrix interactions and causing advanced glycation end product receptor-mediated pathologic changes in gene expression. In animal models, pharmacologic inhibition of advanced glycation end product formation prevents diabetic complications in the retina, glomerulus, peripheral nerve, and artery. Efficacy results from a study in type I diabetic patients with overt nephropathy are anticipated in the third quarter of 1998.

UR - http://www.scopus.com/inward/record.url?scp=0001139913&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0001139913&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:0001139913

VL - 3

SP - 291

EP - 297

JO - Current Opinion in Endocrinology, Diabetes and Obesity

JF - Current Opinion in Endocrinology, Diabetes and Obesity

SN - 1752-296X

IS - 4

ER -