近几十年来,糖尿病患者的数量急剧上升,主要是由于2型糖尿病(T2DM)的发病率上升。几种口服抗糖尿病药物用于治疗T2DM,包括,α-葡萄糖苷酶抑制剂,双胍,磺酰脲类,meglinides,GLP-1受体激动剂,PPAR-γ激动剂,DDP4抑制剂,和SGLT2抑制剂。在这篇综述中,我们关注SGLT2抑制剂对不同身体系统的可能影响。除了糖尿病状态,SGLT2抑制剂已显示出明显的改善心脏重塑的能力,增强心肌功能,降低心力衰竭死亡率。此外,SGLT2抑制剂可以修饰脂肪细胞及其细胞因子的产生,如脂肪因子和脂联素,增强胰岛素敏感性并延迟糖尿病的发病。另一方面,SGLT2抑制剂与T2DM患者的总髋骨矿物质沉积减少和髋骨吸收增加有关。需要更多的数据来评估SGLT2抑制剂对癌症的作用。最后,SGLT2抑制剂对神经保护的作用似乎是直接和间接的,根据利用各种实验模型的科学研究。SGLT2抑制剂改善血管张力,弹性,通过减少氧化应激和收缩性,炎症,胰岛素信号通路,和内皮细胞增殖。它们还能改善大脑功能,突触可塑性,乙酰胆碱酯酶活性,减少淀粉样蛋白斑块的形成,以及大脑中mTOR通路的调节,减少脑损伤和认知能力下降。
The number of diabetic patients has risen dramatically in recent decades, owing mostly to the rising incidence of type 2 diabetes mellitus (T2DM). Several oral antidiabetic medications are used for the treatment of T2DM including, α-glucosidases inhibitors, biguanides, sulfonylureas, meglitinides, GLP-1 receptor agonists, PPAR-γ agonists, DDP4 inhibitors, and SGLT2 inhibitors. In this review we focus on the possible effects of SGLT2 inhibitors on different body systems. Beyond the diabetic state, SGLT2 inhibitors have revealed a demonstrable ability to ameliorate cardiac remodeling, enhance myocardial function, and lower heart failure mortality. Additionally, SGLT2 inhibitors can modify adipocytes and their production of cytokines, such as adipokines and adiponectin, which enhances insulin sensitivity and delays diabetes onset. On the other hand, SGLT2 inhibitors have been linked to decreased total hip bone mineral deposition and increased hip bone resorption in T2DM patients. More data are needed to evaluate the role of SGLT2 inhibitors on cancer. Finally, the effects of SGLT2 inhibitors on neuroprotection appear to be both direct and indirect, according to scientific investigations utilizing various experimental models. SGLT2 inhibitors improve vascular tone, elasticity, and contractility by reducing oxidative stress, inflammation, insulin signaling pathways, and endothelial cell proliferation. They also improve brain function, synaptic plasticity, acetylcholinesterase activity, and reduce amyloid plaque formation, as well as regulation of the mTOR pathway in the brain, which reduces brain damage and cognitive decline.