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JCEM:锻炼方法或对小部分2型糖尿病患者的病情并无改善

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近日,来自来自美国桑福德-伯纳姆医学研究所(Sanford-Burnham Medical Research Institute)的研究人员通过研究发现,参与监督锻炼计划对高达五分之一的2型糖尿病在患者的血糖管理上并不明显改善,相关研究发表于国际杂志Journal of Clinical Endocrinology & Metabolism上。

  近日,来自来自美国桑福德-伯纳姆医学研究所(Sanford-Burnham Medical Research Institute)的研究人员通过研究发现,参与监督锻炼计划对高达五分之一的2型糖尿病在患者的血糖管理上并不明显改善,相关研究发表于国际杂志Journal of Clinical Endocrinology & Metabolism上。

  当个人的机体对胰岛素耐受就会引发2型糖尿病,使得患者机体血液中存在过量的糖,美国CDC的一项研究计划指出,在未来大约有40%的美国人都会患上糖尿病。研究者Lauren Marie Sparks博士表示,肥胖和缺乏体力活动是引发2型糖尿病的两个关键风险因子,医生们经常会建议利用锻炼和其它干预生活方式的策略来抑制个体患上2型糖尿病。

  很多患者都会受益于锻炼计划,而本文研究则显示,由于其自身基因的差异,一小部分的2型糖尿病患者并不会得益于锻炼计划对其疾病的改善。文章中研究人员对2型糖尿病患者进行锻炼体系的研究,同时研究人员也进行了实验动物及遗传学的相关研究。

  研究者发现,大约15%至20%的2型糖尿病患者在血糖控制、胰岛素敏感性或肌肉线粒体密度(测定脂肪燃烧的能力)上并无任何改善;遗传学和动物模型研究揭示,对锻炼产生耐受性是在DNA上进行编码的,而且这种耐受性可以进行世代遗传。

  最后研究者Sparks说道,未来我们需要进行更多的研究来确定哪些2型糖尿病患者对锻炼疗法有效以及哪些患者对锻炼疗法无效,遗传和表观模式研究将可帮助我们有效区分这两组患者;目前利用研究人员的研究结果,研究人员就可以开发对患者有益的靶向特殊干预措施及疗法,未来研究人员希望通过更为深入的研究来开发出对锻炼策略没有反应的2型糖尿病患者的新型治疗方法。(转化医学网360zhyx.com)

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转化医学网推荐的原文摘要:

Resistance to the Beneficial Effects of Exercise in Type 2 Diabetes: Are Some Individuals Programmed to Fail?
Journal of Clinical Endocrinology & Metabolism doi:10.1210/jc.2014-2545
Natalie A. Stephens and Lauren M. Sparks
Context:
Exercise benefits most, but not all, individuals with type 2 diabetes (T2D). The beneficial effects are well studied, but why some individuals do not respond favorably to exercise training is largely unexplored. It is critical to treatment and prevention strategies to identify individuals with T2D that have a blunted metabolic response to exercise and investigate the underlying mechanisms that might predict this “programmed response to fail.”
Evidence Acquisition:
We carried out a systematic review of classic and contemporary primary reports on clinical human and animal exercise studies. We also referenced unpublished data from our previous studies, as well those of collaborators. Genetic and epigenetic components and their associations with the exercise response were also examined.
Evidence Synthesis:
As evidence of the exercise resistance premise, we and others found that supervised exercise training results in substantial response variations in glucose homeostasis, insulin sensitivity, and muscle mitochondrial density, wherein approximately 15–20% of individuals fail to improve their metabolic health with exercise. Classic genetic studies have shown that the extent of the exercise training response is largely heritable, whereas new evidence demonstrates that DNA hypomethylation is linked to the exercise response in skeletal muscle. DNA sequence variation and/or epigenetic modifications may, therefore, dictate the exercise training response.
Conclusions:
Studies dedicated to uncovering the mechanisms of exercise resistance will advance the field of exercise and T2D, allowing interventions to be targeted to those most likely to benefit and identify novel approaches to treat those who do not experience metabolic improvements after exercise training.



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