Research progress on correlations between CD36 and type 2 diabetes mellitus
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摘要: 随着全球经济的飞速发展、人民生活水平的提高及生活方式的改变,糖尿病已成为威胁全人类生命健康的重要非传染性疾病之一,其中,2型糖尿病(T2DM)是其主要类型。目前虽然已有许多针对T2DM不同靶点的药物,但其疗效不尽如人意,且可能伴随如腹胀、恶心呕吐、体重增加、泌尿道感染等副作用。因此,寻找新的药物治疗靶点,开发新的治疗药物迫在眉睫且意义重大。胰岛素抵抗(IR)和(或)胰岛素分泌缺陷是T2DM发生、发展的重要环节,因此,寻找新的途径改善IR及调控胰岛β细胞胰岛素分泌是T2DM治疗的关键手段和重要方向。白细胞分化抗原36(CD36)是一种多功能膜蛋白受体,在机体多种细胞广泛表达,其能通过识别并结合不同的配体参与调节糖脂代谢、粘附、凋亡、炎症反应及免疫应答等多种生理和病理过程,从而参与T2DM的发生与进展。糖尿病环境下,机体主要胰岛素靶组织(包括肝脏、脂肪、骨骼肌)上高表达的CD36通过多种机制参与IR的进程,CD36还通过介导氧化应激、内质网应激、炎症反应等多种病理过程参与胰岛β细胞的分泌和死亡。此外,CD36还能通过介导脂肪感知信号传导调节脂肪偏好及摄食行为,进而参与T2DM的发生及进展过程。因此,通过调控CD36在各个组织器官的表达水平来治疗T2DM有可能成为未来治疗T2DM及相关代谢性疾病的重要途径。Abstract: With the rapid development of the global economy, the improvement of people's living standards and the changes of their life style, diabetes has become one of the most severe noncommunicable diseases threatening the life and health of the whole of humanity, among which type 2 diabetes mellitus (T2DM) accounts for the vast majority of cases. Although there are many kinds of drugs targeting different targets of T2DM, their efficacy is not satisfactory, and may be accompanied by some side-effects, such as abdominal bloating, nausea and vomiting, weight gain, urinary tract infection and so on. Therefore, it is urgent and significant to find new therapeutic targets and develop new therapeutic drugs for T2DM. T2DM is primarily caused by insufficient insulin secretion by the pancreatic β cells and/or insulin resistance (IR) in peripheral tissues. Thus, it is important to find new ways to improve IR and regulate insulin secretion of pancreatic β cells for the treatment of T2DM. Cluster of differentiation 36 (CD36) is a multifunctional membrane protein receptor, which is widely expressed in various cells of the body. It participates in the occurrence and progression of T2DM through recognizing and binding different ligands to regulate lipid metabolism, adhesion, apoptosis, inflammatory response and immune response and other physiological and pathological processes. An increased expression of CD36 induced by hyperglycemia in the main insulin target tissues, including liver, fat and skeletal muscle, is involved in IR through various mechanisms. In addition, CD36 also participates in the process of insulin secretion and pancreatic β cell death by mediating oxidative stress, endoplasmic reticulum stress, inflammation and other pathological processes. Furthermore, CD36 also regulates fat preference and feeding behavior by mediating fat perception signal transduction, participating in the occurrence and progression of T2DM. Therefore, regulation of the expression level of CD36 in various tissues and organs may become an important approach for the treatment of T2DM and related metabolic diseases in the future.
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