Therefore, exogenous AGEs are believed (but not yet conclusively demonstrated) to play a role in the development of diabetes complications in addition to the endogenously generated AGEs.
In the post-prandial period, absorbed and endogenously generated AGEs and MG act synergistically to decrease vascular function by directly scavenging NO and increasing oxidative stress.
We generated AGEs by incubating BSA (25 mg/ml) with 250 mM glucose 6-phosphate at 37 °C for 6 8 weeks in 0.1 M phosphate buffer containing 1.5 mM PMSF, 0.5 mM EDTA, and 1 mM azide.
Formally, (14) h (c ) : = | T | − 1 ∑ T i ∈ T h ¯ (c, T i ) The generated ages always produce a tree, since x ⊂ y ⇒ h ¯ (x, T i ) ≤ h ¯ (y, T i ).
The reduction in endogenously generated AGEs goes beyond the treatment of hyperglycemia, since several treatments that reduce oxidative and carbonyl stress (e.g., angiotensin II receptor inhibitors, antioxidants, aminoguanidine) have proven their efficacy in decreasing AGE levels (19).
We therefore believe that endogenously generated AGEs and precursors act synergistically with the exogenous AGEs to induce oxidative stress and lead to the long-term cardiovascular and diabetes complications.
