Advanced glycation in diabetic patients leads to cataracts

The higher level of advanced glycation end products (AGE) in senile diabetic patients may correlate to a higher rate of cataract development, according to a study published in the May–June 2008 issue of the Journal of Diabetes and its Complications.

Anjuman Gul, MBBS, MPhil of the Department of Biochemistry, Ziauddin University, Pakistan and colleagues performed a noncompetitive enzyme linked immunosorbent assay (ELISA) with a polyclonal anti-AGE antibody to study AGE immunoreactivity and investigate the link between AGE and cataract formation. Four senile study groups were assessed: non-diabetic non-cataract subjects (n=31); diabetic non-cataract subjects (n=33); diabetic cataract subjects (n=30); and non-diabetic cataract subjects (n=30). A fifth group (young non-diabetic non-cataract subjects; n=31) was also included in the evaluation.

Amongst the four senile groups, diabetic patients had significantly increased levels of fasting blood glucose, glycosylated haemoglobin and serum fructosamine when compared with non-diabetic patients, regardless of the presence (or non-presence) of cataracts. Cataract patients had significantly increased levels of serum AGEs compared with non-cataract patients; diabetic subjects also had increased serum AGE levels, but these were higher in those with cataracts than those without. Young patients had significantly lower AGE levels than any other group.

Thus the researchers concluded that senile diabetic subjects are prone to cataract development because of the distribution of AGEs in these subjects. This reinforces the theory that the advanced glycation process may have a role in cataract formation.