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巴西莓果皮摄入可预防胰岛素抵抗诱导的小鼠 tau 磷酸化。

Jaboticaba berry peel intake prevents insulin-resistance-induced tau phosphorylation in mice.

机构信息

Department of Food and Nutrition, Faculty of Food Engineering, University of Campinas, Campinas, SP, Brazil.

Department of Biochemistry and Tissue Biology, Institute of Biology, University of Campinas, Campinas, SP, Brazil.

出版信息

Mol Nutr Food Res. 2017 Oct;61(10). doi: 10.1002/mnfr.201600952. Epub 2017 Jul 3.

DOI:10.1002/mnfr.201600952
PMID:28544198
Abstract

The hyperphosphorylation of microtubule-associated protein tau (tau) in the hippocampus can be caused by central and peripheral insulin resistance and these alterations are related to the development of tauopathies, such as Alzheimer's disease. In this study, we used a high-fat diet to induce obesity and insulin resistance in adult Swiss mice and checked whether supplementation with Myrciaria jaboticaba berry peel for 10 weeks could improve insulin sensitivity, learning/memory performance, and prevent tau phosphorylation in the hippocampus. Furthermore, adipocytokines, inflammatory markers, and oxidative stress were assessed. Myrciaria jaboticaba peel has phenolic compounds (e.g., cyanidin, ellagic acid), dietary fiber and carotenoids, which contribute to great antioxidant capacity. Supplementation of the high-fat diet with 4% M. jaboticaba peel prevented fat weight gain and reduced peripheral insulin resistance. The treated group also showed lower tau phosphorylation in the hippocampus corroborating better learning/memory performance in the Morris water maze test. Maintenance of neuronal viability, lower levels of hippocampal inflammatory markers, and improved brain antioxidant defenses were also related to the consumption of M. jaboticaba peel. These findings contribute to a better understanding of how a high-fat diet supplemented with jaboticaba berry peel counteracts the impairment of cognitive functions caused by high-fat diet intake and diet-induced insulin resistance.

摘要

微管相关蛋白 tau(tau)在海马体中的过度磷酸化可能是由中枢和外周胰岛素抵抗引起的,这些改变与 tau 病的发展有关,如阿尔茨海默病。在这项研究中,我们使用高脂肪饮食诱导成年瑞士小鼠肥胖和胰岛素抵抗,并检查了 10 周补充杨梅果皮是否可以提高胰岛素敏感性、学习/记忆表现,并防止海马体中的 tau 磷酸化。此外,还评估了脂肪细胞因子、炎症标志物和氧化应激。杨梅果皮含有酚类化合物(如矢车菊素、鞣花酸)、膳食纤维和类胡萝卜素,具有很强的抗氧化能力。用 4%的杨梅果皮补充高脂肪饮食可以防止体重增加和外周胰岛素抵抗。治疗组在 Morris 水迷宫测试中也表现出更低的海马体 tau 磷酸化,表明学习/记忆表现更好。神经元存活率的维持、海马体炎症标志物水平的降低以及大脑抗氧化防御能力的提高也与杨梅果皮的摄入有关。这些发现有助于更好地理解高脂肪饮食补充杨梅果皮如何对抗高脂肪饮食摄入和饮食诱导的胰岛素抵抗引起的认知功能障碍。

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