Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2023 Apr 5:14:1135157.
doi: 10.3389/fendo.2023.1135157. eCollection 2023.

Gut microbiota and oleoylethanolamide in the regulation of intestinal homeostasis

Affiliations
Review

Gut microbiota and oleoylethanolamide in the regulation of intestinal homeostasis

Carlotta De Filippo et al. Front Endocrinol (Lausanne). .

Abstract

A vast literature strongly suggests that the endocannabinoid (eCB) system and related bioactive lipids (the paracannabinoid system) contribute to numerous physiological processes and are involved in pathological conditions such as obesity, type 2 diabetes, and intestinal inflammation. The gut paracannabinoid system exerts a prominent role in gut physiology as it affects motility, permeability, and inflammatory responses. Another important player in the regulation of host metabolism is the intestinal microbiota, as microorganisms are indispensable to protect the intestine against exogenous pathogens and potentially harmful resident microorganisms. In turn, the composition of the microbiota is regulated by intestinal immune responses. The intestinal microbial community plays a fundamental role in the development of the innate immune system and is essential in shaping adaptive immunity. The active interplay between microbiota and paracannabinoids is beginning to appear as potent regulatory system of the gastrointestinal homeostasis. In this context, oleoylethanolamide (OEA), a key component of the physiological systems involved in the regulation of dietary fat consumption, energy homeostasis, intestinal motility, and a key factor in modulating eating behavior, is a less studied lipid mediator. In the small intestine namely duodenum and jejunum, levels of OEA change according to the nutrient status as they decrease during food deprivation and increase upon refeeding. Recently, we and others showed that OEA treatment in rodents protects against inflammatory events and changes the intestinal microbiota composition. In this review, we briefly define the role of OEA and of the gut microbiota in intestinal homeostasis and recapitulate recent findings suggesting an interplay between OEA and the intestinal microorganisms.

Keywords: dysbiosis; gut barrier permeability; inflammation; intestinal physiology; metabolic diseases; obesity.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer LO declared a past co-authorship with the authors MP and CF to the Handling Editor.

Similar articles

Cited by

References

    1. Rodriguez de Fonseca F, Navarro M, Gomez R, Escuredo L, Nava F, Fu J, et al. . An anorexic lipid mediator regulated by feeding. Nature (2001) 414(6860):209–12. doi: 10.1038/35102582 - DOI - PubMed
    1. Gaetani S, Oveisi F, Piomelli D. Modulation of meal pattern in the rat by the anorexic lipid mediator oleoylethanolamide. Neuropsychopharmacology (2003) 28(7):1311–6. doi: 10.1038/sj.npp.1300166 - DOI - PubMed
    1. Oveisi F, Gaetani S, Eng KT, Piomelli D. Oleoylethanolamide inhibits food intake in free-feeding rats after oral administration. Pharmacol Res (2004) 49(5):461–6. doi: 10.1016/j.phrs.2003.12.006 - DOI - PubMed
    1. Piomelli D. A fatty gut feeling. Trends Endocrinol Metab (2013) 24(7):332–41. doi: 10.1016/j.tem.2013.03.001 - DOI - PMC - PubMed
    1. DiPatrizio NV, Piomelli D. Intestinal lipid-derived signals that sense dietary fat. J Clin Invest (2015) 125(3):891–8. doi: 10.1172/JCI76302 - DOI - PMC - PubMed