International Journal of Preventive Medicine (Int J Prev Med)2008-78021452023060628202820ENDepartment of Sport Sciences, University of Isfahan, IsfahanDepartment of Sport Sciences, University of Isfahan, IsfahanDepartment of Sport Sciences, University of Isfahan, IsfahanDepartment of Sport Sciences, Shahrekord University, ShahrekordDepartment of Neuroscience, Shahrekord University of Medical Sciences, Shahrekord20230606Background: Both aging and diabetes are two well‑established risk factors related to type 3 diabetes and memory deficits. Accordingly, diabetes multiplies the effects of aging on cognition impairments once these conditions occur simultaneously. Methods: In this present experimental study, 56 male Wistar rats with HFD/STZ‑induced T2D were randomized into seven groups (n = eight animals per group): (1) sedentary old non‑diabetic (C); (2) sedentary HFD/STZ‑induced T2D (D); (3) sedentary HFD/STZ‑induced T2D plus UA (UA) (DU); (4) endurance‑trained HFD/STZ‑induced T2D (DE); (5) resistance‑trained HFD/STZ‑induced T2D (DR); (6) endurance‑trained HFD/STZ‑induced T2D plus UA (DEU); and (7) resistance‑trained STZ‑diabetic plus UA (DRU) rats. Two‑way ANOVA was applied to measure the training, supplementation, and interaction effect on serum and gene expression outcomes. Result: The study results established no significant interaction effect between the UA supplementation and the resistance/endurance training with regard to the levels of glucose (P = 0.534), insulin (P = 0.327), brain‑derived neurotrophic factor (P = 0.191), and insulin‑like growth factor‑1 (P = 0.448). Conclusions: To develop novel practical nutritional strategies involving UA intake, further studies are thus needed to clarify how chronic consumption of UA with/without resistance/endurance training reverses cognition disorder process in old male Wistar rats with HFD/STZ‑induced T2D.http://ijpm.mui.ac.ir/index.php/ijpm/article/view/2820http://ijpm.mui.ac.ir/index.php/ijpm/article/download/2820/717718661