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短期饥饿与线粒体功能障碍——导致术后胰岛素抵抗的可能机制。

Short-term starvation and mitochondrial dysfunction - a possible mechanism leading to postoperative insulin resistance.

机构信息

Division of Gastrointestinal Surgery, Nottingham Digestive Diseases Centre Biomedical Research Unit, Nottingham University Hospitals, Queen's Medical Centre, Nottingham, UK.

出版信息

Clin Nutr. 2009 Oct;28(5):497-509. doi: 10.1016/j.clnu.2009.04.014. Epub 2009 May 17.

DOI:10.1016/j.clnu.2009.04.014
PMID:19446932
Abstract

BACKGROUND

Preoperative starvation results in the development of insulin resistance. Measures to attenuate the development of insulin resistance, such as preoperative carbohydrate loading, lead to clinical benefits. However, the mechanisms that underlie the development of insulin resistance during starvation and its attenuation by preoperative carbohydrate loading remain to be defined. Insulin resistance associated with type 2 diabetes and ageing has been linked to mitochondrial dysfunction. The metabolic consequences of preoperative starvation and carbohydrate loading and mechanisms linking insulin resistance to impaired mitochondrial function are discussed.

METHODS

Searches of the Medline and Science Citation Index databases were performed using various key words in combinations with the Boolean operators AND, OR and NOT. Key journals, nutrition and metabolism textbooks and the reference lists of key articles were also hand searched.

RESULTS

Animal studies have shown that short-term energy deprivation decreases mitochondrial ATP synthesis capacity and complex activity, and increases oxidative injury. Furthermore, evidence from human studies suggests that the development of insulin resistance during starvation may be linked to impaired mitochondrial function.

CONCLUSIONS

There is evidence from animal studies that short-term starvation causes mitochondrial dysfunction. Future studies should investigate whether mitochondrial dysfunction underlies the development of insulin resistance in patients undergoing elective surgery.

摘要

背景

术前禁食会导致胰岛素抵抗的发生。减轻胰岛素抵抗发展的措施,如术前碳水化合物负荷,会带来临床获益。然而,在禁食期间发生胰岛素抵抗的机制及其通过术前碳水化合物负荷减轻的机制仍有待确定。与 2 型糖尿病和衰老相关的胰岛素抵抗与线粒体功能障碍有关。讨论了术前禁食和碳水化合物负荷的代谢后果,以及将胰岛素抵抗与受损的线粒体功能联系起来的机制。

方法

使用各种关键词组合使用布尔运算符 AND、OR 和 NOT 在 Medline 和 Science Citation Index 数据库中进行搜索。还查阅了重点期刊、营养和代谢教科书以及重点文章的参考文献。

结果

动物研究表明,短期能量剥夺会降低线粒体 ATP 合成能力和复合物活性,并增加氧化损伤。此外,来自人类研究的证据表明,在饥饿期间发生的胰岛素抵抗可能与线粒体功能受损有关。

结论

动物研究有证据表明短期禁食会导致线粒体功能障碍。未来的研究应该调查在接受择期手术的患者中,线粒体功能障碍是否是胰岛素抵抗发展的基础。

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