https://scholars.lib.ntu.edu.tw/handle/123456789/593997
標題: | Consumption of non-nutritive sweetener, acesulfame potassium exacerbates atherosclerosis through dysregulation of lipid metabolism in apoe−/− mice | 作者: | Lin, Cheng-Hsin HUNG-YUAN LI SHU-HUEI WANG Chen, Yue-Hwa Chen, Yang-Ching Wu, Hung-Tsung |
關鍵字: | acesulfame potassium; apolipoprotein E; atherosclerosis; dysregulation; lipid metabolism;Acesulfame potassium; Apolipoprotein E; Atherosclerosis; Dysregulation; Lipid metabolism | 公開日期: | 9-十一月-2021 | 出版社: | MDPI | 卷: | 13 | 期: | 11 | 來源出版物: | Nutrients | 摘要: | Obesity is associated with the risk of cardiovascular disease, and non-nutritive sweetener, such as acesulfame potassium (AceK) has been used to combat obesity. However, the effects of AceK on cardiovascular disease are still unclear. In this study, high cholesterol diet (HCD)-fed ApoE-/- mice had dysregulated plasma lipid profile, and developed atherosclerosis, determined by atherosclerotic plaque in the aorta. Supplement of AceK in HCD worsened the dyslipidemia and increased atherosclerotic plaque, as compared with HCD-fed ApoE-/- mice. Since treatment of AceK in RAW264.7 macrophages showed no significant effects on inflammatory cytokine expressions, we then investigated the impacts of AceK on lipid metabolism. We found that AceK consumption enhanced hepatic lipogenesis and decreased β-oxidation in ApoE-/- mice. In addition, AceK directly increased lipogenesis and decreased β-oxidation in HepG2 cells. Taken together, a concurrent consumption of AceK exacerbated HCD-induced dyslipidemia and atherosclerotic lesion in ApoE-/- mice, and AceK might increase the risk of atherosclerosis under HCD. |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/593997 | ISSN: | 2072-6643 | DOI: | 10.3390/nu13113984 | SDG/關鍵字: | acesulfame; apolipoprotein E; cytokine; nonnutritive sweetener; potassium; RNA; acetosulfame; apolipoprotein E; autacoid; cytokine; nonnutritive sweetener; thiazine derivative; animal cell; animal experiment; animal model; animal tissue; aorta; apolipoprotein E knockout mouse; Article; atherosclerosis; atherosclerotic plaque; cardiovascular disease; cardiovascular risk factor; cell culture; cholesterol diet; controlled study; disease exacerbation; dyslipidemia; fatty acid oxidation; gene expression; Hep-G2 cell line; lipid blood level; lipid diet; lipid metabolism; lipogenesis; liver; macrophage; male; mouse; nonhuman; obesity; protein expression; protein function; RAW 264.7 cell line; real time polymerase chain reaction; Western blotting; animal; atherosclerosis; complication; disease exacerbation; dyslipidemia; gene expression regulation; genetics; homeostasis; human; knockout mouse; metabolism; pathology; Animals; Apolipoproteins E; Atherosclerosis; Cytokines; Diet, High-Fat; Disease Progression; Dyslipidemias; Gene Expression Regulation; Hep G2 Cells; Homeostasis; Humans; Inflammation Mediators; Lipid Metabolism; Male; Mice; Mice, Knockout; Non-Nutritive Sweeteners; RAW 264.7 Cells; Thiazines |
顯示於: | 解剖學暨細胞生物學科所 |
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