Palmitoylethanolamide counteracts hepatic metabolic inflexibility modulating mitochondrial function and efficiency in diet-induced obese mice
Laboratory studyHumansOther animals
- Design
- Laboratory study
- Subjects
- Mice fed a high-fat diet, plus human HepG2 liver cells challenged with palmitate; numbers not stated in the abstract
- Dose used in the study
- Palmitoylethanolamide 30 mg/kg per day by mouth in mice; concentration in cells not stated
- Duration
- Described as long-term; exact length not stated in the abstract
- What was measured
- Liver fat, energy expenditure and insulin resistance in mice; oxidative capacity and efficiency of isolated liver mitochondria; mitochondrial bioenergetics, fat accumulation and fatty acid oxidation in HepG2 cells; the role of AMPK.
What the authors reported
This lab study found:
- Long-term oral PEA limited liver fat accumulation, increased energy expenditure and markedly reduced insulin resistance in high-fat-fed mice.
- In isolated mitochondria PEA changed oxidative capacity and efficiency, with less lipid accumulation and oxidative stress.
- In insulin-resistant HepG2 cells PEA recovered mitochondrial function, reduced fat and increased fatty acid oxidation.
- Blocking AMPK limited these effects.
Limits of this study
A mouse and cell study; it cannot show effect in people. Study length and animal numbers are not in the abstract. Funding and conflicts not stated in the abstract.
Source
PubMed 31914699 · doi:10.1096/fj.201901510RR
Entry checked against the abstract on PubMed on 2026-09-22. The dose shown is the dose the researchers used. It is not a recommendation. How to read this page.