Cholecystectomy: a way forward and back to metabolic syndrome?

被引:26
|
作者
Garruti, Gabriella [1 ]
Wang, David Q-H [2 ]
Di Ciaula, Agostino [3 ]
Portincasa, Piero [4 ]
机构
[1] Univ Bari Aldo Moro, Med Sch, Dept Emergency & Organ Transplantat, Sect Endocrinol, Bari, Italy
[2] Albert Einstein Coll Med, Marion Bessin Liver Res Ctr, Dept Med, Div Gastroenterol & Liver Dis, Bronx, NY 10467 USA
[3] Hosp Bisceglie, Div Internal Med, Bisceglie, Italy
[4] Univ Bari, Med Sch, Dept Biomed Sci & Human Oncol, Clin Med A Murri, Bari, Italy
关键词
FATTY LIVER-DISEASE; GROWTH-FACTOR; 19; GALLSTONE DISEASE; BILE-ACIDS; ASSOCIATION; RECEPTOR; OBESITY;
D O I
10.1038/labinvest.2017.129
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The gallbladder provides rhythmic secretion of concentrated bile acids (BAs) during fasting and postprandially contributes to digestion of dietary lipids. In addition, BAs activate metabolic pathways governing gluco-lipid homeostasis and energy expenditure via the farnesoid X nuclear receptor (FXR), G protein-coupled BA receptor 1 (GPBAR-1), and fibroblast growth factor 19 (FGF19) in the liver, intestine, brown fat, and muscle. Cholecystectomy is standard treatment worldwide for symptomatic gallstone patients. As excellently reviewed by Chen et al, cholecystectomy may disrupt enterohepatic recycling of, and signaling by, BAs. Further studies are needed to investigate whether gallbladder removal is an independent risk factor for development of the metabolic syndrome.
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页码:4 / 6
页数:3
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