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Diabetes:服用改造益生菌可有效治疗患者糖尿病

首页 » 研究 » 糖尿病 2015-01-28 转化医学网 赞(8)
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近日,一篇发表于国际杂志Diabetes上的研究论文中,来自康奈尔大学的研究人员表示,未来终有一天人类服用一粒益生菌药片就可以治疗糖尿病。

  近日,一篇发表于国际杂志Diabetes上的研究论文中,来自康奈尔大学的研究人员表示,未来终有一天人类服用一粒益生菌药片就可以治疗糖尿病。

  这项研究中,研究人员对人类肠道中的常见益生菌——乳酸菌进行工程化操作,使其分泌胰高血糖素样的肽类(GPL-1),随后对大鼠进行口服GPL-190天,结果显示,接受工程化益生菌的大鼠的高血糖水平下降了30%;后期研究者将加大工程化益生菌的使用剂量来观察是否可以实现对大鼠的完整疗法。

  研究者发现,糖尿病大鼠的上部肠道组织的上皮细胞可以转化成为类似于胰腺β细胞样的细胞,后者可以监测机体的血糖水平并且及时分泌出胰岛素来平衡健康个体机体中的血糖水平。研究者March说道,利用这种新型的工程化益生菌可以使得糖尿病大鼠在餐后血糖降低所需的总时间同正常大鼠一样。

  这种工程化的益生菌就使得调节血糖的胰腺中心转移到了肠道上部组织中,尽管其取代了糖尿病大鼠产生胰岛素的能力,当研究人员在健康大鼠机体中进行实验发现其并不会影响健康大鼠的血糖水平;当然如果大鼠可以自行控制血糖那么就不需要再额外注射胰岛素了。

  最后研究者说道,将来我们有望开发出一种益生菌药片来更快速便捷地帮助治疗糖尿病患者。(转化医学网360zhyx.com)

  以上为转化医学网原创翻译整理。如需转载,请联系 info@360zhyx.com。
转化医学网推荐的原文阅读:

Engineered Commensal Bacteria Reprogram Intestinal Cells Into Glucose-Responsive Insulin-Secreting Cells for the Treatment of Diabetes
Diabetes doi: 10.2337/db14-0635
Franklin F. Duan, Joy H. Liu and John C. March⇑
The inactive full-length form of GLP-1(1–37) stimulates conversion of both rat and human intestinal epithelial cells into insulin-secreting cells. We investigated whether oral administration of human commensal bacteria engineered to secrete GLP-1(1–37) could ameliorate hyperglycemia in a rat model of diabetes by reprogramming intestinal cells into glucose-responsive insulin-secreting cells. Diabetic rats were fed daily with human lactobacilli engineered to secrete GLP-1(1–37). Diabetic rats fed GLP-1-secreting bacteria showed significant increases in insulin levels and, additionally, were significantly more glucose tolerant than those fed the parent bacterial strain. These rats developed insulin-producing cells within the upper intestine in numbers sufficient to replace ∼25–33% of the insulin capacity of nondiabetic healthy rats. Intestinal tissues in rats with reprogrammed cells expressed MafA, PDX-1, and FoxA2. HNF-6 expression was observed only in crypt epithelia expressing insulin and not in epithelia located higher on the villous axis. Staining for other cell markers in rats treated with GLP-1(1–37)-secreting bacteria suggested that normal function was not inhibited by the close physical proximity of reprogrammed cells. These results provide evidence of the potential for a safe and effective nonabsorbed oral treatment for diabetes and support the concept of engineered commensal bacterial signaling to mediate enteric cell function in vivo.

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