Experimental/clinical condition | Animal species/region of gut | Adaptive changes | Reference |
Croton oil-induced ileitis | Mouse, small intestine | Increased CB1 protein expression and FAAH activity. No changes in endocannabinoid levels | 32 |
Cholera toxin-induced diarrhoea | Mouse, small intestine | Increased levels of anandamide (but not 2-AG) and CB1 mRNA; no changes in FAAH activity | 26 |
Acetic acid-induced ileus | Mouse, small intestine | Increased levels of anandamide (but not 2-AG) and CB1 expression; no changes in FAAH | 25 |
Colitis induced by DNBS | Mouse, colon | Increased number of CB1-expressing neurons | 33 |
Colitis induced by oil of mustard or by dextran sulfate sodium | Mouse, colon | Immunohistochemistry revealed strong upregulation of CB1 receptors in myenteric neurons and endothelial cells; CB2 immunostaining was more marked in infiltrated immune cells in colitis | 34 |
Preneoplastic lesions induced by azoxymethane | Mouse, colon | Increased levels of 2-AG | 41 |
Coeliac-like atrophy induced by methotrexate | Rat, duodenum | Increased levels of both anandamide and 2-AG (in both muscle/serosa and mucosa layers) | 37 |
Toxin A-induced ileitis | Rat, ileum | Increased levels of anandamide and 2-AG | 40 |
Coeliac disease | Humans, duodenum | Increased levels of anandamide and a trend towards an increase of 2-AG; increased CB1 receptor immunofluorescence | 37 |
Colorectal cancer/adenomatous polyps | Humans, colon | Increased levels of anandamide and 2-AG; No changes in CB1, CB2 and FAAH expression | 36 |
Diverticulitis | Humans, colon | Increased levels of anandamide, decreased levels of 2-AG. No changes in CB1 and CB2 mRNA expression | 38 |
Inflammatory bowel disease | Humans, colon | More intense epithelial CB1 immunoreactivity in the acute phase IBD and Crohn’s disease; CB2 receptor immunoreactivity evident in the epithelium of colonic tissue characteristic of IBD; increased levels of anandamide (but not 2-AG) | 29,35 |
2-AG, 2-arachydonylglycerol; DNBS, dinitrobenzene sulfonic acid; FAAH, fatty acid amide hydrolase; IBD, inflammatory bowel disease.