Genetic Ablation of Solute Carrier Family 7a3a Leads to Hepatic Steatosis in Zebrafish During Fasting
Gu, Qilin1,2; Yang, Xiaojie1,2; Lin, Li3; Li, Shaoyang3; Li, Qing1; Zhong, Shan3; Peng, Jinrong4; Cui, Zongbin1
2014-12-01
Source PublicationHEPATOLOGY
ISSN0270-9139
Volume60Issue:6Pages:1929-1941
AbstractNonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder caused by abnormal lipid metabolisms, such as reduced hepatic fatty acid oxidation (FAO), but intracellular control of FAO under physio-and pathological conditions remains largely undefined. Here, we demonstrate that deprivation of Slc7a3a leads to hepatic steatosis in fasted zebrafish as a result of defects in arginine-dependent nitric oxide (NO) synthesis. Fast-induced hepatic steatosis in slc7a3a-null mutants can be rescued by treatments with NO donor, cyclic guanosine monophosphate analog, adenosinemonophosphate- activated protein kinase (AMPK) activator, or peroxisome proliferatoractivated receptor alpha (PPAR-alpha) agonist. In contrast, inhibitors of NO synthases, AMPK, or soluble guanylate cyclase and liver-specifically expressed dominant negatives of peroxisome proliferator-activated receptor-gamma coactivator 1 alpha and PPAR-alpha are sufficient to induce hepatic steatosis in fasted wild-type larvae. Moreover, knockdown of Slc7a3 in mice or SLC7A3 in human liver cells impaired AMPK-PPAR-alpha signaling and resulted in lipid accumulation under fasting or glucose starvation, respectively. Conclusion: These findings have revealed a NO-AMPK-PPAR-alpha-signaling pathway that is crucial for the control of hepatic FAO in vertebrates.
SubtypeArticle
KeywordFatty Liver-disease Magnetic-resonance Elastography Nonalcoholic Steatohepatitis Noninvasive Evaluation Stiffness Measurement Mr Elastography Natural-history United-states Xl Probe Fibrosis
DOI10.1002/hep.27356
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
Indexed BySCI
Language英语
WOS Research AreaGastroenterology & Hepatology
WOS SubjectGastroenterology & Hepatology
WOS KeywordFATTY LIVER-DISEASE ; MAGNETIC-RESONANCE ELASTOGRAPHY ; NONALCOHOLIC STEATOHEPATITIS ; NONINVASIVE EVALUATION ; STIFFNESS MEASUREMENT ; MR ELASTOGRAPHY ; NATURAL-HISTORY ; UNITED-STATES ; XL PROBE ; FIBROSIS
WOS IDWOS:000345517000058
Citation statistics
Cited Times:36[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.ihb.ac.cn/handle/342005/20374
Collection藻类生物学及应用研究中心_水生生物分子与细胞生物学研究中心
Affiliation1.Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol, Wuhan 430072, Peoples R China
2.Univ Chinese Acad Sci, Beijing, Peoples R China
3.Wuhan Univ, Wuhan 430072, Peoples R China
4.Zhejiang Univ, Hangzhou 310003, Zhejiang, Peoples R China
Recommended Citation
GB/T 7714
Gu, Qilin,Yang, Xiaojie,Lin, Li,et al. Genetic Ablation of Solute Carrier Family 7a3a Leads to Hepatic Steatosis in Zebrafish During Fasting[J]. HEPATOLOGY,2014,60(6):1929-1941.
APA Gu, Qilin.,Yang, Xiaojie.,Lin, Li.,Li, Shaoyang.,Li, Qing.,...&Cui, Zongbin.(2014).Genetic Ablation of Solute Carrier Family 7a3a Leads to Hepatic Steatosis in Zebrafish During Fasting.HEPATOLOGY,60(6),1929-1941.
MLA Gu, Qilin,et al."Genetic Ablation of Solute Carrier Family 7a3a Leads to Hepatic Steatosis in Zebrafish During Fasting".HEPATOLOGY 60.6(2014):1929-1941.
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