Evidence map›Paper›PMID 35685876›Full record

ArticleFrontiers in nutrition2022

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

Hung-Tsung Wu, Ching-Han Lin, Hsiu-Ling Pai, Yi-Cheng Chen, Kai-Pi Cheng, Hsin-Yu Kuo, Chung-Hao Li, Horng-Yih Ou

Open access · goldAbstract read
In one paragraph

Article in Frontiers in nutrition, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.3field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 32 citations in OpenAlex.

  1. Long-term artificial sweetener exposure increases the risk of atherosclerosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026
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  10. Biological and Behavioral Responses ofInternational journal of molecular sciences · 2025
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  16. Food sweeteners: Angels or clowns for human health?Current research in food science · 2025
    Review
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  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 1 country.

Hung-Tsung WuDepartment of Internal Medicine, School of Medicine, College of Medicine, National Cheng Kung University, Tainan City, Taiwan.
Ching-Han LinDivision of Endocrinology and Metabolism, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan City, Taiwan.
Hsiu-Ling PaiGraduate Institute of Metabolism and Obesity Sciences, College of Nutrition, Taipei Medical University, Taipei City, Taiwan.
Yi-Cheng ChenDepartment of Medical Research, Ditmanson Medical Foundation Chia-Yi Christian Hospital, Chiayi City, Taiwan.
Kai-Pi ChengDivision of Endocrinology and Metabolism, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan City, Taiwan.
Hsin-Yu KuoDivision of Gastroenterology and Hepatology, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan City, Taiwan.
Chung-Hao LiDepartment of Family Medicine, Tainan Municipal An-Nan Hospital, China Medical University, Tainan City, Taiwan.
Horng-Yih OuDepartment of Internal Medicine, School of Medicine, College of Medicine, National Cheng Kung University, Tainan City, Taiwan.
National Cheng Kung University Hospital · TWChia-Yi Christian Hospital · TWChina Medical University · TWNational Cheng Kung University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

artificial sweetenerendoplasmic reticulum stresshepatic steatosishigh fat dietsucralose

Identifiers

PMID35685876
PMCPMC9171434
OpenAlexW4281386567

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.