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缺铁饮食诱导成年大鼠纹状体和海马中与能量代谢相关的独特蛋白质谱。

Iron-deficient diet induces distinct protein profile related to energy metabolism in the striatum and hippocampus of adult rats.

机构信息

Departamento de Bioquímica, Universidade Federal de São Paulo, São Paulo, Brazil.

Departamento de Biociência, Universidade Federal de São Paulo, São Paulo, Brazil.

出版信息

Nutr Neurosci. 2022 Feb;25(2):207-218. doi: 10.1080/1028415X.2020.1740862. Epub 2020 Mar 17.

DOI:10.1080/1028415X.2020.1740862
PMID:32183604
Abstract

Iron deficiency is a public health problem that affects all age groups. Its main consequence is anemia, but it can also affect cognitive functions. Although the negative effects of iron deficiency on cognitive function have been extensively described, the underlying mechanism has not been fully investigated. Thus, to gain an unbiased insight into the effects of iron deficiency (ID) on discrete brain regions, we performed a proteomic analysis of the striatum and hippocampus of adult rats subjected to an iron restricted (IR) diets for 30 days. We found that an IR diet caused major alterations in proteins related to glycolysis and lipid catabolism in the striatum. In the hippocampus, a larger portion of proteins related to oxidative phosphorylation and neurodegenerative diseases were altered. These alterations in the striatum and hippocampus occurred without a reduction in local iron levels, although there was a drastic reduction in liver iron and ferritin. Moreover, the IR group showed higher fasting glycaemia than the control group. These results suggest that brain iron content is preserved during acute iron deficiency, but the alterations of other systemic metabolites such as glucose may trigger distinct metabolic adaptations in each brain region. Abnormal energy metabolism precedes and persists in many neurological disorders. Thus, altered energy metabolism can be one of the mechanisms by which iron deficiency affects cognitive functions.

摘要

缺铁是一个影响所有年龄段的公共健康问题。其主要后果是贫血,但它也会影响认知功能。尽管缺铁对认知功能的负面影响已经得到广泛描述,但潜在的机制尚未得到充分研究。因此,为了深入了解缺铁(ID)对大脑特定区域的影响,我们对接受 30 天缺铁饮食的成年大鼠的纹状体和海马体进行了蛋白质组学分析。我们发现,缺铁饮食会导致纹状体中与糖酵解和脂类分解相关的蛋白质发生重大变化。在海马体中,与氧化磷酸化和神经退行性疾病相关的更多蛋白质发生了改变。这些纹状体和海马体的改变并没有导致局部铁水平降低,尽管肝脏铁和铁蛋白的含量急剧下降。此外,IR 组的空腹血糖水平高于对照组。这些结果表明,在急性缺铁期间,大脑中的铁含量得以保留,但葡萄糖等其他系统代谢物的改变可能会在每个大脑区域引发不同的代谢适应。异常的能量代谢先于许多神经退行性疾病发生并持续存在。因此,能量代谢的改变可能是缺铁影响认知功能的机制之一。

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