Page 32 - N. Metabolism and metabolic diseases
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[N. Metabolism and metabolic diseases-17]
Lipid metabolic dysfunction in mice with DSS-induced
ulcerative colitis
Jeonghyeon Kwon¹, Chungho Lee¹, Sungbaek Heo¹, Chanmi So¹, Yerin Kim¹, Bobae Kim¹, Chang-Kee Hyun¹˙*
¹School of Life Science, Handong Global University, Pohang 37554, Republic of Korea
Inflammatory bowel disease (IBD) is a group of intestinal disorders, accompanied by various complications. In this
study, we examined the connection between IBD and metabolic disorders using dextran sodium sulfate (DSS)-
induced IBD model mice. Mice with chronic colitis induced by 3 cycles of 7-day DSS administration followed by 7-
day of DSS-free water developed fatty liver and dyslipidemia. DSS caused direct damage to the colonic epithelial
barrier, which led to an increased intestinal permeability and consequent endotoxemia. There was a significant
reduction in expression of crucial metabolic regulators such as SIRT1, FGF21, irisin, and adiponectin. Accompanied
with this reduction, the expression of genes involved in fat metabolism including fatty acid oxidation, lipolysis, and
lipogenesis in the liver and adipose tissues, and also in cholesterol metabolism such as cholesterol synthesis, bile
acid synthesis, and reverse cholesterol transport in the liver decreased. BAT thermogenesis and SAT browning was
also suppressed. Our findings provide a potential molecular mechanism that links IBD to lipid metabolic dysfunction
and hepatic steatosis. [This work was supported by the National Research Foundation of Kore grant funded by the
Korea government (2019R1F1A1059860).]

