剑桥大学研究发现，2型糖尿病患者的胰岛素抵抗先于线粒体功能障碍

Insulin resistance precedes mitochondrial dysfunction in type 2 diabetics, Cambrige study finds

 

根据剑桥大学研究人员的一项新研究，在2型糖尿病患者中常见的胰岛素抵抗可能是线粒体功能失调所致。这些发现有助于解答多年来困扰糖尿病研究者的一个长期谜题。

 

人们早就知道，患有2型糖尿病的人通常会在线粒体中出现功能障碍，线粒体是细胞内的细胞器(细胞的发电厂），能产生能量。然而，目前还不清楚这些线粒体异常是否导致了胰岛素抵抗和糖尿病，或者是一种先前存在的差异导致了胰岛素抵抗和线粒体功能受损。

 

研究这些症状是困难的，因为大多数表现一种症状的人也有另一种症状。因此，很难确定哪一个先出现。然而，研究人员想出了一个解决这个问题的独特方法。

 

他们的研究发表在《临床研究杂志》(Journal of Clinical Investigation)上，他们对出生在胰岛素受体基因缺陷的个体进行了研究。这些受体负责调节胰岛素的作用，而功能紊乱会使个体对激素产生抵抗力，模仿2型糖尿病的症状。

 

研究人员测试了这些人锻炼后的磷酸肌酸恢复时间。这被认为是对人体骨骼肌线粒体功能的测量。与健康个体相比，胰岛素受体突变患者的恢复时间明显减慢。

 

这些结果表明，胰岛素信号障碍和胰岛素抵抗是线粒体功能障碍的根本原因。这些发现很可能解释了为什么许多患2型糖尿病的人也会受到这些细胞器的损害。

　

 

经过进一步的检查，研究人员发现，胰岛素抵抗的参与者的睡眠代谢率要快得多。他们推测这可能是由于线粒体功能受损，可能需要增加营养氧化以维持能量水平。

 

这些发现有助于回答长期困扰糖尿病专家的问题。通过证明胰岛素抵抗实际上是导致线粒体功能障碍的原因，而不是相反，研究结果可以为未来研究人员提供方向，他们希望解决这两种情况下的健康后果。

 

除了与2型糖尿病相关的健康并发症风险外，线粒体功能障碍还会导致肌肉无力、听力障碍和视力丧失。这可能很难治疗。

　

　

 

Insulin resistance precedes mitochondrial dysfunction in type 2 diabetics, study finds

 

Insulin resistance, which is common in individuals with type 2 diabetes, may result from dysfunctions in the mitochondria, according to a new study from researchers at the University of Cambridge. The findings help answer an enduring mystery that has perplexed diabetes investigators for years.

 

It has long been known that individuals with type 2 diabetes often suffer from dysfunctions in their mitochondria, which are organelles contained within cells that produce energy. However, it was not known whether these mitochondrial irregularities were the cause of insulin resistance and diabetes, or whether a single preexisting difference accounted for both insulin resistance and impaired mitochondrial function.

 

Studying these conditions is difficult, because most people who exhibit one of the symptoms also has the other. Therefore, it is difficult to determine which came first. However, the researchers came up with a unique solution to this problem.

 

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For their study, which was published in the Journal of Clinical Investigation, they examined individuals born with genetic defects in their insulin receptors. These receptors are responsible for mediating the effects of insulin, and a dysfunction can leave individuals resistant to the hormone, mimicking the symptoms of type 2 diabetes.

 

 

 

The researchers tested phosphocreatine recovery time in these individuals after they exercised. This is considered to be a measure of skeletal muscle mitochondrial function in the body. Compared to healthy individuals, those with insulin receptor mutations had significantly slower recovery times.

 

These results indicated to the investigation team that insulin signaling dysfunction and insulin resistance are the root cause of mitochondrial dysfunctions. These findings likely explain why many individuals with type 2 diabetes also experience the damage to these organelles.

 

Upon further examination, the researchers found that insulin-resistant participants had much faster sleeping metabolic rates. They speculated that this could be because impaired mitochondrial function may necessitate increased nutrient oxidation to maintain energy levels.

 

The findings help answer a question that had long plagued diabetes experts. By showing that insulin resistance is in fact the cause of mitochondrial dysfunction rather than the other way around, the results could provide direction to future researchers who are looking to solve the health consequences that can result from either condition.

 

Aside from the risk of health complications associated with type 2 diabetes, mitochondrial dysfunction can lead to muscle weakness, hearing problems and loss of vision. It can be difficult to treat.

　

https://www.endocrineweb.com/news/type-2-diabetes/5593-insulin-resistance-precedes-