TY - JOUR
T1 - Plasma Levels of Advanced Glycation Endproducts N-is an element of-(carboxymethyl)lysine, N-is an element of-(carboxyethyl)lysine, and Pentosidine Are not Independently Associated With Cardiovascular Disease in Individuals With or Without Type 2 Diabetes: The Hoorn and CODAM Studies
AU - Hanssen, Nordin M. J.
AU - Engelen, Lian
AU - Ferreira, Isabel
AU - Scheijen, Jean L. J. M.
AU - Huijberts, Maya S.
AU - van Greevenbroek, Marleen M. J.
AU - van der Kallen, Carla J. H.
AU - Dekker, Jacqueline M.
AU - Nijpels, Giel
AU - Stehouwer, Coen D. A.
AU - Schalkwijk, Casper G.
PY - 2013/8
Y1 - 2013/8
N2 - Objective: Experimental and histological data suggest a role for advanced glycation end products (AGEs) in cardiovascular disease (CVD), particularly in type 2 diabetes (T2DM). However, the epidemiological evidence of an adverse association between AGEs and CVD remains inconclusive. We therefore investigated, in individuals with various degrees of glucose metabolism, the associations of plasma AGEs with prevalent CVD. Research Design and Methods: We measured plasma levels of protein-bound N-is an element of-(carboxymethyl)lysine (CML), N-is an element of-(carboxyethyl)lysine (CEL), and pentosidine, in participants from two Dutch cohort studies (n = 1291, mean age 64.7 +/- 8.3 years, 45% women), including 573 individuals with normal glucose metabolism, 304 with impaired glucose metabolism, and 414 with T2DM. In addition, we measured free CML, CEL, and 5-hydro-5-methylimidazolone in a subset of participants (n = 554). Data were analyzed with multiple logistic or linear regression analyses. Results: CEL (32 [interquartile range: 2540 vs 28 [22-35] nmol/mmol lysine]) and pentosidine (0.53 [0.43-0.67] vs 0.48 [0.40-0.59] nmol/mmol lysine) as well as free CEL (48 [39-62] vs 45 [36-56] nmol/L) and 5-hydro-5-methylimidazolone (141 [96-209] vs 116 [84-165] nmol/L) were higher in individuals with vs without CVD, whereas protein-bound CML was lower (33 [27-38] vs 34 [29-39] nmol/mmol lysine). However, these differences disappeared after adjustment for confounders. The associations did not differ consistently between individuals with and without T2DM. Conclusions: We found no independent adverse associations of plasma AGEs with CVD in individuals with normal glucose metabolism, impaired glucose metabolism, and T2DM.
AB - Objective: Experimental and histological data suggest a role for advanced glycation end products (AGEs) in cardiovascular disease (CVD), particularly in type 2 diabetes (T2DM). However, the epidemiological evidence of an adverse association between AGEs and CVD remains inconclusive. We therefore investigated, in individuals with various degrees of glucose metabolism, the associations of plasma AGEs with prevalent CVD. Research Design and Methods: We measured plasma levels of protein-bound N-is an element of-(carboxymethyl)lysine (CML), N-is an element of-(carboxyethyl)lysine (CEL), and pentosidine, in participants from two Dutch cohort studies (n = 1291, mean age 64.7 +/- 8.3 years, 45% women), including 573 individuals with normal glucose metabolism, 304 with impaired glucose metabolism, and 414 with T2DM. In addition, we measured free CML, CEL, and 5-hydro-5-methylimidazolone in a subset of participants (n = 554). Data were analyzed with multiple logistic or linear regression analyses. Results: CEL (32 [interquartile range: 2540 vs 28 [22-35] nmol/mmol lysine]) and pentosidine (0.53 [0.43-0.67] vs 0.48 [0.40-0.59] nmol/mmol lysine) as well as free CEL (48 [39-62] vs 45 [36-56] nmol/L) and 5-hydro-5-methylimidazolone (141 [96-209] vs 116 [84-165] nmol/L) were higher in individuals with vs without CVD, whereas protein-bound CML was lower (33 [27-38] vs 34 [29-39] nmol/mmol lysine). However, these differences disappeared after adjustment for confounders. The associations did not differ consistently between individuals with and without T2DM. Conclusions: We found no independent adverse associations of plasma AGEs with CVD in individuals with normal glucose metabolism, impaired glucose metabolism, and T2DM.
U2 - 10.1210/jc.2013-1068
DO - 10.1210/jc.2013-1068
M3 - Article
C2 - 23780372
SN - 0021-972X
VL - 98
SP - E1369-E1373
JO - Journal of Clinical Endocrinology & Metabolism
JF - Journal of Clinical Endocrinology & Metabolism
IS - 8
ER -