N-Palmitoylethanolamine Maintains Local Lipid Homeostasis to Relieve Sleep Deprivation-Induced Dry Eye Syndrome
Laboratory studyOther animals
- Design
- Laboratory study
- Subjects
- Mice in a "stick over water" sleep deprivation model; numbers not stated in the abstract
- Dose used in the study
- Exogenous palmitoylethanolamide; dose and route not stated in the abstract
- Duration
- Not stated in the abstract
- What was measured
- Palmitoylethanolamide levels and synthetic enzyme expression in the lacrimal gland; lipid deposition, cell structure and secretory function of the gland; corneal barrier function and dry eye signs; the role of PPAR-alpha.
What the authors reported
Sleep deprivation lowered palmitoylethanolamide in the lacrimal gland, mainly through reduced expression of its synthetic enzyme NAPE-PLD. Giving PEA restored lipid balance in the gland, reduced lipid deposits, preserved endoplasmic reticulum and mitochondrial structure and improved acinar secretion. PEA also prevented corneal barrier damage and improved dry eye signs. PPAR-alpha mediated these effects.
Limits of this study
A mouse model of sleep-deprivation dry eye; it cannot show effect in people. Dose, route and animal numbers are not given in the abstract. Funding and conflicts not stated in the abstract.
Source
PubMed 32047441 · doi:10.3389/fphar.2019.01622
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.