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腾讯登录Sci Transl Med：性无能药物育亨宾或可治疗2型糖尿病
| 导读 | 近日在一项发表在国际杂志Science Translational Medicine上的研究中，来自隆德大学的研究人员发现，治疗性无能的药物育亨宾或许可以帮助治疗那些因特殊基因突变而引发胰岛素产量减少的2型糖尿病患者。 |
目前有很多药物可以降低血糖，而且患者结合饮食锻炼完全可以有效控制2型糖尿病的发展，研究者指出，2型糖尿病也是一种生活方式不当引发的疾病，换句话说生活因子会诱发该疾病，但是疾病的严重性和易感性往往是由遗传突变所影响的。生活方式的改变，比如饮食、锻炼及体重的减轻都将是控制2型糖尿病发展的良策。（转化医学网360zhyx.com）
转化医学网推荐的原文摘要：
Genotype-based treatment of type 2 diabetes with an α2A-adrenergic receptor antagonist
Sci Transl Med DOI: 10.1126/scitranslmed.3009934
Yunzhao Tang1,2,*, Annika S. Axelsson1,*, Peter Spégel1,*, Lotta E. Andersson1, Hindrik Mulder1, Leif C. Groop1, Erik Renström1 and Anders H. Rosengren1,†
The feasibility of exploiting genomic information for individualized treatment of polygenic diseases remains uncertain. A genetic variant in ADRA2A, which encodes the α2A-adrenergic receptor (α2AAR), was recently associated with type 2 diabetes. This variant causes receptor overexpression and impaired insulin secretion; thus, we hypothesized that blocking α2AAR pharmacologically could improve insulin secretion in patients with the risk genotype. A total of 50 type 2 diabetes patients were recruited on the basis of ADRA2A genotype for a randomized placebo-controlled intervention study with the α2AAR antagonist yohimbine. The patients received 0, 10, or 20 mg of yohimbine at three separate visits. The primary endpoint was insulin secretion at 30 min (Ins30) during an oral glucose tolerance test (OGTT). Patients with the risk variant had 25% lower Ins30 than those without risk genotype. After administration of 20 mg of yohimbine, Ins30 was enhanced by 29% in the risk group, making secretion similar to patients carrying the low-risk allele. The corrected insulin response and disposition index in individuals with the high-risk (but not low-risk) allele were improved by 59 ± 18% and 43 ± 14%, respectively. The beneficial effect of yohimbine was not a consequence of improved insulin sensitivity. In summary, the data show that the insulin secretion defect in patients carrying the ADRA2A risk genotype can be corrected by α2AAR antagonism. The findings show that knowledge of genetic risk variants can be used to guide therapeutic interventions that directly target the underlying pathophysiology and demonstrate the potential of individualized genotype-specific treatment of type 2 diabetes.
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