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限时进食改善了高脂饮食诱导的肥胖大鼠模型的血管内皮功能。

Time-Restricted Feeding Improved Vascular Endothelial Function in a High-Fat Diet-Induced Obesity Rat Model.

作者信息

Azemi Ahmad Khusairi, Siti-Sarah Abdul Rahim, Mokhtar Siti Safiah, Rasool Aida Hanum Ghulam

机构信息

Department of Pharmacology, School of Medical Sciences, Health Campus, Universiti Sains Malaysia, Kota Bharu 16150, Kelantan, Malaysia.

Hospital Universiti Sains Malaysia, Kubang Kerian, Kota Bharu 16150, Kelantan, Malaysia.

出版信息

Vet Sci. 2022 Apr 28;9(5):217. doi: 10.3390/vetsci9050217.

DOI:10.3390/vetsci9050217
PMID:35622745
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9147025/
Abstract

Obesity, where there is enhancement of stored body fat in adipose tissues, is associated with cardiovascular complications that are mainly related to atherosclerosis. Time-restricted feeding (TRF) is a form of restricted eating aimed at reducing weight in obese subjects. The present study aims to investigate changes in vascular endothelial function, endothelial nitric oxide synthase (eNOS), and protein kinase B (Akt) protein expressions with TRF in obese and normal rats. Male Sprague Dawley rats were divided into two normal and three obese groups; obesity was induced in the obese groups by feeding with a high-fat diet (HFD) for six weeks. After six weeks, rats were equally divided into five groups ( = 7 per group): Normal group (NR) which continued on a standard diet for six more weeks, normal group switched to TRF with a standard diet for six weeks (NR + TRFSD), obese group (OR) which continued on HFD for six more weeks, obese group switched to TRF of HFD (OR + TRFHFD), and obese group switched to TRF of a standard diet (OR + TRFSD). TRF was practiced for six weeks, after which the rats were sacrificed. Aortic endothelium-dependent and endothelium-independent relaxations and contractions were assessed using the organ bath. Aortic eNOS and Akt protein expressions were determined using immunoblotting. Fasting blood glucose, body weight, body mass index (BMI), serum lipid profile, Lee's index, serum insulin levels, and sensitivity (HOMA-IR) were also measured. Endothelium-dependent relaxation was significantly impaired, while endothelium-dependent contraction increased in obese rats compared to that in normal rats. Both obese groups which underwent TRF with a HFD and standard diet improved their impairments in endothelium-dependent relaxation and reduced endothelium-dependent contraction; these were associated with increased expressions of aortic eNOS and Akt protein. Both obese groups with TRF reduced body weight, BMI, Lee's index, total cholesterol, triglycerides, low-density lipoprotein cholesterol, and improved insulin sensitivity. TRF improved endothelium-dependent relaxation and reduced endothelium-dependent contraction, thus attenuating endothelial dysfunction in obese rats. These were associated with increased aortic eNOS and Akt protein expressions.

摘要

肥胖是指脂肪组织中储存的身体脂肪增加,它与主要与动脉粥样硬化相关的心血管并发症有关。限时进食(TRF)是一种旨在减轻肥胖受试者体重的限制性饮食形式。本研究旨在探讨肥胖和正常大鼠中TRF对血管内皮功能、内皮型一氧化氮合酶(eNOS)和蛋白激酶B(Akt)蛋白表达的影响。雄性Sprague Dawley大鼠分为两个正常组和三个肥胖组;通过高脂饮食(HFD)喂养六周诱导肥胖组肥胖。六周后,大鼠平均分为五组(每组 = 7只):正常组(NR)继续标准饮食六周,正常组改为标准饮食的TRF六周(NR + TRFSD),肥胖组(OR)继续HFD六周,肥胖组改为HFD的TRF(OR + TRFHFD),肥胖组改为标准饮食的TRF(OR + TRFSD)。进行TRF六周,之后处死大鼠。使用器官浴评估主动脉内皮依赖性和非内皮依赖性舒张和收缩。使用免疫印迹法测定主动脉eNOS和Akt蛋白表达。还测量了空腹血糖、体重、体重指数(BMI)、血脂谱、李氏指数、血清胰岛素水平和敏感性(HOMA-IR)。与正常大鼠相比,肥胖大鼠的内皮依赖性舒张明显受损,而内皮依赖性收缩增加。接受HFD和标准饮食TRF的两个肥胖组均改善了内皮依赖性舒张的损伤并减少了内皮依赖性收缩;这些与主动脉eNOS和Akt蛋白表达增加有关。两个接受TRF的肥胖组均降低了体重、BMI、李氏指数、总胆固醇、甘油三酯、低密度脂蛋白胆固醇,并改善了胰岛素敏感性。TRF改善了内皮依赖性舒张并减少了内皮依赖性收缩,从而减轻了肥胖大鼠的内皮功能障碍。这些与主动脉eNOS和Akt蛋白表达增加有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75d6/9147025/f31bdfb67e71/vetsci-09-00217-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75d6/9147025/de4a07340eec/vetsci-09-00217-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75d6/9147025/60f9a5027763/vetsci-09-00217-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75d6/9147025/49248e57e5aa/vetsci-09-00217-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75d6/9147025/bb044b1b4763/vetsci-09-00217-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75d6/9147025/e235c9d7a9fa/vetsci-09-00217-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75d6/9147025/f31bdfb67e71/vetsci-09-00217-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75d6/9147025/de4a07340eec/vetsci-09-00217-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75d6/9147025/60f9a5027763/vetsci-09-00217-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75d6/9147025/49248e57e5aa/vetsci-09-00217-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75d6/9147025/bb044b1b4763/vetsci-09-00217-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75d6/9147025/e235c9d7a9fa/vetsci-09-00217-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75d6/9147025/f31bdfb67e71/vetsci-09-00217-g006.jpg

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