Advanced glycation end-products in myocardium-supported vessels: Effects of heart failure and diabetes mellitus

Nożyński, Jerzy; Zakliczyńśki, Michał; Konecka-Mrowka, D.; Przybylski, Roman; Zembala, Marian; Zielińska, Teresa; Mrówka, A.; Lange, Dariusz; Zembala‐Nożyńska, Ewa; Nikiel, Barbara; Młynarczyk-Liszka, Joanna

doi:10.1016/j.healun.2010.11.006

Cited by 14 publications

(5 citation statements)

References 20 publications

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“…8 The above suggests that the associations between circulating AGEs and LV function and structure are not straightforward. Studies conducted on human 7,[26][27][28][29][30][31][32] or animal [33][34][35][36][37][38] cardiac tissue have shown that AGEs accumulate within the myocardium, 7,[26][27][28][29][30][31][32][33][34] even more so in T2DM [26][27][28][29][30][31]34 or IGM. 33 In addition, these studies showed that the myocardial accumulation of AGEs was associated with impaired diastolic function 30,[33][34][35][36] and/or impaired systolic function.…”

Section: Discussionmentioning

confidence: 99%

Serum advanced glycation endproducts are associated with left ventricular dysfunction in normal glucose metabolism but not in type 2 diabetes: The Hoorn Study

Linssen

Henry

Schalkwijk³

et al. 2016

Diabetes and Vascular Disease Research

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Objective: To investigate whether serum advanced glycation endproducts are associated with left ventricular systolic and diastolic function in participants with normal glucose metabolism, impaired glucose metabolism and type 2 diabetes mellitus. Methods: Participants from a cross-sectional, population-based study (n = 280 with normal glucose metabolism, n = 171 with impaired glucose metabolism, n = 242 with type 2 diabetes mellitus) underwent echocardiography. Serum proteinbound advanced glycation endproducts [i.e. Nε-(carboxymethyl)lysine, pentosidine and Nε-(carboxyethyl)lysine] were measured. Linear regression analyses were used and stratified according to glucose metabolism status. Results: In normal glucose metabolism, higher Nε-(carboxymethyl)lysine and pentosidine levels were associated with worse diastolic function (left atrial volume index and left atrial volume × left ventricular mass index product term) and higher Nε-(carboxymethyl)lysine and Nε-(carboxyethyl)lysine levels with worse systolic function (ejection fraction). In impaired glucose metabolism, a similar pattern emerged, though less consistent. In type 2 diabetes mellitus, these associations were non-existent for diastolic function or even reversed for systolic function. Conclusion: This suggests that serum advanced glycation endproducts are associated with impaired left ventricular function in normal glucose metabolism, but that with deteriorating glucose metabolism status, serum advanced glycation endproducts may not mirror heart failure risk.

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Section: Discussionmentioning

confidence: 99%

Serum advanced glycation endproducts are associated with left ventricular dysfunction in normal glucose metabolism but not in type 2 diabetes: The Hoorn Study

Linssen

Henry

Schalkwijk³

et al. 2016

Diabetes and Vascular Disease Research

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“…Hyperglycaemia can have detrimental consequences on glucose deposition, which can mediate and further cause pathology in the heart of individuals with diabetes. Formation of AGEs in the heart is increased by hyperglycaemia and can be further aggravated by diabetes [63]. These form on intra-and extracellular proteins, generating protein cross-linking, and can increase free radical and reactive oxygen species (ROS) activity, leading to biochemical damage and further cardiac impairment in diabetic cardiomyopathy [64].…”

Section: Glucotoxicity and Lipotoxicitymentioning

confidence: 99%

“…Prior to the development of fibrosis, if the heart of an individual with diabetes is exposed to excess glucose, glucotoxicity may occur due to the build-up of a glucose gradient across the sarcolemma [67]. Since myocardial glucose oxidation is decreased in diabetes [20], this can lead to hyperglycaemia and the subsequent accumulation of glycolytic intermediates and products which can further contribute towards AGEs production [63], as well as increased anaplerosis and lipogenesis [68].…”

Section: Glucotoxicity and Lipotoxicitymentioning

confidence: 99%

Metabolic, structural and biochemical changes in diabetes and the development of heart failure

Karwi

Connolly

et al. 2022

Diabetologia

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Diabetes contributes to the development of heart failure through various metabolic, structural and biochemical changes. The presence of diabetes increases the risk for the development of cardiovascular disease (CVD), and since the introduction of cardiovascular outcome trials to test diabetic drugs, the importance of improving our understanding of the mechanisms by which diabetes increases the risk for heart failure has come under the spotlight. In addition to the coronary vasculature changes that predispose individuals with diabetes to coronary artery disease, diabetes can also lead to cardiac dysfunction independent of ischaemic heart disease. The hyperlipidaemic, hyperglycaemic and insulin resistant state of diabetes contributes to a perturbed energy metabolic milieu, whereby the heart increases its reliance on fatty acids and decreases glucose oxidative rates. In addition to changes in cardiac energy metabolism, extracellular matrix remodelling contributes to the development of cardiac fibrosis, and impairments in calcium handling result in cardiac contractile dysfunction. Lipotoxicity and glucotoxicity also contribute to impairments in vascular function, cardiac contractility, calcium signalling, oxidative stress, cardiac efficiency and lipoapoptosis. Lastly, changes in protein acetylation, protein methylation and DNA methylation contribute to a myriad of gene expression and protein activity changes. Altogether, these changes lead to decreased cardiac efficiency, increased vulnerability to an ischaemic insult and increased risk for the development of heart failure. This review explores the above mechanisms and the way in which they contribute to cardiac dysfunction in diabetes.

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“…Positive correlations of serum level of AGEs with ventricular isovolumetric relaxation time, arterial stiffness and carotid intimal thickness have been shown in diabetic patients. 37) 38) 39) A recent study conducted in transplant hearts by Jerzy Nozynski et al 40) reported that chronic heart failure increases AGE deposition mostly in veins, whereas type 2 DM predisposes arterioles to AGE accumulation. Receptors for advanced glycosylation end product (RAGE) also participate in the pathogenesis of DCM.…”

Section: Pathological Mechanismsmentioning

confidence: 99%

Diabetic Cardiomyopathy; Summary of 41 years

et al. 2015

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Patients with diabetes have an increased risk for development of cardiomyopathy, even in the absence of well known risk factors like coronary artery disease and hypertension. Diabetic cardiomyopathy was first recognized approximately four decades ago. To date, several pathophysiological mechanisms thought to be responsible for this new entity have also been recognized. In the presence of hyperglycemia, non-enzymatic glycosylation of several proteins, reactive oxygen species formation, and fibrosis lead to impairment of cardiac contractile functions. Impaired calcium handling, increased fatty acid oxidation, and increased neurohormonal activation also contribute to this process. Demonstration of left ventricular hypertrophy, early diastolic and late systolic dysfunction by sensitive techniques, help us to diagnose diabetic cardiomyopathy. Traditional treatment of heart failure is beneficial in diabetic cardiomyopathy, but specific strategies for prevention or treatment of cardiac dysfunction in diabetic patients has not been clarified yet. In this review we will discuss clinical and experimental studies focused on pathophysiology of diabetic cardiomyopathy, and summarize diagnostic and therapeutic approaches developed towards this entity.

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Advanced glycation end-products in myocardium-supported vessels: Effects of heart failure and diabetes mellitus

Cited by 14 publications

References 20 publications

Serum advanced glycation endproducts are associated with left ventricular dysfunction in normal glucose metabolism but not in type 2 diabetes: The Hoorn Study

Serum advanced glycation endproducts are associated with left ventricular dysfunction in normal glucose metabolism but not in type 2 diabetes: The Hoorn Study

Metabolic, structural and biochemical changes in diabetes and the development of heart failure

Diabetic Cardiomyopathy; Summary of 41 years

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