Protein glycosylation and advanced glycosylated endproducts (AGEs) accumulation: an avian solution?

The objectives of this study were to determine the effect of diet restriction (DR) and the crosslinking inhibitor, aminoguanidine (AG), on PMA-induced respiratory burst, concentrations of uric acid, and the rate of pentosidine accumulation in the skin (Ps) of naturally hyperglycemic broiler breeder hens. Female chicks (n = 450) were randomly assigned to four groups from 8 to 92 weeks after hatch: ad libitum (AL), diet restricted (DR), AL and DR groups supplemented with 400 ppm AG each (AL + AG and DR + AG). No consistent effects of treatments were observed on plasma concentrations of glucose. The accumulation of Ps in AL birds increased linearly with age (p < .001) and was significantly retarded in all treatment groups (p < .001). Ps in the AL + AG group was comparable to that in the DR or DR + AG groups. PMA-induced respiratory bursts in blood leukocytes were significantly retarded in DR or AG-supplemented (p < .0001) groups. Although there was a marginal increase in overall mean concentrations of plasma uric acid for the DR group, no consistent differences were observed on individual time points. It is concluded that the glycosylation process may not be the primary cause of glucose-derived crosslinks and that the accumulation of Ps can be retarded by DR and AG in broiler breeder hens.