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Absence of stearoyl-CoA desaturase-1 does not promote DSS-induced acute colitis

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Title: Absence of stearoyl-CoA desaturase-1 does not promote DSS-induced acute colitis
Author: Vallance, Bruce A.; Bissada, Nagat; MacDonald, Marcia L. E.; Hayden, Michael R.
Subject Keywords Dose-response relationship;Lipids;Dextran sulfate;Inflammation
Issue Date: 2009-08-17
Publicly Available in cIRcle 2009-09-21
Citation: MacDonald ML, Bissada N, Vallance BA, Hayden MR. Absence of stearoyl-CoA desaturase-1 does not promote DSS-induced acute colitis. Biochim Biophys Acta. Epub 2009 Aug 17. DOI: 10.1016/j.bbalip.2009.08.001. http://dx.doi.org/10.1016/j.bbalip.2009.08.001
Abstract: Absence of stearoyl-CoA desaturase-1 (SCD1) in mice leads to chronic inflammation of the skin and increased susceptibility to atherosclerosis, while also increasing plasma inflammatory markers. A recent report suggested that SCD1 deficiency also increases disease severity in a mouse model of inflammatory bowel disease, induced by dextran sulfate sodium (DSS). However, SCD1-deficient mice are known to consume increased amounts of water, which would also be expected to increase the intake of DSS-treated water. The aim of this study was to determine the effect of SCD1 deficiency on DSS-induced acute colitis with DSS dosing adjusted to account for genotype differences in fluid consumption. Wild-type controls were treated with 3.5% DSS for 5 days to induce moderately severe colitis, while the concentration of DSS given to SCD1-deficient mice was lowered to 2.5% to control for increased fluid consumption. Colonic inflammation was assessed by clinical and histological scoring. Although SCD1-deficient mice consumed a total intake of DSS that was greater than that of wild-type controls, colonic inflammation, colon length and fecal blood were not altered by SCD1-deficiency in DSS-induced colitis, while diarrhea and total weight loss were modestly improved. Despite SCD1 deficiency leading to chronic inflammation of the skin and increased susceptibility to atherosclerosis, it does not accelerate inflammation in the DSS-induced model of acute colitis when DSS intake is controlled. These observations suggest that SCD1 deficiency does not play a significant role in colonic inflammation in this model. [The original version of this article, along with updated information and services is located on the World Wide Web at: http://dx.doi.org/10.1016/j.bbalip.2009.08.001]
Affiliation: Child and Family Research Institute (CFRI)Molecular Medicine and Therapeutics, Centre forMedical Genetics, Dept of
URI: http://hdl.handle.net/2429/12927
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