小鼠2型糖尿病及其合并症的遗传学。

Iqbal M Lone, Fuad A Iraqi
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引用次数: 15

摘要

2型糖尿病(T2D)是一种多基因、多因素的复杂疾病,定义为慢性代谢紊乱。这是一个主要的全球健康问题,估计有4.63亿20-79岁的成年人患有糖尿病,预计到2045年将增加到7亿。据报告,糖尿病是2012年导致非传染性疾病死亡的四大主要原因之一。环境因素在多基因型糖尿病的发展中起一定作用。多基因型糖尿病常在家族中发生。幸运的是,T2D占1型糖尿病(T1D)、T2D、单基因糖尿病综合征(MGDS)和妊娠期糖尿病(Gestational diabetes mellitus)四种糖尿病的90-95%,可以通过改变营养和生活方式以及药物干预来预防或延迟。T2D的典型症状是高血糖和机体的全面胰岛素抵抗,产生糖耐量受损。t2dm的糖耐量受损伴有广泛的健康并发症,包括心血管疾病(CVD),其发病率和死亡率在人群中各不相同。T2D的发病机制因人群和/或种族而异,已知主要由遗传成分和环境因素引起。很明显,遗传背景在决定宿主对特定环境条件的反应中起着关键作用,无论是否发生T2D(易感性与抗性)。T2D被认为是一种无声的疾病,可在诊断前发展数年。一旦诊断为T2D,许多代谢障碍被观察到,无论是作为副作用还是作为独立的合并症。小鼠模型已被证明是绘制T2D发展及其合并症易感性遗传因素的有力工具。在这里,我们对从20世纪90年代初到撰写本文时的所有已发表的数据进行了全面的检索,以寻找已经报道的与小鼠T2D和合并症相关的数量性状位点(QTL),这些模型包含不同的遗传背景。我们的研究结果发现了54个与T2D相关的qtl,以及72个与该疾病相关的合并症相关的qtl。我们以图形形式总结了这些qtl的基因组位置,以显示这些qtl之间的重叠位置,这可能表明这些qtl可以通过共享基因/s来强调。最后,我们回顾并讨论了已发表的报告,这些报告显示已鉴定的小鼠qtl /与人类疾病相关的基因成功翻译。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Genetics of murine type 2 diabetes and comorbidities.

Type 2 diabetes (T2D) is a polygenic and multifactorial complex disease, defined as chronic metabolic disorder. It's a major global health concern with an estimated 463 million adults aged 20-79 years with diabetes and projected to increase up to 700 million by 2045. T2D was reported to be one of the four leading causes of non-communicable disease (NCD) deaths in 2012. Environmental factors play a part in the development of polygenic forms of diabetes. Polygenic forms of diabetes often run-in families. Fortunately, T2D, which accounts for 90-95% of the entire four types of diabetes including, Type 1 diabetes (T1D), T2D, monogenic diabetes syndromes (MGDS), and Gestational diabetes mellitus, can be prevented or delayed through nutrition and lifestyle changes as well as through pharmacologic interventions. Typical symptom of the T2D is high blood glucose levels and comprehensive insulin resistance of the body, producing an impaired glucose tolerance. Impaired glucose tolerance of T2D is accompanied by extensive health complications, including cardiovascular diseases (CVD) that vary in morbidity and mortality among populations. The pathogenesis of T2D varies between populations and/or ethnic groupings and is known to be attributed extremely by genetic components and environmental factors. It is evident that genetic background plays a critical role in determining the host response toward certain environmental conditions, whether or not of developing T2D (susceptibility versus resistant). T2D is considered as a silent disease that can progress for years before its diagnosis. Once T2D is diagnosed, many metabolic malfunctions are observed whether as side effects or as independent comorbidity. Mouse models have been proven to be a powerful tool for mapping genetic factors that underline the susceptibility to T2D development as well its comorbidities. Here, we have conducted a comprehensive search throughout the published data covering the time span from early 1990s till the time of writing this review, for already reported quantitative trait locus (QTL) associated with murine T2D and comorbidities in different mouse models, which contain different genetic backgrounds. Our search has resulted in finding 54 QTLs associated with T2D in addition to 72 QTLs associated with comorbidities associated with the disease. We summarized the genomic locations of these mapped QTLs in graphical formats, so as to show the overlapping positions between of these mapped QTLs, which may suggest that some of these QTLs could be underlined by sharing gene/s. Finally, we reviewed and addressed published reports that show the success of translation of the identified mouse QTLs/genes associated with the disease in humans.

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