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白蛋白缺乏症可减少饮食诱导肥胖小鼠模型的肝脂肪变性并改善葡萄糖代谢。

Albumin Deficiency Reduces Hepatic Steatosis and Improves Glucose Metabolism in a Mouse Model of Diet-Induced Obesity.

机构信息

Department of Nutrition Science, Purdue University, West Lafayette, IN 47907, USA.

Department of Comparative Pathobiology, Purdue University, West Lafayette, IN 47907, USA.

出版信息

Nutrients. 2023 Apr 25;15(9):2060. doi: 10.3390/nu15092060.

DOI:10.3390/nu15092060
PMID:37432201
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10181153/
Abstract

Serum albumin facilitates the transport of free fatty acids (FFAs) from adipose tissue to other organs. It was not known if impeding this process could protect from hepatic steatosis and metabolic dysfunction in obesity. We tested whether albumin knockout (Alb) mice would exhibit a reduction in plasma FFA concentration, reduced hepatic lipid accumulation, and improved glucoregulation as compared to wild-type (WT) mice. Male homozygous albumin knockout mice (Alb) and WT controls were fed a low-fat diet (LFD) or high-fat diet (HFD). Alb mice exhibited a similar body weight gain and body composition as WT on both diets. Despite HFD-induced obesity, Alb mice were protected from various comorbidities. Compared to WT mice on the HFD, Alb exhibited lower plasma FFA levels, lower blood glucose levels during glucose tolerance and insulin tolerance tests, and lower hepatic steatosis and inflammation. Alb mice on HFD also exhibited elevated expression of multiple genes in the liver and adipose tissues, such as peroxisome proliferator-activated receptor α in both tissues, as well as glucose transporter-4 and adiponectin in adipose tissues. The results indicate that albumin's FFA transport function may be involved in the development of hepatic lipid accumulation and dysregulated glucose metabolism in obesity.

摘要

血清白蛋白促进游离脂肪酸(FFA)从脂肪组织转运到其他器官。目前尚不清楚,如果阻止这一过程是否可以防止肥胖中的肝脂肪变性和代谢功能障碍。我们测试了白蛋白敲除(Alb)小鼠与野生型(WT)小鼠相比,其血浆 FFA 浓度是否降低,肝脂质积累是否减少,葡萄糖调节是否改善。雄性纯合白蛋白敲除小鼠(Alb)和 WT 对照小鼠分别喂食低脂饮食(LFD)或高脂饮食(HFD)。在两种饮食中,Alb 小鼠的体重增加和身体成分与 WT 相似。尽管 HFD 诱导肥胖,但 Alb 小鼠仍能预防多种合并症。与 HFD 上的 WT 小鼠相比,Alb 小鼠的血浆 FFA 水平较低,葡萄糖耐量和胰岛素耐量试验期间的血糖水平较低,肝脂肪变性和炎症程度较低。HFD 上的 Alb 小鼠肝脏和脂肪组织中多种基因的表达也升高,例如两种组织中的过氧化物酶体增殖物激活受体-α,以及脂肪组织中的葡萄糖转运蛋白-4 和脂联素。结果表明,白蛋白的 FFA 转运功能可能参与肥胖中肝脂质积累和葡萄糖代谢失调的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/99aa6ebf0f02/nutrients-15-02060-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/d9cda01da6ae/nutrients-15-02060-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/9473c81297d6/nutrients-15-02060-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/5f8a7dc4afb3/nutrients-15-02060-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/6c2027bd97a0/nutrients-15-02060-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/ccf6e4a148f0/nutrients-15-02060-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/c48f8d5f0cd5/nutrients-15-02060-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/0845707406aa/nutrients-15-02060-g007a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/cc6e3f295d13/nutrients-15-02060-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/99aa6ebf0f02/nutrients-15-02060-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/d9cda01da6ae/nutrients-15-02060-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/9473c81297d6/nutrients-15-02060-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/5f8a7dc4afb3/nutrients-15-02060-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/6c2027bd97a0/nutrients-15-02060-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/ccf6e4a148f0/nutrients-15-02060-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/c48f8d5f0cd5/nutrients-15-02060-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/0845707406aa/nutrients-15-02060-g007a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/cc6e3f295d13/nutrients-15-02060-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a10b/10181153/99aa6ebf0f02/nutrients-15-02060-g009.jpg

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