Nonenzymatic glycosylation of macromolecules: Prospects of pharmacologic modulation

Michael Brownlee

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

Diabetes increases the risk of developing atherosclerotic arterial disease significantly. Although elevated glycohemoglobin was shown to be an independent risk factor in older women in the Framingham Heart Study, the relationship between hyperglycemia and macrovascular disease is complicated by the many other factors that influence atherogenesis in nondiabetic people. Studies in vitro suggest that chronic hyperglycemia may accelerate the atherogenic process through excessive glycation of various components of the arterial wall. These data are reviewed critically, and the biochemistry and pharmacological potential of the glycation-inhibitor aminoguanidine is discussed.

Original languageEnglish (US)
Pages (from-to)57-60
Number of pages4
JournalDiabetes
Volume41
Issue numberSUPPL. 2
StatePublished - 1992

Fingerprint

Glycosylation
Hyperglycemia
Biochemistry
Atherosclerosis
Pharmacology
In Vitro Techniques
pimagedine

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Internal Medicine

Cite this

Nonenzymatic glycosylation of macromolecules : Prospects of pharmacologic modulation. / Brownlee, Michael.

In: Diabetes, Vol. 41, No. SUPPL. 2, 1992, p. 57-60.

Research output: Contribution to journalArticle

Brownlee, Michael. / Nonenzymatic glycosylation of macromolecules : Prospects of pharmacologic modulation. In: Diabetes. 1992 ; Vol. 41, No. SUPPL. 2. pp. 57-60.
@article{041e4268249e4f6aacf23270cb333f10,
title = "Nonenzymatic glycosylation of macromolecules: Prospects of pharmacologic modulation",
abstract = "Diabetes increases the risk of developing atherosclerotic arterial disease significantly. Although elevated glycohemoglobin was shown to be an independent risk factor in older women in the Framingham Heart Study, the relationship between hyperglycemia and macrovascular disease is complicated by the many other factors that influence atherogenesis in nondiabetic people. Studies in vitro suggest that chronic hyperglycemia may accelerate the atherogenic process through excessive glycation of various components of the arterial wall. These data are reviewed critically, and the biochemistry and pharmacological potential of the glycation-inhibitor aminoguanidine is discussed.",
author = "Michael Brownlee",
year = "1992",
language = "English (US)",
volume = "41",
pages = "57--60",
journal = "Diabetes",
issn = "0012-1797",
publisher = "American Diabetes Association Inc.",
number = "SUPPL. 2",

}

TY - JOUR

T1 - Nonenzymatic glycosylation of macromolecules

T2 - Prospects of pharmacologic modulation

AU - Brownlee, Michael

PY - 1992

Y1 - 1992

N2 - Diabetes increases the risk of developing atherosclerotic arterial disease significantly. Although elevated glycohemoglobin was shown to be an independent risk factor in older women in the Framingham Heart Study, the relationship between hyperglycemia and macrovascular disease is complicated by the many other factors that influence atherogenesis in nondiabetic people. Studies in vitro suggest that chronic hyperglycemia may accelerate the atherogenic process through excessive glycation of various components of the arterial wall. These data are reviewed critically, and the biochemistry and pharmacological potential of the glycation-inhibitor aminoguanidine is discussed.

AB - Diabetes increases the risk of developing atherosclerotic arterial disease significantly. Although elevated glycohemoglobin was shown to be an independent risk factor in older women in the Framingham Heart Study, the relationship between hyperglycemia and macrovascular disease is complicated by the many other factors that influence atherogenesis in nondiabetic people. Studies in vitro suggest that chronic hyperglycemia may accelerate the atherogenic process through excessive glycation of various components of the arterial wall. These data are reviewed critically, and the biochemistry and pharmacological potential of the glycation-inhibitor aminoguanidine is discussed.

UR - http://www.scopus.com/inward/record.url?scp=0026701935&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026701935&partnerID=8YFLogxK

M3 - Article

C2 - 1526337

AN - SCOPUS:0026701935

VL - 41

SP - 57

EP - 60

JO - Diabetes

JF - Diabetes

SN - 0012-1797

IS - SUPPL. 2

ER -