Mol. Cells 2011; 31(5): 461-470
Published online April 21, 2011
https://doi.org/10.1007/s10059-011-1009-3
© The Korean Society for Molecular and Cellular Biology
Wookju Jang1,4, Nam Ho Jeoung2,4, and Kyung-Hyun Cho1,3,*
Correspondence to : *Correspondence: chok@yu.ac.kr
Long-term consumption of artificial sweeteners (AS) has been the recent focus of safety concerns. However, the potential risk of the AS in cardiovascular disease and lipoprotein metabolism has not been investigated sufficiently. We compared the influence of AS (aspartame, acesulfame K, and saccharin) and fructose in terms of functional and structural correlations of apolipoprotein (apo) A-I and high-density lipoproteins (HDL), which have atheroprotective effects. Long-term treatment of apoA-I with the sweetener at physiological concentration (3 mM for 168 h) resulted in loss of antioxidant and phospholipid binding activities with modification of secondary structure. The AS treated apoA-I exhibited proteolytic cleavage to produce 26 kDa-fragment. They showed pro-atherogenic properties in acetylated LDL phagocytosis of macrophages. Each sweetener alone or sweetener-treated apoA-I caused accelerated senescence in human dermal fibroblasts. These results suggest that long-term consumption of AS might accelerate atherosclerosis and senescence via impairment of function and structure of apoA-I and HDL.
Keywords apolipoprotein A-I, artificial sweetener, atherosclerosis, high-density lipoprotein, senescence
Mol. Cells 2011; 31(5): 461-470
Published online May 31, 2011 https://doi.org/10.1007/s10059-011-1009-3
Copyright © The Korean Society for Molecular and Cellular Biology.
Wookju Jang1,4, Nam Ho Jeoung2,4, and Kyung-Hyun Cho1,3,*
1School of Biotechnology, Yeungnam University, Gyeongsan 712-749, Korea, 2Department of Fundamental Medical and Pharmaceutical Sciences, CU-Leaders College, Catholic University of Daegu, Gyeongsan 712-702, Korea, 3Research Institute of Protein Sensor, Yeungnam University, Gyeongsan 712-749, Korea, 4These authors contributed equally to this work.
Correspondence to:*Correspondence: chok@yu.ac.kr
Long-term consumption of artificial sweeteners (AS) has been the recent focus of safety concerns. However, the potential risk of the AS in cardiovascular disease and lipoprotein metabolism has not been investigated sufficiently. We compared the influence of AS (aspartame, acesulfame K, and saccharin) and fructose in terms of functional and structural correlations of apolipoprotein (apo) A-I and high-density lipoproteins (HDL), which have atheroprotective effects. Long-term treatment of apoA-I with the sweetener at physiological concentration (3 mM for 168 h) resulted in loss of antioxidant and phospholipid binding activities with modification of secondary structure. The AS treated apoA-I exhibited proteolytic cleavage to produce 26 kDa-fragment. They showed pro-atherogenic properties in acetylated LDL phagocytosis of macrophages. Each sweetener alone or sweetener-treated apoA-I caused accelerated senescence in human dermal fibroblasts. These results suggest that long-term consumption of AS might accelerate atherosclerosis and senescence via impairment of function and structure of apoA-I and HDL.
Keywords: apolipoprotein A-I, artificial sweetener, atherosclerosis, high-density lipoprotein, senescence
Kyung-Hyun Cho
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