Aims: Human studies of links between advanced glycation end-products (AGEs) and disease phenotypes are less common than studies of animal and cell models. Here, we examined the association of total AGEs with diabetes risk factors in a predominately type 2 diabetes (T2D) affected cohort.
Methods: AGEs were measured using an enzyme linked immunosorbant assay in 816 individuals from the DHS Mind Study (n=709 T2D affected), and association analyses were completed.
Results: Total AGEs were associated with estimated glomerular filtration rate (p=0.0054; β=-0.1291) and coronary artery calcification (p=0.0352; β=1.1489) in the entire cohort. No significant associations were observed when individuals with T2D were analyzed separately. In individuals without T2D, increased circulating AGEs were associated with increased BMI (p=0.02, β=0.138), low density lipoproteins (p=0.046, β=17.07) and triglycerides (p=0.0004, β=0.125), and decreased carotid artery calcification (p=0.0004, β=-1.2632) and estimated glomerular filtration rate (p=0.0018, β=-0.1405). Strong trends were also observed for an association between AGEs and poorer cognitive performance on the digit symbol substitution test (p=0.046, β=-6.64) and decreased grey matter volume (p=0.037, β=-14.87).
Conclusions: AGEs may play an important role in a number of phenotypes and diseases, although not necessarily in interindividual variation in people with T2D. Further evaluation of specific AGE molecules may shed more light on these relationships.
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http://dx.doi.org/10.1016/j.jdiacomp.2015.11.025 | DOI Listing |
J Diabetes Res
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Diabetes Center, Dallah Hospital, Riyadh, Saudi Arabia.
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Hebei Key Laboratory of Organ Fibrosis, School of Public Health, North China University of Science and Technology, Tangshan, Hebei 063210, China. Electronic address:
Epithelial-mesenchymal transition (EMT) is implicated in the pathogenesis of silicosis. High mobility group box 1 (HMGB1) has been found to induce EMT in fibrotic diseases. Previous studies have revealed a critical role of HMGB1 in silicosis, whereas the detail mechanisms still obscure.
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Department of Pharmacology, Graduate School of Medicine, Yamaguchi University, Yamaguchi, Japan; Research Institute for Cell Design Medical Science, Yamaguchi University, Yamaguchi, Japan. Electronic address:
Impaired fracture healing in diabetic patients leads to prolonged morbidity and increased healthcare costs. Methylglyoxal (MG), a reactive metabolite elevated in diabetes, is implicated in various complications, but its direct impact on bone healing remains unclear. Here, using a non-diabetic murine tibial fracture model, we demonstrate that MG directly impairs fracture healing.
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Pharmacognosy Department, Faculty of Pharmacy, Cairo University, Kasr El-Aini, Cairo 11562, Egypt.
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View Article and Find Full Text PDFJ Clin Med
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Cardiothoracovascular Department, Azienda Sanitaria Universitaria Giuliano Isontina, 34100 Trieste, Italy.
Despite notable advancements in cardiovascular medicine, morbidity and mortality rates associated with myocardial infarction (MI) remain high. The unfavourable prognosis and absence of robust post-MI protocols necessitate further intervention. In this comprehensive review, we will focus on well-established and novel biomarkers that can provide insight into the processes that occur after an ischemic event.
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