Please use this identifier to cite or link to this item: https://doi.org/10.1038/srep19377
Title: Notch1 deficiency decreases hepatic lipid accumulation by induction of fatty acid oxidation
Authors: Song, N.-J
Yun, U.J
Yang, S
Wu, C
Seo, C.-R
Gwon, A.-R
Baik, S.-H 
Choi, Y
Choi, B.Y
Bahn, G
Kim, S
Kwon, S.-M
Park, J.S
Baek, S.H
Park, T.J
Yoon, K
Kim, B.-J
Mattson, M.P
Lee, S.-J
Jo, D.-G
Park, K.W
Keywords: fatty acid
Notch1 receptor
adipocyte
adverse effects
animal
cell line
deficiency
diet
drug effects
fatty liver
gene silencing
genetics
human
insulin resistance
lipid metabolism
liver
metabolism
mouse
obesity
oxidation reduction reaction
oxidative stress
pathology
RNA interference
signal transduction
Adipocytes
Animals
Cell Line
Diet
Fatty Acids
Fatty Liver
Gene Knockdown Techniques
Humans
Insulin Resistance
Lipid Metabolism
Liver
Mice
Obesity
Oxidation-Reduction
Oxidative Stress
Receptor, Notch1
RNA Interference
Signal Transduction
Issue Date: 2016
Publisher: Nature Publishing Group
Citation: Song, N.-J, Yun, U.J, Yang, S, Wu, C, Seo, C.-R, Gwon, A.-R, Baik, S.-H, Choi, Y, Choi, B.Y, Bahn, G, Kim, S, Kwon, S.-M, Park, J.S, Baek, S.H, Park, T.J, Yoon, K, Kim, B.-J, Mattson, M.P, Lee, S.-J, Jo, D.-G, Park, K.W (2016). Notch1 deficiency decreases hepatic lipid accumulation by induction of fatty acid oxidation. Scientific Reports 6 : 19377. ScholarBank@NUS Repository. https://doi.org/10.1038/srep19377
Rights: Attribution 4.0 International
Abstract: Notch signaling pathways modulate various cellular processes, including cell proliferation, differentiation, adhesion, and communication. Recent studies have demonstrated that Notch1 signaling also regulates hepatic glucose production and lipid synthesis. However, the effect of Notch1 signaling on hepatic lipid oxidation has not yet been directly investigated. To define the function of Notch1 signaling in hepatic lipid metabolism, wild type mice and Notch1 deficient antisense transgenic (NAS) mice were fed a high-fat diet. High-fat diet-fed NAS mice exhibited a marked reduction in hepatic triacylglycerol accumulation compared with wild type obese mice. The improved fatty liver was associated with an increased expression of hepatic genes involved in fatty acid oxidation. However, lipogenic genes were not differentially expressed in the NAS liver, suggesting lipolytic-specific regulatory effects by Notch1 signaling. Expression of fatty acid oxidative genes and the rate of fatty acid oxidation were also increased by inhibition of Notch1 signaling in HepG2 cells. In addition, similar regulatory effects on lipid accumulation were observed in adipocytes. Taken together, these data show that inhibition of Notch1 signaling can regulate the expression of fatty acid oxidation genes and may provide therapeutic strategies in obesity-induced hepatic steatosis.
Source Title: Scientific Reports
URI: https://scholarbank.nus.edu.sg/handle/10635/182514
ISSN: 2045-2322
DOI: 10.1038/srep19377
Rights: Attribution 4.0 International
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