Trends in Endocrinology & Metabolism
Brief reviewThe role of oxidation and glycation in the pathogenesis of diabetic atherosclerosis
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Cited by (19)
Resistance to glycation in the zebra finch: Mass spectrometry-based analysis and its perspectives for evolutionary studies of aging
2022, Experimental GerontologyCitation Excerpt :Further reactions yield a highly heterogeneous group of advanced glycation end products (AGEs, (Poulsen et al., 2013; Ramasamy et al., 2010)). Abnormal glycation levels in humans, e.g. when glycaemia is high, promotes oxidative stress and diabetes, cardiovascular and neurodegenerative diseases, and may ultimately contribute to aging (Masoro et al., 1989; O'Brien and Timmins, 1994; Sell et al., 1996; Semba et al., 2010; Ulrich and Cerami, 2001). Recent hypotheses put forward to explain the bird paradox “high glucose – low glycation – long lifespan” included a lower propensity to accumulate AGEs over time (Klandorf et al., 1999; Rattiste et al., 2015), a lower permeability to glucose and/or a shorter half-life of certain cell types that are sensitive to AGEs accumulation (i.e. red blood cells) or specificities of avian protein sequences that may limit potential for Amadori reactions (Holmes et al., 2001; Zuck et al., 2017).
Type 1 diabetes increases retention of low-density lipoprotein in the atherosclerosis-prone area of the murine aorta
2017, AtherosclerosisCitation Excerpt :First, the diabetic arterial wall is characterized by increased expression of extracellular proteoglycans, as well as the accumulation of glycated proteins, which may mediate LDL retention [30]. Second, prolonged hyperglycaemia is associated with excessive cross-linking of collagen and ECM proteins in the vascular wall, resulting mainly from glycation of proteins and formation of advanced glycation end products (AGEs), which could lead to both accumulation and subsequent oxidative modification of LDL [31,32]. Third, changes in LDL retention could lead to changes in the distribution of atherosclerosis.
Diabetes status modifies the association between carotid intima-media thickness and incident heart failure: The Atherosclerosis Risk in Communities study
2017, Diabetes Research and Clinical PracticeCitation Excerpt :Carotid IMT may have been increased in persons with abnormal glucose metabolism, compared to those with a NFG, for a number of reasons including a direct effect of chronic hyperglycaemia on the carotid artery walls or an indirect effect of diabetes-related metabolic abnormalities. Chronic hyperglycaemia, advanced glycosylation end-products [21,22], and the acceleration of lipoprotein oxidation [23], might increase the risk of carotid atherosclerosis in these individuals. In addition, T2D is also associated with CHD risk factors, including dyslipidaemia and hypertension [20], both of which have been linked to greater CIMT.
In vitro and in vivo antioxidant properties of gliclazide
2000, Journal of Diabetes and its ComplicationsGlycation of apolipoprotein E impairs its binding to heparin: Identification of the major glycation site
1999, Biochimica et Biophysica Acta - Molecular Basis of Disease