Therapeutic targets for the prevention of type 1 diabetes mellitus.

N Singh, J P Palmer
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引用次数: 13

Abstract

The pathogenesis of type 1 diabetes is multifactorial, involving genetic susceptibility, autoimmune mechanisms, and environmental factors. This article will focus on two main strategies for altering the underlying disease process in type 1 diabetes. The first strategy is to identify individuals at risk for the development of diabetes and to halt the immune process before it leads to overt clinical disease, Promising in vitro and animal studies with nicotinamide, parenteral insulin, and oral insulin led to large clinical prevention studies, such as the European Nicotinamide Diabetes Intervention Trial and the Diabetes Prevention Trial (DPT-1). These studies failed to show that nicotinamide and insulin prevented the disease in at risk relatives of patients with type 1 diabetes and left many questions unanswered. The second strategy focuses on intervention shortly after diagnosis in order to arrest the destruction of beta cells and to preserve residual beta-cell function as long as possible. Cyclosporin was an effective immunosuppressive but was rejected as a potential treatment for type 1 diabetes because of its renal toxicity. Recently, more attention has been focused on an anti-CD3 antibody, on DiaPep277, and on glutamic acid decarboxylase (GAD). Animal studies and small short-term human trials with these compounds have suggested that they may be effective interventions in patients recently diagnosed with type 1 diabetes.

预防1型糖尿病的治疗靶点。
1型糖尿病的发病机制是多因素的,涉及遗传易感性、自身免疫机制和环境因素。本文将重点讨论改变1型糖尿病潜在疾病过程的两种主要策略。第一个策略是识别有糖尿病发展风险的个体,并在其导致明显的临床疾病之前停止免疫过程。烟酰胺、肠外胰岛素和口服胰岛素的体外和动物研究前景良好,导致了大型临床预防研究,如欧洲烟酰胺糖尿病干预试验和糖尿病预防试验(DPT-1)。这些研究未能证明烟酰胺和胰岛素能在1型糖尿病患者的高危亲属中预防这种疾病,并且留下了许多未解之谜。第二种策略侧重于在诊断后不久进行干预,以阻止β细胞的破坏,并尽可能长时间地保留剩余的β细胞功能。环孢素是一种有效的免疫抑制剂,但由于其肾毒性而被拒绝作为1型糖尿病的潜在治疗方法。近年来,人们对抗cd3抗体、DiaPep277和谷氨酸脱羧酶(GAD)的研究越来越关注。这些化合物的动物研究和小型短期人体试验表明,它们可能是最近诊断为1型糖尿病患者的有效干预措施。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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