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|Title:||Effect of feeding a high fat diet on hydrogen sulfide (H2S) metabolism in the mouse||Authors:||Kumar, Srinivasan Dinesh
Peh, Meng Teng
Anwar, Azzahra Binti
Ng, David S.W.
Atan, Mohamed Shirhan Bin Mohamed
Moore, Philip K.
|Issue Date:||2014||Source:||Peh, M. T., Anwar, A. B., Ng, D. S., Atan, M. S. B. M., Kumar, S. D., & Moore, P. K. (2014). Effect of feeding a high fat diet on hydrogen sulfide (H2S) metabolism in the mouse. Nitric Oxide, 41, 138-145.||Series/Report no.:||Nitric Oxide||Abstract:||Hydrogen sulfide (H2S) has complex effects in inflammation with both pro- and anti-inflammatory actions of this gas reported. Recent work suggests that a deficiency of H2S occurs in, and may contribute to, the chronic inflammation which underpins ongoing atherosclerotic disease. However, whether a high fat diet, predisposing to atherosclerosis, affects H2S metabolism is not known. In this study we assessed H2S metabolism in different tissues of mice fed a high fat diet for up to 16 weeks. Ex vivo biosynthesis of H2S was reduced in liver, kidney and lung of high fat fed mice. Western blotting revealed deficiency of cystathionine γ lyase (CSE) in liver and lung with increased expression of cystathionine β synthetase (CBS) in liver and kidney. Expression of 3-mercaptopyruvate sulfurtransferase (3-MST) was reduced in liver but not other tissues. Aortic endothelial cell CSE was also reduced in high fat fed animals as determined immunohistochemically. Plasma H2S concentration was not changed in these animals. No evidence of lipid deposition was apparent in aortae from high fat fed animals and plasma serum amyloid A (SAA) and C-reactive protein (CRP) were also unchanged suggesting lack of frank atherosclerotic disease. Plasma IL-6, IL12p40 and G-CSF levels were increased by high fat feeding whilst other cytokines including IL-1α, IL-1b and TNF-α were not altered. These results suggest that deficiency of tissue CSE and H2S occurs in mice fed a high fat diet and that this change takes place prior to development of frank atherosclerotic disease.||URI:||https://hdl.handle.net/10356/81770
|ISSN:||1089-8603||DOI:||10.1016/j.niox.2014.03.002||Rights:||© 2014 Elsevier Inc. This is the author created version of a work that has been peer reviewed and accepted for publication by Nitric Oxide, Elsevier Inc. It incorporates referee’s comments but changes resulting from the publishing process, such as copyediting, structural formatting, may not be reflected in this document. The published version is available at: [http://dx.doi.org/10.1016/j.niox.2014.03.002].||Fulltext Permission:||open||Fulltext Availability:||With Fulltext|
|Appears in Collections:||LKCMedicine Journal Articles|
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