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IBD and IBS: palmitoylethanolamide, a natural treatment focussing on gut homeostasis

Inflammatory bowel diseases (IBD) and irritable bowel syndrome (IBS), lead to abdominal pain and motility disturbances. In the gut endogenous lipids play a physiological role in gut homeostasis. Various enzymes, such as FAAH and FAAA are crucially involved in the modulation of physiological processes mediated by biolipids in the gastrointestinal (GI) tract such as palmitoylethanolamide.

In particular, for inflammatory bowel diseases (IBD) and irritable bowel syndrome (IBS), whose symptoms are based on chronic irritation and inflammation in the gut as well as on motility disorders, molecules as PEA may replace in future conventional therapies for IBD and IBS.

The authors of the article:

‘Inhibition of fatty acid amide hydrolase (FAAH) as a novel therapeutic strategy in the treatment of pain and inflammatory diseases in the gastrointestinal tract’

focus unnecessary on new chemical enzyme inhibitors for reaching higher endogenous levels of the protectove biollipids such as PEA. Simple oral ingestion of PEA as in PeaPure replenishes the system and leads to the same goal, without side effects often dose-limiting for enzyme inhibitors.

Source: Sałaga M, Sobczak M, Fichna J. Inhibition of fatty acid amide hydrolase (FAAH) as a novel therapeutic strategy in the treatment of pain and inflammatory diseases in the gastrointestinal tract. Eur J Pharm Sci. 2013 Nov 22. pii: S0928-0987(13)00451-X. doi: 10.1016/j.ejps.2013.11.012.

Addendum 1

Effect of palmitoylethanolamide in a murine model of colitis

S. Petrosino1, F. Borrelli, E. Pagano, V. Di Marzo, A.A. Izzo et al

Although the presence of palmitoylethanolamide (PEA) in mammalian tissues has been known since the 1960s, this compound has emerged only recently as an important local pro-homeostatic mediator that, due to its chemical stability, can be also administered exogenously to exert, among others, analgesic and anti-inflammatory properties (Re et al. 2007). On the other hand, little is known about the effect of PEA in inflammatory bowel diseases (IBDs), which include ulcerative colitis and Crohn’s disease, and are chronic recurrent inflammatory disorders of the intestine which affect millions of individuals (Lichtenstein et al., 2006). Here, we investigated the effect of PEA in a murine model of colitis. Colitis was induced in mice by intracolonic administration of dinitrobenzene sulphonic acid (DNBS) and inflammation was assessed by evaluating inflammatory markers/parameters (colon weight/colon length ratio and myeloperoxidase activity).

A potential ‘curative effect’ on inflammation was tested: 1) in a first experiment, where PEA (0.1-1 mg/kg) was administered intraperitoneally (i.p.) for three consecutive days starting 24 hours after DNBS administration; and 2) in a second experiment, where PEA (0.1-1 mg/kg) was administered orally (per os) for three consecutive days starting 24 hours after DNBS administration. Animals were killed three days after DNBS administration. Our results show that: 1) in the first experiment PEA (i.p.) inhibited the loss of body weight induced by DNBS administration and reduced colon weight/colon length ratio in a dose-dependent manner; and 2) in the second experiment PEA (per os) inhibited the loss of body weight induced by DNBS, reduced colon weight/colon length ratio and myeloperoxidase activity, as well as the number of animals with diarrhea.

In conclusion, these results suggest a massive curative effect of PEA in a murine model of IBD.
Experiments are ongoing to establish the mechanism of action of PEA ‘curative’ effects in this model of colitis.

Effect of palmitoylethanolamide in a murine model of colitis

Addendum 2

Palmitoylethanolamide ameliorates development of colitis caused by injection of dinitrobenzene sulfonic
acid (DNBS) in mice by D. Impellizzeri1, E. Esposito1, R. Di Paola1 et al.

The inflammatory bowel diseases (IBDs) has a worldwide distribution, but its pathogenesis is not clearly understood. A major advance in the study of IBD has been the discovery and subsequent analysis of a number of models of mucosal inflammation that resemble IBD. Dinitrobenzene sulfonic acid (DNBS)—induced colitis in experimental animals has proven to be a useful model of IBD, as it possesses many of the cell and humoral immunity characteristics found in human IBD (Esposito et al., 2010).

N-palmitoylethanolamine (PEA) is an endogenous fatty acid amide belonging to the family of the N-acylethanolamines
(NAEs). Recently, several studies demonstrated that PEA is an important analgesic, anti-inflammatory and neuroprotective mediator, acting at several molecular targets in both central and sensory nervous systems as well as immune cells (Esposito et al., 2013). PEA has been proposed to act as a protective endogenous mediator produced during inflammatory conditions to counteract inflammation, neuronal damage and pain. In fact, several studies demonstrate that the tissue concentrations of PEA are altered during different pathological conditions (Re et al., 2007). For its chemical stability, it can be also administered exogenously as the active principle of current anti-inflammatory and analgesic preparations (Balvers et al., 2013).

N-palmitoylethanolamine (PEA) is an endogenous fatty acid amide belonging to the family of the N-acylethanolamines (NAEs). Recently, several studies demonstrated that PEA is an important analgesic, anti-inflammatory and neuroprotective mediator, acting at several molecular targets in both central and sensory nervous systems as well as immune cells (Esposito et al., 2013). PEA has been proposed to act as a protective endogenous mediator produced during inflammatory conditions to counteract inflammation, neuronal damage and pain. In fact, several studies demonstrate that the tissue concentrations of PEA are altered during different pathological conditions (Re et al., 2007). For its chemical stability, it can be also administered exogenously as the active principle of current anti-inflammatory and analgesic preparations
(Balvers et al., 2013).

Effect of palmitoylethanolamide in a murine model of colitis

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