Oral Presentation Joint Annual Scientific Meeting of the Nutrition Society of NZ and the Nutrition Society of Australia

Emu oil prevents bodyweight loss in a mouse model of chronic ulcerative colitis (296)

Romina Ghaemi 1 2 , Gordon S Howarth 1 2 3 , Ian C Lawrance 4 , Suzanne Mashtoub 1 2 4
  1. Discipline of Physiology, School of Medical Sciences, The University of Adelaide, Adelaide, South Australia
  2. Gastroenterology Department, Women’s and Children’s Hospital, North Adelaide, South Australia
  3. School of Animal & Veterinary Sciences, The University of Adelaide, Roseworthy, South Australia
  4. School of Medicine and Pharmacology, The University of Western Australia, Murdoch, Western Australia

Background/Aims: Ulcerative colitis (UC), a type of inflammatory bowel disease, is characterised by colonic inflammation and ulceration. Orally-administered Emu Oil (EO), extracted from Emu fat, accelerated the intestinal repair process in a pre-clinical model of acute UC. We hypothesized that EO would reduce the severity of dextran sulphate sodium (DSS)-induced chronic UC in mice.

Methods: Female C57BL6 mice (n=10/group) were gavaged with water or EO (80microL or 160microL) thrice weekly. Mice were subjected to two cycles each consisting of ad libitum access to water or DSS (2% w/v) for one week and two weeks water recovery. Followed by one week water or DSS and mice culled two days later. Bodyweight, blood profile, organ data and myeloperoxidase activity were assessed. p<0.05 was considered significant.

Results: DSS decreased bodyweight (days 6-19 and 26-30; maximum of 24%), compared to normal controls (p<0.001). In DSS-treated mice, high dose EO significantly increased bodyweight (days 6-12), compared to controls (p<0.05). DSS decreased red blood cell count, compared to normal controls (p<0.05); an effect not improved by EO. Compared to normal controls, DSS increased liver (16%), spleen (45%), lung (19%) and small intestine (20%) weights (p<0.05), although EO had no significant effect (p>0.05). DSS increased colon myeloperoxidase activity compared to normal controls (p<0.05), however, EO was unable to significantly reduce these levels.

Conclusions: EO prevented bodyweight loss in this mouse model of chronic colitis, however, was unable to improve other preliminary parameters. Analyses currently underway include chronic inflammatory markers, histological morphometry and cell kinetics.

Funding source: N/A