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肥胖诱导的脑胰岛素抵抗、脑线粒体功能障碍与痴呆之间的联系

Links Between Obesity-Induced Brain Insulin Resistance, Brain Mitochondrial Dysfunction, and Dementia.

作者信息

Sripetchwandee Jirapas, Chattipakorn Nipon, Chattipakorn Siriporn C

机构信息

Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.

Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.

出版信息

Front Endocrinol (Lausanne). 2018 Aug 31;9:496. doi: 10.3389/fendo.2018.00496. eCollection 2018.

DOI:10.3389/fendo.2018.00496
PMID:30233495
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6127253/
Abstract

It is widely recognized that obesity and associated metabolic changes are considered a risk factor to age-associated cognitive decline. Inflammation and increased oxidative stress in peripheral areas, following obesity, are patently the major contributory factors to the degree of the severity of brain insulin resistance as well as the progression of cognitive impairment in the obese condition. Numerous studies have demonstrated that the alterations in brain mitochondria, including both functional and morphological changes, occurred following obesity. Several studies also suggested that brain mitochondrial dysfunction may be one of underlying mechanism contributing to brain insulin resistance and cognitive impairment in the obese condition. Thus, this review aimed to comprehensively summarize and discuss the current evidence from various , and clinical studies that are associated with obesity, brain insulin resistance, brain mitochondrial dysfunction, and cognition. Contradictory findings and the mechanistic insights about the roles of obesity, brain insulin resistance, and brain mitochondrial dysfunction on cognition are also presented and discussed. In addition, the potential therapies for obese-insulin resistance are reported as the therapeutic strategies which exert the neuroprotective effects in the obese-insulin resistant condition.

摘要

人们普遍认为,肥胖及相关代谢变化被视为与年龄相关的认知衰退的一个风险因素。肥胖后外周区域的炎症和氧化应激增加显然是导致脑胰岛素抵抗严重程度以及肥胖状态下认知障碍进展的主要因素。大量研究表明,肥胖后大脑线粒体发生了改变,包括功能和形态变化。一些研究还表明,脑线粒体功能障碍可能是肥胖状态下导致脑胰岛素抵抗和认知障碍的潜在机制之一。因此,本综述旨在全面总结和讨论来自各种基础和临床研究的当前证据,这些证据与肥胖、脑胰岛素抵抗、脑线粒体功能障碍和认知有关。还介绍并讨论了关于肥胖、脑胰岛素抵抗和脑线粒体功能障碍对认知作用的矛盾发现和机制见解。此外,还报告了肥胖 - 胰岛素抵抗的潜在治疗方法,作为在肥胖 - 胰岛素抵抗状态下发挥神经保护作用的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0f2/6127253/3f062b4ae9ca/fendo-09-00496-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0f2/6127253/4800be03ec9c/fendo-09-00496-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0f2/6127253/069fae855ef1/fendo-09-00496-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0f2/6127253/3f062b4ae9ca/fendo-09-00496-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0f2/6127253/4800be03ec9c/fendo-09-00496-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0f2/6127253/069fae855ef1/fendo-09-00496-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0f2/6127253/3f062b4ae9ca/fendo-09-00496-g0003.jpg

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