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饮食诱导肥胖大鼠中非酒精性脂肪肝(NAFLD)的相对恢复。

Relative Recovery of Non-Alcoholic Fatty Liver Disease (NAFLD) in Diet-Induced Obese Rats.

机构信息

Laboratory Animal Research Center, Qatar University, Doha P.O. Box 2713, Qatar.

Anti-Doping Laboratory Qatar, Sports City Road, Doha P.O. Box 2713, Qatar.

出版信息

Nutrients. 2023 Dec 28;16(1):115. doi: 10.3390/nu16010115.

DOI:10.3390/nu16010115
PMID:38201945
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10780646/
Abstract

Consumption of a high-carbohydrate diet has a critical role in the induction of weight gain and obesity-related pathologies. This study tested the hypothesis that a carbohydrate-rich diet induces weight gain, ectopic fat deposition, associated metabolic risks and development of non-alcoholic fatty liver disease (NAFLD), which are partially reversible following carbohydrate reduction. Sprague Dawley (SD) rats were fed a carbohydrate-enriched cafeteria diet (CAF) or normal chow (NC) ad libitum for 16-18 weeks. In the reversible group (REV), the CAF was replaced with NC for a further 3 weeks (18-21 weeks). Animals fed the CAF diet showed significantly increased body weight compared to those fed NC, accompanied by abnormal changes in their systemic insulin and triglycerides, elevation of hepatic triglyceride and hepatic steatosis. In the REV group, when the CAF diet was stopped, a modest, non-significant weight loss was associated with improvement in systemic insulin and appearance of the liver, with lower gross fatty deposits and hepatic triglyceride. In conclusion, a carbohydrate-enriched diet led to many features of metabolic syndrome, including hyperinsulinemia, while a dietary reduction in this macronutrient, even for a short period, was able to restore normoinsulinemia, and reversed some of the obesity-related hepatic abnormalities, without significant weight loss.

摘要

高碳水化合物饮食在诱导体重增加和肥胖相关病理方面起着关键作用。本研究检验了以下假设:富含碳水化合物的饮食会导致体重增加、异位脂肪沉积、相关代谢风险和非酒精性脂肪性肝病 (NAFLD) 的发展,而减少碳水化合物摄入后这些情况部分是可以逆转的。SD 大鼠自由喂食富含碳水化合物的自助餐厅饮食(CAF)或正常饲料(NC)16-18 周。在可逆转组(REV)中,CAF 被 NC 取代进一步 3 周(18-21 周)。与喂食 NC 的大鼠相比,喂食 CAF 饮食的大鼠体重明显增加,伴随全身胰岛素和甘油三酯的异常变化、肝甘油三酯升高和肝脂肪变性。在 REV 组中,当停止 CAF 饮食时,体重适度、非显著下降与全身胰岛素改善和肝脏外观改善相关,肝内脂肪沉积和肝甘油三酯降低。总之,富含碳水化合物的饮食导致了许多代谢综合征的特征,包括高胰岛素血症,而即使在短时间内减少这种宏量营养素,也能够恢复正常胰岛素血症,并逆转一些与肥胖相关的肝异常,而不会显著减轻体重。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/10780646/fbc7b3506c9a/nutrients-16-00115-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/10780646/f34e5c3cf14a/nutrients-16-00115-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/10780646/11966119fc82/nutrients-16-00115-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/10780646/63cac4c0dcd4/nutrients-16-00115-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/10780646/86655b08ab1e/nutrients-16-00115-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/10780646/fbc7b3506c9a/nutrients-16-00115-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/10780646/f34e5c3cf14a/nutrients-16-00115-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/10780646/11966119fc82/nutrients-16-00115-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/10780646/63cac4c0dcd4/nutrients-16-00115-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/10780646/86655b08ab1e/nutrients-16-00115-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d655/10780646/fbc7b3506c9a/nutrients-16-00115-g005.jpg

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