Advanced Glycation End Products Associated With Cataract Formation in Individuals with Diabetes

by | May 2, 2017 | 2009, Diabetes, Eye Health

Written by Angeline A. De Leon, Staff Writer. In all four senile groups, the serum AGEs were significantly (Pb.001) lower in young control subjects thus corroborating the hypothesis that the advanced glycation process might have a role in cataract formation, which in diabetic patients is far more prevalent compared to nondiabetic cataract patients. 

eye healthNatural metabolic functions involve glycation, a process whereby sugar in the bloodstream attaches to fats and proteins in the body. Directly resulting from this is the formation of advanced glycation end products (AGE), toxic waste products which cause deformation of protein fibers and other important types of connective tissue (1). While associated with normal aging, in diabetic patients who experience sustained high blood sugar, advanced glycation contributes to pathological complications, including cataract formation (2). Studies, in fact, report diabetes as a major risk factor for the development of cataracts (3), with experimental evidence showing that AGE accumulation leads to structural damage of the eye lens (4, 5), eventually resulting in visual impairment. To date, research on serum AGEs (s-AGEs) and cataract development has focused mainly on senile diabetic patients. In an exploratory study of the role of s-AGEs in cataract formation in diabetic and nondiabetic subjects, a 2009 study published in the Journal of Diabetes and Its Complications compared serum levels of AGEs in senile diabetic and nondiabetic patients with cataract to normal senile and young subjects.

Participants consisted of five different subgroups: (1) senile Type 2 diabetic patients with cataract (n = 30); (2) senile Type 2 diabetic patients without cataract (n = 33); (3) senile nondiabetic patients with cataracts (n = 30); (4) normal senile subjects (n = 31); and (5) normal young subjects (n = 31). Participants in the senile groups were selected from patients over 60 years of age, and healthy individuals aged 20-25 were recruited as control subjects. Participants underwent a 10-hour overnight fast after which a whole blood sample was collected in the fasting state. Researchers assessed levels of fasting blood glucose, glycosylated hemoglobin (HbA1C), and serum fructosamine as measures of glycemic control. Samples were then chemically analyzed using a technique capable of detecting low serum levels of AGE fractions.

Results of the study provided the following key findings:

  1. In comparison to senile nondiabetic patients with cataract and senile control subjects, senile diabetic patients with and without cataract showed significantly higher levels of fasting blood glucose, HbA1C, and serum fructosamine (p < 0.001).
  2. In comparison to senile and young control subjects, serum AGEs were significantly increased in senile diabetic patients with cataract (p < 0.001), senile nondiabetic patients with cataract (p < 0.001), and senile diabetic patients without cataract (p < 0.001) (presented from highest to lowest concentrations of s-AGEs).
  3. In comparison to all four senile groups, young controls showed significantly lower serum AGEs (p < 0.001). When comparing senile subjects to young controls, the senile group showed about a 35% relative increase in s-AGEs (p < 0.001).

In general, evidence demonstrates a linear relationship between s-AGE levels and age, supporting previous findings on increasing trends of AGE formation over the course of normal biological aging. Findings also reveal the accelerating effect of both AGEs and diabetes on cataract formation. Implications of the study underscore the critical role of lifestyle factors in actively protecting against advanced glycation and its neurodegenerative effects, particularly in older age.

Source: Gul A, Rahman MA, Salim A, et al. Advanced glycation end products in senile diabetic and nondiabetic patients with cataract. Journal of Diabetes and Its Complications. 2009; 23: 343-348. DOI: 10.1016/j.jdiacomp.2008.04.001.

© 2009 Elsevier Inc. All rights reserved.

Posted May 2, 2017.

Angeline A. De Leon, M.A., graduated from the University of Illinois at Urbana-Champaign in 2010, completing a bachelor’s degree in psychology, with a concentration in neuroscience. She received her master’s degree from The Ohio State University in 2013, where she studied clinical neuroscience within an integrative health program. 

References:

  1. Luthra M, Balasubramania D. Nonenzymatic glycation alters protein structure and stability. A study of two eye lens crystallins. Journal of Biological Chemistry. 1993; 268: 18119-18127.
  2. Ahmed N. Advanced glycation end products role in pathology of diabetic complications. Diabetes Research and Clinical Practice. 2005; 67: 3-21.
  3. Bron A J, Brown NAP, Harding JJ, et al. The lens and cataract in diabetes. International Opthamology Clinics. 1998; 38: 37-67.
  4. Virgolici B, Stoian I, Muscurel C, et al. Plasma redox status and premature onset of senile cataract. Romanian Journal of Internal Medicine. 2007; 45: 59-65.
  5. Nass N, Bartling B, Navarrete Santos A, et al. Advanced glycation end products, diabetes, and ageing. Zeitschrift fur Gerontologie und Geriatrie. 2007; 40: 349-356.