The glycation pathway in type 2 diabetes and cardiovascular disease

L. Engelen

doi:10.26481/dis.20121012le

The glycation pathway in type 2 diabetes and cardiovascular disease

L. Engelen

Research output: Thesis › Doctoral Thesis › Internal

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Abstract

The increased formation of glycated proteins (advanced glycation end products (AGE’s)) is a possible mechanism to explain the increased risk of cardiovascular diseases with diabetes. Although earlier (animal) experimental studies have shown this role of AGE’s, research for this dissertation does not establish a connection between AGE’s in the blood and cardiovascular diseases in persons with diabetes type 2. Moreover, there is no definite epidemiologic proof for favourable effects of specific AGE-inhibiting treatments and for decreasing AGE’s in blood by existing treatments. This does not mean that AGE’s are unimportant in the development of diabetes 2 related cardiovascular diseases, but it does mean that the current biomarkers in blood don’t sufficiently reflect damage in tissues as a result of AGE’s. Better biomarkers are therefore needed.

Original language	English
Qualification	Doctor of Philosophy
Awarding Institution	Maastricht University
Supervisors/Advisors	Stehouwer, Coen, Supervisor Schalkwijk, Casper, Supervisor Ferreira de Sousa, Maria, Co-Supervisor
Award date	12 Oct 2012
Place of Publication	Maastricht
Publisher	Ipskamp Drukkers B.V., Enschede
Print ISBNs	978 94 6191 421 7
DOIs	https://doi.org/10.26481/dis.20121012le
Publication status	Published - 1 Jan 2012

Keywords

cardiovascular diseases
diabetes type 2
glycated proteins
biomarkers

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10.26481/dis.20121012le

Full TextFinal published version, 10.3 MB
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Cite this

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abstract = "The increased formation of glycated proteins (advanced glycation end products (AGE{\textquoteright}s)) is a possible mechanism to explain the increased risk of cardiovascular diseases with diabetes. Although earlier (animal) experimental studies have shown this role of AGE{\textquoteright}s, research for this dissertation does not establish a connection between AGE{\textquoteright}s in the blood and cardiovascular diseases in persons with diabetes type 2. Moreover, there is no definite epidemiologic proof for favourable effects of specific AGE-inhibiting treatments and for decreasing AGE{\textquoteright}s in blood by existing treatments. This does not mean that AGE{\textquoteright}s are unimportant in the development of diabetes 2 related cardiovascular diseases, but it does mean that the current biomarkers in blood don{\textquoteright}t sufficiently reflect damage in tissues as a result of AGE{\textquoteright}s. Better biomarkers are therefore needed. ",

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