Sucralose, a Non-nutritive Artificial Sweetener Exacerbates High Fat Diet-Induced Hepatic Steatosis Through Taste Receptor Type 1 Member 3

Frontiers in Nutrition

Chung-Hao Li¹  Hung-Tsung Wu²  Yi-Cheng Chen³  Horng-Yih Ou⁴  Ching-Han Lin⁴  Kai-Pi Cheng⁴  Hsiu-Ling Pai⁶  Hsin-Yu Kuo⁷ 

[1] Department of Family Medicine, Tainan Municipal An-Nan Hospital, China Medical University, Tainan City, Taiwan;Department of Internal Medicine, School of Medicine, College of Medicine, National Cheng Kung University, Tainan City, Taiwan;Department of Medical Research, Ditmanson Medical Foundation Chia-Yi Christian Hospital, Chiayi City, Taiwan;Division of Endocrinology and Metabolism, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan City, Taiwan;Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan City, Taiwan;Graduate Institute of Metabolism and Obesity Sciences, College of Nutrition, Taipei Medical University, Taipei City, Taiwan;Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan City, Taiwan;

关键词: artificial sweetener;    endoplasmic reticulum stress;    hepatic steatosis;    high fat diet;    sucralose;   

DOI  :  10.3389/fnut.2022.823723

来源: DOAJ

【 摘 要 】

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease globally, and it is strongly associated with obesity. To combat obesity, artificial sweeteners are often used to replace natural sugars, and sucralose is one of the most extensively used sweeteners. It was known that sucralose exerted effects on lipid metabolism dysregulation, and hepatic inflammation; however, the effects of sucralose on hepatic steatosis were still obscure. In this study, we found that supplements of sucralose enhanced high-fat-diet (HFD)-induced hepatic steatosis. In addition, treatment of sucralose increased reactive oxygen species (ROS) generation and induced endoplasmic reticulum (ER) stress in HepG2 cells. Pretreatment of ROS or ER stress inhibitors reversed the effects of sucralose on lipogenesis. Furthermore, pretreatment of taste receptor type 1 membrane 3 (T1R3) inhibitor or T1R3 knockdown reversed sucralose-induced lipogenesis in HepG2 cells. Taken together, sucralose might activate T1R3 to generate ROS and promote ER stress and lipogenesis, and further accelerate to the development of hepatic steatosis.

【 授权许可】

Unknown