The association between advanced glycation end products (AGEs) and ABC (hemoglobin A1C, blood pressure, and low-density lipoprotein cholesterol) control parameters among patients with type 2 diabetes mellitus

Abstract

Background Diabetes-induced chronic hyperglycemia results in the formation and aggregation of advanced glycation end-products (AGEs), which are products of non-enzymatic glycosylation of lipids or proteins. The development of diabetic complications can be accelerated by AGEs. In the current study, we aimed to explore the relationship between AGEs levels and ABC goals of diabetes control (A: Hemoglobin A1C < 7.0%, B: Blood pressure < 140/90 mmHg, and C: low-density lipoprotein cholesterol [LDL] < 100 mg/dL). Methods In the current cross-sectional study, 293 patients with type 2 diabetes mellitus (T2D), were enrolled. Demographic and clinical characteristics of the individuals were collected. AGEs levels were measured using quantitative fluorescence spectroscopy. Finally, the association of AGEs levels with patients' characteristics and ABC goals was assessed. Results Higher serum AGEs concentration was detected in older age, smoking patients and those with higher diastolic blood pressure, lower high-density lipoprotein (HDL) level, lower body mass index (BMI) and retinopathy. Moreover, the T2D patients who achieved higher numbers of ABC goals of diabetes were younger age (P-value = 0.003), with lower hemoglobin A1C (P-value = 0.001), fasting blood sugar (P-value = 0.002) diastolic blood pressure (P-value = 0.001), systolic blood pressure (P-value = 0.001), cholesterol (P-value = 0.001), LDL (P-value = 0.001), and AGEs (P-value = 0.023) levels. Diabetic patients with AGEs levels above 73.9% were about 2.2 times more likely to achieve none of ABC treatment goals (95% CI 1.107–3.616). Conclusion Our results revealed the relationship between AGEs and ABC goal achievement, and microvascular diabetic complications, and imply that AGEs measurement may be valuable in the monitoring of diabetic patients' complications and treatment adjustment.

Clinical value of noninvasive lens advanced glycation end product detection in early screening and severity evaluation of patients with diabetic kidney disease

“…We also found that the concentration of noninvasive lens AGEs was an independent risk factor for the severity of DKD and had a high regression coefficient, which indicates that it has certain clinical value in evaluating the severity of DKD. Rezaei Mohaddeseh et al [ 26 ] found that plasma AGE concentrations were positively correlated with diabetic retinopathy, but no correlation was found between plasma AGE concentrations and DKD. In this study, by measuring the contents of AGEs in the lens, we found that they were correlated with DKD.…”

The Role of Advanced Glycation End-Product Levels Measured by Skin Autofluorescence in the Development of Mitral Annular Calcification

“…This leads to an increase in the level of microvascular complications of DM. Rezaei, M. et al support this assumption; their studies show that AGEs measurements are valuable in the follow-up of DM complications, but they were unable to prove a relationship between HbA1c levels and blood sugar regulation and AGE levels in their work [ 26 ]. One reason for the development of MAC may be the accumulation of AGEs in MVA; to confirm this, further tissue analyses are required.…”

Risk Factors for Diabetic Retinopathy in Latin America (Mexico) and the World: A Systematic Review and Meta-Analysis

“…Affecting the nonenzymatic glycation process in the formation of Amadori products, which are initially the basis for the generation and accumulation of advanced glycation products (AGEs) that play an important pathophysiological role in DR, damage to the blood vessels of the retina is caused by the accumulation of AGEs ions within the cells and in the extracellular matrix, which leads to hardening of the blood vessels, which does not allow them to vasodilate and cause them to rupture or become blocked and cause a reduction in blood flow. Additionally, AGEs cause mitochondrial deterioration, and both events cause retinal hypoxia [45].…”