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Transgenic overexpression of Niemann-Pick C2 protein promotes cholesterol gallstone formation in mice.

Abstract：

BACKGROUND & AIMS:Niemann-Pick C2 (NPC2) is a lysosomal protein involved in the egress of low-density lipoprotein-derived cholesterol from lysosomes to other intracellular compartments. NPC2 has been detected in several tissues and is also secreted from the liver into bile. We have previously shown that NPC2-deficient mice fed a lithogenic diet showed reduced biliary cholesterol secretion as well as cholesterol crystal and gallstone formation. This study aimed to investigate the consequences of NPC2 hepatic overexpression on liver cholesterol metabolism, biliary lipid secretion, gallstone formation and the effect of NPC2 on cholesterol crystallization in model bile. METHODS:We generated NPC2 transgenic mice (Npc2.Tg) and fed them either chow or lithogenic diets. We studied liver cholesterol metabolism, biliary lipid secretion, bile acid composition and gallstone formation. We performed cholesterol crystallization studies in model bile using a recombinant NPC2 protein. RESULTS:No differences were observed in biliary cholesterol content or secretion between wild-type and Npc2.Tg mice fed the chow or lithogenic diets. Interestingly, Npc2.Tg mice showed an increased susceptibility to the lithogenic diet, developing more cholesterol gallstones at early times, but did not show differences in the bile acid hydrophobicity and gallbladder cholesterol saturation indices compared to wild-type mice. Finally, recombinant NPC2 decreased nucleation time in model bile. CONCLUSIONS:These results suggest that NPC2 promotes cholesterol gallstone formation by decreasing the cholesterol nucleation time, indicating a pro-nucleating function of NPC2 in bile.

journal_name

J Hepatol

journal_title

Journal of hepatology

authors

Acuña M,González-Hódar L,Amigo L,Castro J,Morales MG,Cancino GI,Groen AK,Young J,Miquel JF,Zanlungo S

doi

10.1016/j.jhep.2015.10.002

subject

Has Abstract

pub_date

2016-02-01 00:00:00

pages

361-369

issue

2

eissn

0168-8278

issn

1600-0641

pii

S0168-8278(15)00669-8

journal_volume

64

pub_type

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