Jeremy N Adams1, Susan E Martelle1, Laura M Raffield1, Barry I Freedman2, Carl D Langefeld3, Fang-Chi Hsu3, Joseph A Maldjian4, Jeff D Williamson5, Christina E Hugenschmidt5, J Jeffery Carr1, Amanda J Cox6, Donald W Bowden7. 1. Center for Genomics and Personalized Medicine Research, Wake Forest School of Medicine, Winston - Salem, NC, USA. 2. Department of Internal Medicine, Nephrology, Wake Forest School of Medicine, Winston - Salem, NC, USA. 3. Department of Biostatistical Sciences, Wake Forest University Health Sciences, Winston Salem, North Carolina. 4. Radiologic Sciences and Advanced NeuroScience Imaging (ANSIR) Laboratory, Wake Forest School of Medicine, Winston-Salem, NC, USA. 5. Department of Internal Medicine, Gerontology and Geriatric Medicine, Wake Forest School of Medicine, Winston - Salem, NC, USA. 6. Molecular Basis of Disease, Griffith University, Southport, QLD, Australia. 7. Center for Genomics and Personalized Medicine Research, Wake Forest School of Medicine, Winston - Salem, NC, USA. Electronic address: dbowden@wakehealth.edu.
Abstract
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.
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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