本文選題：二肽基肽酶-4抑制劑 + β-細胞��； 參考：《重慶醫(yī)科大學》2015年碩士論文

【摘要】：第一部分：DPP-4抑制劑對胰島β-細胞功能的影響糖尿病發(fā)生發(fā)展的根本原因在于胰島功能的進行性衰竭,其中既包括胰島β-細胞分泌胰島素(INS)缺陷,同時也存在α-細胞不適當?shù)姆置谝雀哐撬匾约巴庵芙M織存在的胰島素抵抗作用。如何改善糖尿病患者的胰島功能,進而延緩疾病進展已成為目前糖尿病治療的新熱點。二肽基肽酶-4(DPP-4)抑制劑(DPP-4I)是近年來一種新型降血糖藥物,在各種糖尿病(DM)動物模型中可見DPP-4I能增加β-細胞團,修復損傷的胰島細胞分布,增加胰島素量。而臨床研究中,研究者們雖選用的評價手段各不同,劑量及療程長短不一,但無論在空腹或糖負荷下都觀察到DPP-4I治療后可增加患者胰島素分泌、減輕胰島素抵抗等從而改善β-細胞功能。目前,大多數(shù)臨床研究表明DPP-4I降低血糖的療效值得肯定,其對胰島β-細胞功能的改善是顯著的；其療效甚至不受胰島素抵抗程度、BMI、病程長短的影響。第二部分：DPP-4抑制劑對胰島α-細胞功能的影響正常人體內,胰島素與胰高血糖素共同參與并維持血糖穩(wěn)態(tài),存在血糖調節(jié)紊亂的糖尿病患者中,不僅存在β-細胞功能異常,同時存在α-細胞功能受損,胰高血糖素分泌紊亂�！半p激素”理論更加全面的體現(xiàn)了糖尿病的發(fā)生發(fā)展機制。在多數(shù)糖尿病患者中,研究者觀察到胰高血糖素水平異常增高,其機制仍不十分明了,目前發(fā)現(xiàn)可能與a-細胞對葡萄糖的反應性降低、胰島素對胰高血糖素的抑制作用減弱、腸促胰素的調節(jié)作用異常、α-細胞的胰島素抵抗、胰高血糖素對β-細胞的促分泌作用、神經(jīng)系統(tǒng)調節(jié)受損、α-細胞原發(fā)功能障礙等因素有關。二肽基肽酶-4抑制劑(DPP-4I)作為近年來一種新型降血糖藥物,許多研究者在糖尿病動物模型中觀察到其可作用于α-細胞,修復細胞的分布紊亂,同時降低胰高血糖素水平。臨床研究中,無論是短期或長期應用DPP-4I都能有效的降低2型糖尿病患者胰高血糖素水平,改善α-細胞分泌紊亂,從而更好的控制血糖水平。在糖耐量受損、1型糖尿病以及類固醇性糖尿病患者中,此作用亦存在。
[Abstract]:The first part: the effect of 1: DPP-4 inhibitor on the function of islet 尾-cells. The fundamental cause of the development of diabetes is the progressive failure of islet function, which includes the deficiency of insulin secretion by islet 尾-cells. At the same time, there is also an inappropriate secretion of glucagon by 偽-cells and insulin resistance in peripheral tissues. How to improve the islet function of diabetic patients and delay the progress of diabetes has become a new focus of diabetes treatment. Dipeptidyl peptidase-4 (DPP-4) inhibitor is a new type of hypoglycemic drug in recent years. DPP-4I can increase 尾 -cell mass, repair the distribution of damaged islet cells and increase the amount of insulin in various animal models of diabetes mellitus (DM). In clinical studies, although the different evaluation methods, dose and duration of treatment were different, the researchers observed that the insulin secretion was increased after DPP-4I treatment on an empty stomach or under glucose load. To reduce insulin resistance and improve the function of 尾-cells. At present, most clinical studies show that the effect of DPP-4I on reducing blood glucose is worthy of recognition, and the improvement of islet 尾-cell function is significant, and the effect is not even affected by the degree of insulin resistance and the duration of the disease. The second part: the effect of DPP-4 inhibitor on the function of islet 偽-cells in normal human body, insulin and glucagon participate in and maintain blood glucose homeostasis together, and there is not only 尾-cell dysfunction in diabetic patients with impaired blood glucose regulation. At the same time, 偽-cell function was impaired and glucagon secretion was disturbed. The "double hormone" theory reflects the development mechanism of diabetes more comprehensively. In most patients with diabetes, researchers have observed an abnormal increase in glucagon levels, the mechanism of which is still unclear, and it has been found that there may be a decrease in the responsiveness of a-cell to glucose and a decrease in the inhibitory effect of insulin on glucagon The regulation of glucagon is abnormal, the insulin resistance of 偽 -cell, the effect of glucagon on 尾 -cell secretion, the damage of nervous system regulation, the primary dysfunction of 偽 -cell, and so on. Dipeptidyl peptidase-4 inhibitor (DPP-4I) is a new hypoglycemic drug in recent years. Many researchers have observed that DPP-4I can act on 偽-cells in diabetic animal models, repair the disorder of cell distribution, and decrease the level of glucagon at the same time. In clinical research, whether short-term or long-term application of DPP-4I can effectively reduce the level of glucagon in patients with type 2 diabetes, improve the disorder of 偽 -cell secretion, and control the level of blood sugar better. This effect is also present in patients with impaired glucose tolerance and type 1 diabetes and steroid diabetes.
【學位授予單位】：重慶醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2015
【分類號】：R587.1

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