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新基因疗法有望改善肥胖症治疗

来源:生物谷 2012-09-24 12:13

2012年9月22日 讯 /生物谷BIOON/ --来自加拿大阿尔伯塔大学的医学研究人员发现一种利用基因疗法治疗肥胖症的新方法。这种治疗在吃高脂肪和高糖的食物的实验室模式动物中获得成功:接受治疗后,它们体重增加较少、较高的活动水平和下降的胰岛素耐药性。相关研究结果于近期刊登在Nutrition and Diabetes期刊上。

在之前的研究中,科学家们一直利用病毒来运送治疗肥胖症的药物,但是长期而言只能取得有限的成功。在这项研究中,阿尔伯塔大学医学与口腔学系研究员Jason Dyck和同事们发现一种通过DNA而不是病毒运送治疗肥胖症的药物。他们的研究结果证实了其他研究人员执行短期研究或利用更为风险性的基因传送方法时所获得的研究发现。

Dyck说,“我认为我们的发现可能让这种治疗方法更加接近临床试验,这是因为这种方法似乎要比常规性基因疗法更加安全。”

这种肥胖症治疗方法重点在于增加脂肪细胞分泌的脂联素(adiponectin)水平。当一个人体重增加和脂肪细胞变得更大时,身体分泌更少的脂联素。体瘦的人们分泌高水平的脂联素。

Dyck说,“这种激素似乎抵抗许多疾病,包括糖尿病和心血管疾病和体重增加。但是当人们增重时,身体分泌更少的脂联素,从而失去与这种激素相关联的有益影响。”

当吃高脂肪、高糖食物的实验室模式动物接受这种治疗方法时,与那些吃同样食物但不接受这种抗肥胖症治疗的动物相比,它们体重增加较少,燃烧更多的热量,更加活跃,消耗更多的氧气,因而更好抵抗葡萄糖耐受不良和胰岛素耐受性。Dyck希望其他的研究团队继续开展他的这项研究。(生物谷Bioon.com)

Adiponectin gene therapy ameliorates high-fat, high-sucrose diet-induced metabolic perturbations in mice

A D Kandasamy1, M M Sung1, J J Boisvenue1, A J Barr1 and J R B Dyck

Background and Design: Adiponectin is an adipokine secreted primarily from adipose tissue that can influence circulating plasma glucose and lipid levels through multiple mechanisms involving a variety of organs. In humans, reduced plasma adiponectin levels induced by obesity are associated with insulin resistance and type 2 diabetes, suggesting that low adiponectin levels may contribute the pathogenesis of obesity-related insulin resistance.

Methods and Results: The objective of the present study was to investigate whether gene therapy designed to elevate circulating adiponectin levels is a viable strategy for ameliorating insulin resistance in mice fed a high-fat, high-sucrose (HFHS) diet. Electroporation-mediated gene transfer of mouse adiponectin plasmid DNA into gastrocnemius muscle resulted in elevated serum levels of globular and high-molecular weight adiponectin compared with control mice treated with empty plasmid. In comparison to HFHS-fed mice receiving empty plasmid, mice receiving adiponectin gene therapy displayed significantly decreased weight gain following 13 weeks of HFHS diet associated with reduced fat accumulation, and exhibited increased oxygen consumption and locomotor activity as measured by indirect calorimetry, suggesting increased energy expenditure in these mice. Consistent with improved whole-body metabolism, mice receiving adiponectin gene therapy also had lower blood glucose and insulin levels, improved glucose tolerance and reduced hepatic gluconeogenesis compared with control mice. Furthermore, immunoblot analysis of livers from mice receiving adiponectin gene therapy showed an increase in insulin-stimulated phosphorylation of insulin signaling proteins.

Conclusion: Based on these data, we conclude that adiponectin gene therapy ameliorates the metabolic abnormalities caused by feeding mice a HFHS diet and may be a potential therapeutic strategy to improve obesity-mediated impairments in insulin sensitivity.

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