Inhibition of Advanced Glycation End Products: A Nexus of Chicken Hyperglycemia and Inflammation Absence.

Poultry have higher blood glucose concentrations, which are 1.5-2 times those of their mammalian counterparts with equivalent body mass, yet do not show any adverse effects. However, the underlying mediators that inhibit systemic inflammation under hyperglycemia are unclear. In this study, chickens and rats were chosen as representatives of poultry and mammals, and the physiological differences in blood glucose regulation between them were investigated under control conditions and streptozotocin (STZ)-induced hyperglycemia, respectively, to explore the internal causes of hyperglycemia without symptoms in poultry. Firstly, the fasting blood glucose (FBG) and glucagon concentrations increased significantly (p < 0.01) and the insulin concentrations decreased when chickens and rats were treated with STZ (p < 0.001). STZ injections in rats resulted in higher oral glucose tolerance test (OGTT) and intraperitoneal insulin tolerance test (IPITT) levels (p < 0.001), but there was no significant difference in chickens. In addition, the body weight development of STZ-inducted rats was retarded, while it was not the case for chickens receiving STZ. Secondly, high glucose metabolism products, including advanced glycation end products (AGEs) were detected in STZ-inducted rats and chickens. The AGEs concentration in the rats receiving STZ was significantly higher than that in control group rats (p < 0.001); however, there was no significant difference in chickens. Also, the concentrations of free amino acids inhibiting AGEs were further explored, and higher concentrations of taurine, leucine, and lysine were observed in chickens than those observed in rats (p < 0.05). Moreover, the concentrations were decreased significantly in STZ-treated chickens (p < 0.05). Finally, the inflammation in tissues vulnerable to high blood glucose was examined, and it was found that there were significantly increased mRNA and protein expression levels of inflammatory factors such as nuclear factor-κB (NF-κB) and interleukin-1β (IL-1β) in STZ-injected rats (p < 0.001), while there was no obvious effect in STZ-induced chickens. The results revealed the damage and inflammation resulting from STZ-induced hyperglycemia in chickens were significantly lower compared to rats. This may be attributed to the high concentrations of free amino acids in chickens, which inhibit AGE formation by functioning as carbonyl scavengers. This study elucidates the underlying causes of the absence of inflammation in chickens compared to rats under hyperglycemic conditions, offering new insights for controlling diabetic complications.