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营养策略会导致记忆损伤,并改变生化参数,而不会引起神经炎症。

Nutritional strategies cause memory damage and alter biochemical parameters without causing neuroinflammation.

机构信息

Laboratory of Neurobiology of Inflammatory and Metabolic Processes, Postgraduate Program in Health Sciences, University of Southern Santa Catarina, Av. José Acácio Moreira, 787, Tubarão, Santa Catarina, 88704-900, Brazil.

Laboratory of Experimental Pathophysiology, Postgraduate Program in Health Sciences, University of the Extreme South of Santa Catarina, Criciúma, Santa Catarina, Brazil.

出版信息

Metab Brain Dis. 2024 Apr;39(4):635-648. doi: 10.1007/s11011-023-01311-6. Epub 2024 Mar 2.

DOI:10.1007/s11011-023-01311-6
PMID:38429463
Abstract

Obesity results from an energy imbalance and has been considered an epidemic due to its increasing rates worldwide. It is classified as a low-grade chronic inflammatory disease and has associated comorbidities. Different nutritional strategies are used for the purpose of weight loss, highlighting low-carbohydrate (LC) diets, ketogenic diets, and intermittent fasting (IF). These strategies can lead to metabolic and behavioral changes as they stimulate different biochemical pathways. Therefore, this study evaluated memory, energy metabolism, neuroinflammation, oxidative stress, and antioxidant defense parameters in mice subjected to an LC diet, ketogenic diet (KD), or IF. Eighty male Swiss mice, 60 days old, were divided into 4 groups: control, LC, KD, or IF. Body weight was measured weekly, and food intake every 48 h. After 15 days of nutritional interventions, the animals were subjected to the behavioral object recognition test and subsequently euthanized. Then, visceral fat was removed and weighed, and the brain was isolated for inflammatory and biochemical analysis. We concluded from this study that the LC and KD strategies could damage memory, IF improves the production of adenosine triphosphate (ATP), and the LC, KD, and IF strategies do not lead to neuroinflammatory damage but present damage at the level of oxidative stress.

摘要

肥胖是由能量失衡引起的,由于其在全球范围内的发病率不断上升,已被视为一种流行病。它被归类为一种低度慢性炎症性疾病,并伴有相关的合并症。不同的营养策略被用于减肥,突出了低碳水化合物(LC)饮食、生酮饮食(KD)和间歇性禁食(IF)。这些策略可以通过刺激不同的生化途径导致代谢和行为的改变。因此,本研究评估了接受 LC 饮食、KD 或 IF 的小鼠的记忆、能量代谢、神经炎症、氧化应激和抗氧化防御参数。将 80 只 60 天大的雄性瑞士小鼠分为 4 组:对照组、LC 组、KD 组或 IF 组。每周测量体重,每 48 小时测量一次食物摄入量。在营养干预 15 天后,动物接受行为物体识别测试,然后处死。然后取出内脏脂肪并称重,并分离大脑进行炎症和生化分析。我们从这项研究中得出结论,LC 和 KD 策略可能会损害记忆,IF 会提高三磷酸腺苷(ATP)的产生,LC、KD 和 IF 策略不会导致神经炎症损伤,但会在氧化应激水平上造成损伤。

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本文引用的文献

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Chronic Ketosis Modulates HIF1α-Mediated Inflammatory Response in Rat Brain.慢性酮症调节大鼠脑内 HIF1α 介导的炎症反应。
Adv Exp Med Biol. 2022;1395:75-79. doi: 10.1007/978-3-031-14190-4_13.
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Prefrontal Cortex and Hippocampus Inflammation in Mice Fed High-Carbohydrate or High-Fat Diets.高糖或高脂肪饮食喂养的小鼠前额叶皮层和海马炎症。
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Intermittent fasting enhances long-term memory consolidation, adult hippocampal neurogenesis, and expression of longevity gene Klotho.
间歇性禁食增强长期记忆巩固、成年海马神经发生和长寿基因 Klotho 的表达。
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A Low-Carbohydrate Diet Improves Glucose Metabolism in Lean Insulinopenic Akita Mice Along With Sodium-Glucose Cotransporter 2 Inhibitor.低碳水化合物饮食联合钠-葡萄糖协同转运蛋白2抑制剂可改善瘦型胰岛素缺乏型秋田小鼠的葡萄糖代谢。
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[Establishment of high-fat diet-induced obesity and insulin resistance model in rats].[高脂饮食诱导大鼠肥胖及胰岛素抵抗模型的建立]
Beijing Da Xue Xue Bao Yi Xue Ban. 2020 Jun 18;52(3):557-563. doi: 10.19723/j.issn.1671-167X.2020.03.024.
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Carbohydrate-restricted diet alters the gut microbiota, promotes senescence and shortens the life span in senescence-accelerated prone mice.碳水化合物限制饮食改变肠道微生物群,促进衰老并缩短加速衰老-prone 小鼠的寿命。
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