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硝苯地平改善生酮饮食对大鼠胰岛素抵抗诱导的认知功能障碍的影响。

Nifedipine Improves the Ketogenic Diet Effect on Insulin-Resistance-Induced Cognitive Dysfunction in Rats.

作者信息

Abdel-Kareem Nancy M, Elshazly Shimaa M, Abd El Fattah May A, Aldahish Afaf A, Zaitone Sawsan A, Ali Sahar K, Abd El-Haleim Enas A

机构信息

Department of Pharmacology and Toxicology, Faculty of Pharmacy, Sinai University-Arish Branch, Arish 45511, Egypt.

Department of Pharmacology and Toxicology, Faculty of Pharmacy, Zagazig University, Zagazig 44519, Egypt.

出版信息

Pharmaceuticals (Basel). 2024 Aug 10;17(8):1054. doi: 10.3390/ph17081054.

DOI:10.3390/ph17081054
PMID:39204160
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11359371/
Abstract

Insulin resistance, induced by high fructose consumption, affects cognitive function negatively. Nifedipine may be suggested for neurological disorders. This study aimed to assess the effect of nifedipine with either a normal diet (ND) or a ketogenic diet (KD) in cognitive dysfunction. Male Wistar rats received 10% fructose in drinking water for 8 weeks to induce insulin resistance. Rats received nifedipine (5.2 mg/kg/day; p.o.) later with ND or KD for an additional five weeks. One and two-way ANOVAs were used in analyzing the data. Reversion to the ND improved insulin resistance and lipid profile, besides brain-derived neurotrophic factor (BDNF), glycogen synthase kinase-3 beta (GSK3β), and insulin-degrading enzyme (IDE) levels. Rats fed KD alone and those that received nifedipine with KD did not show similar improvement in the previously mentioned parameters as the ND group. However, nifedipine-ND rats showed improvement in cognitive behavior and insulin resistance. Treatment with nifedipine-KD ameliorated GSK3β, amyloid β (Aβ), and tau protein levels. As the nifedipine-KD combination succeeded in diminishing the accumulated Aβ and tau protein, KD may be used for a while due to its side effects, then nifedipine treatment could be continued with an ND. This conclusion is based on the finding that this combination mitigated insulin resistance with the associated improved behavior.

摘要

高果糖摄入诱导的胰岛素抵抗对认知功能有负面影响。硝苯地平可能适用于神经系统疾病。本研究旨在评估硝苯地平与正常饮食（ND）或生酮饮食（KD）对认知功能障碍的影响。雄性Wistar大鼠饮用含10%果糖的水8周以诱导胰岛素抵抗。之后大鼠接受硝苯地平（5.2毫克/千克/天；口服），同时搭配ND或KD，持续另外五周。使用单因素方差分析和双因素方差分析来分析数据。恢复到ND饮食可改善胰岛素抵抗、血脂谱，以及脑源性神经营养因子（BDNF）、糖原合酶激酶-3β（GSK3β）和胰岛素降解酶（IDE）水平。单独喂食KD的大鼠以及接受硝苯地平与KD联合处理的大鼠，在上述参数方面并未表现出与ND组类似的改善情况。然而，硝苯地平与ND联合处理的大鼠在认知行为和胰岛素抵抗方面有所改善。硝苯地平与KD联合处理改善了GSK3β、β淀粉样蛋白（Aβ）和tau蛋白水平。由于硝苯地平与KD联合成功减少了Aβ和tau蛋白的积累，鉴于KD有副作用，可先使用一段时间KD，然后继续用ND进行硝苯地平治疗。这一结论基于该联合处理减轻了胰岛素抵抗并改善了相关行为这一发现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/b85e50fe3cd0/pharmaceuticals-17-01054-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/9bfe18bdd12d/pharmaceuticals-17-01054-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/fca19ede4109/pharmaceuticals-17-01054-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/629d81ca10cf/pharmaceuticals-17-01054-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/73fdcae998e5/pharmaceuticals-17-01054-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/2e68c45e09b9/pharmaceuticals-17-01054-g008a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/b85e50fe3cd0/pharmaceuticals-17-01054-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/9bfe18bdd12d/pharmaceuticals-17-01054-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/f8b705f71cab/pharmaceuticals-17-01054-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/d61a57af659e/pharmaceuticals-17-01054-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/5e7ddf2ba7b9/pharmaceuticals-17-01054-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/fca19ede4109/pharmaceuticals-17-01054-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/629d81ca10cf/pharmaceuticals-17-01054-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/73fdcae998e5/pharmaceuticals-17-01054-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/2e68c45e09b9/pharmaceuticals-17-01054-g008a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e986/11359371/b85e50fe3cd0/pharmaceuticals-17-01054-g009.jpg

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