糖尿病性骨质疏松症是一种常见的健康问题，与骨代谢紊乱有关。 A2A 腺苷受体 (A2AAR) 信号传导似乎在骨稳态中发挥着关键作用。本研究旨在评估 A2AAR 刺激与胰岛素治疗相比，对糖尿病引起的骨质疏松症的治疗效果。将 40 只成年雄性大鼠分配为对照组 (C)、未治疗的糖尿病引起的骨质疏松症 (DIO)、胰岛素治疗的 DIO (I-DIO) 和 A2AAR 激动剂治疗的 DIO (A-DIO) 组。胰岛素和 A2AAR 激动剂治疗均显着增加血清胰岛素水平、谷胱甘肽过氧化物酶 (GPx) 活性、骨保护素 (Opg) 和 β-连环蛋白 (Ctnnb1) 的骨表达以及皮质骨和小梁骨厚度，同时降低血清空腹血糖、丙二醛。 MDA)、肿瘤坏死因子 α (TNF-α)、核因子 kappa-B 配体受体激活剂 (Rankl)、runt 相关转录因子 2 (Runx2) 和硬化素 (Sost) 与未治疗 DIO 组的骨表达。 A2AAR 激动剂治疗在改善糖尿病骨质疏松症方面比胰岛素更有效。这可能归因于 β-连环蛋白基因表达的上调，增强其对骨的合成代谢作用，以及 A2AAR 激动剂的抗氧化、抗炎和抗糖尿病作用。

Diabetic osteoporosis is a common health problem that is associated with a disruption in bone metabolism. A2A adenosine receptor (A2AAR) signaling seems to play a critical role in bone homeostasis. This study aimed to evaluate the effect of A2AAR stimulation on the treatment of diabetic-induced osteoporosis versus insulin treatment. Forty adult male rats were allocated into control (C), untreated diabetic-induced osteoporosis (DIO), insulin-treated DIO (I-DIO), and A2AAR agonist-treated DIO (A-DIO) groups. Both insulin and A2AAR agonist treatments significantly increased serum insulin level, glutathione peroxidase (GPx) activity, bone expression of osteoprotegerin (Opg) and β-catenin (Ctnnb1), and cortical and trabecular bone thickness, whereas they decreased serum fasting glucose, malondialdehyde (MDA), tumor necrosis factor α (TNF-α), bone expression of receptor activator of nuclear factor kappa-B ligand (Rankl), runt-related transcription factor-2 (Runx2), and sclerostin (Sost) versus the untreated DIO groups. A2AAR agonist treatment was more effective than insulin in ameliorating diabetic osteoporosis. This might be attributed to the upregulation of β-catenin gene expression, enhancing its anabolic effect on bone, in addition to the A2AAR agonist's anti-oxidative, anti-inflammatory, and anti-diabetic effects.