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Vitamin C deficiency inhibits non-alcoholic fatty liver disease progression through impaired de novo lipogenesis

Title
Vitamin C deficiency inhibits non-alcoholic fatty liver disease progression through impaired de novo lipogenesis
Authors
Lee, Seoung-WooBaek, Su-MinKang, Kyung-KuLee, A-RangKim, Tae-UnChoi, Seong-KyoonRoh, Yoon-SeokHong, Il-HwaPark, Sang-JoonKim, Tae-HwanJeong, Kyu-ShikPark, Jin-Kyu
DGIST Authors
Lee, Seoung-Woo; Baek, Su-Min; Kang, Kyung-Ku; Lee, A-Rang; Kim, Tae-Un; Choi, Seong-Kyoon; Roh, Yoon-Seok; Hong, Il-Hwa; Park, Sang-Joon; Kim, Tae-Hwan; Jeong, Kyu-Shik; Park, Jin-Kyu
Issue Date
2021-09
Citation
American Journal of Pathology, 191(9), 1550-1563
Type
Article
Keywords
HEPATIC STEATOSISGENE-EXPRESSIONCHOLESTEROLMICENAFLDACIDSUPPLEMENTATIONBIOSYNTHESISEPIDEMIOLOGYANTIOXIDANT
ISSN
0002-9440
Abstract
Despite the increasing clinical importance of nonalcoholic fatty liver disease (NAFLD), little is known about its underlying pathogenesis or specific treatment. The senescence marker protein 30 (SMP30), which regulates the biosynthesis of vitamin C (VC) in many mammals, except primates and humans, was recently recognized as a gluconolactonase. However, the precise relation between VC and lipid metabolism in NAFLD is not completely understood. Therefore, this study aimed to clearly reveal the role of VC in NAFLD progression. SMP30 knockout (KO) mice were used as a VC-deficient mouse model. To investigate the precise role of VC on lipid metabolism, 13- to 15-week–old SMP30 KO mice and wild-type mice fed a 60% high-fat diet were exposed to tap water or VC-containing water (1.5 g/L) ad libitum for 11 weeks. Primary mouse hepatocytes isolated from the SMP30 KO and wild-type mice were used to demonstrate the relation between VC and lipid metabolism in hepatocytes. Long-term VC deficiency significantly suppressed the progression of simple steatosis. The high-fat diet–fed VC-deficient SMP30 KO mice exhibited impaired sterol regulatory element-binding protein-1c activation because of excessive cholesterol accumulation in hepatocytes. Long-term VC deficiency inhibits de novo lipogenesis through impaired sterol regulatory element-binding protein-1c activation. © 2021 American Society for Investigative Pathology
URI
http://hdl.handle.net/20.500.11750/15272
DOI
10.1016/j.ajpath.2021.05.020
Publisher
American Society for Investigative Pathology
Related Researcher
Files:
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Collection:
Division of Biotechnology1. Journal Articles


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