Immunomodulation by helminths: Similar impact on type 1 and type 2 diabetes?

Immunomodulation by helminths: Similar impact on type 1 and type 2 diabetes?
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DOI:
10.1111/pim.12401
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发表时间:
2017-05
影响因子:
2.2
通讯作者:
J. Surendar;K. Indulekha;A. Hoerauf;M. Hübner
J. Surendar;K. Indulekha;A. Hoerauf;M. Hübner
中科院分区:
医学4区
文献类型:
--
作者:
J. Surendar;K. Indulekha;A. Hoerauf;M. Hübner

文献摘要

相似文献

1 型 (T1D) 和 2 型糖尿病 (T2D) 的发病率都在急剧增加,预计到 2035 年,全球糖尿病患病率将达到近 6 亿例。尽管两种类型糖尿病的发病机制不同,但免疫系统都积极参与这两种疾病的发生。遗传和环境因素决定了患 T1D 的风险。另一方面,久坐的生活方式、食物摄入过多等生活方式的改变也会导致T2D发病率的增加。通过高质量的医疗改善卫生条件是过去几十年来导致包括蠕虫感染在内的传染病持续减少的一个环境因素。最近,越来越多的证据表明,在人类和动物模型中,蠕虫感染与糖尿病之间存在负相关。在这篇综述中,我们讨论了一些研究,这些研究为蠕虫感染对 T1D 和 T2D 的有益影响提供了证据。提出了蠕虫通过减轻胰腺炎症来预防 1 型糖尿病发作的可能机制,并通过提高胰岛素敏感性、减轻炎症、促进脂肪组织褐变以及改善脂质代谢和胰岛素信号传导来预防 2 型糖尿病。
The incidence of both type 1 (T1D) and type 2 diabetes (T2D) is drastically increasing, and it is predicted that the global prevalence of diabetes will reach almost 600 million cases by 2035. Even though the pathogenesis of both types of diabetes is distinct, the immune system is actively involved in both forms of the disease. Genetic and environmental factors determine the risk to develop T1D. On the other hand, sedentary life style, surplus of food intake and other lifestyle changes contribute to the increase of T2D incidence. Improved sanitation with high‐quality medical treatment is such an environmental factor that has led to a continuous reduction of infectious diseases including helminth infections over the past decades. Recently, a growing body of evidence has implicated a negative association between helminth infections and diabetes in humans as well as animal models. In this review, we discuss studies that have provided evidence for the beneficial impact of helminth infections on T1D and T2D. Possible mechanisms are presented by which helminths prevent T1D onset by mitigating pancreatic inflammation and confer protection against T2D by improving insulin sensitivity, alleviating inflammation, augmenting browning of adipose tissue and improving lipid metabolism and insulin signalling.