Acesulfame K and fatty liver in mice
What it found
In mice on a high-fat diet, long-term acesulfame K in drinking water increased liver fat and worsened glucose tolerance.
These effects were absent in mice lacking the PPARα gene.
What they found
Animal and lab studies
Liver fat in mice
Acesulfame K increased liver fat and triglycerides by about 10% in normal mice on a high-fat diet, but not in mice without PPARα.
Glucose tolerance in mice
Acesulfame K raised the peak blood sugar by about 25% and impaired glucose tolerance in normal mice, but not in mice without PPARα.
Liver cells in lab
In Hepa1-6 and Huh-7 liver cells, acesulfame K increased fat accumulation and activated PLCβ in a dose-dependent way. Blocking PPARα stopped these effects.
PPARα activation in mice
Drugs that activate PPARα reduced liver fat and lowered PLCβ activation in mice given acesulfame K. This protective effect was not seen in mice without PPARα.
Body weight and food intake
Acesulfame K did not change body weight gain in either type of mice, but it reduced food intake and increased water consumption.
What the authors conclude
“These findings demonstrated that chronic AK intake exacerbates NAFLD progression via PLCβ activation in hepatic STR signaling and that PLCβ activation depends on physiological PPARα activity.”
Also in their conclusions
- They conclude that chronic acesulfame K intake worsens fatty liver by activating PLCβ in the liver's sweet taste receptor signaling, and that this depends on PPARα.
- They say that activating PPARα with drugs protects against acesulfame K-induced fatty liver by suppressing PLCβ.
- They advise that the potential liver and metabolic risks of long-term non-nutritive sweetener consumption should be fully addressed to protect public health.
How it was done
The authors wanted to know whether chronic acesulfame K consumption affects nonalcoholic fatty liver disease and what role the PPARα protein plays, since this was previously unclear.
They gave male wild-type and PPARα-null mice a 60% high-fat diet and acesulfame K (2 mg/ml) in drinking water for 12 weeks. They also tested acesulfame K in liver cells and used drugs to activate or block PPARα.
What it can’t tell you
- These are animal and cell studies. They cannot show what happens in people.
- The study used a high-fat diet and a specific dose of acesulfame K, so the results may not apply to other diets or doses.
- The authors note that the sample size was limited, so the findings need confirmation in larger studies.
Who paid
- Conflicts
- The authors declare that they have no competing interests.
- Authors work at
- The First Affiliated Hospital of Ningbo University, P.R. China; Zhejiang University, P.R. China; Ningbo University, P.R. China
The paper
- Title
- Peroxisome proliferator‑activated receptor α regulates acesulfame‑K‑induced NAFLD via hepatic PLCβ: Foe and friend
- Type
- Study
- Evidence
- Animals and lab studies
- Summarised from
- Full text
- Cite
- Lin PY, Xie JR, Qian TC, et al (2026). Peroxisome proliferator‑activated receptor α regulates acesulfame‑K‑induced NAFLD via hepatic PLCβ: Foe and friend. International journal of molecular medicine. doi:10.3892/ijmm.2026.5773Free full textPubMed 41789618DOI
Summary written 26 Sep 2026. Check it against the paper before it changes what you eat. How we summarise papers · Report an error