Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, C067

Oral Communications


B. A. Çevlikli2, C. Tanman2, E. Yircali2, A. Ürpekli2, F. C. yildiz2, Z. N. Özdemir Kumral1, S. Arabaci Tamer1, D. Gökçeoğlu8, D. Akakin8, D. Özbeyli4, L. Sen1, K. Ozguler5, B. Aksu5, C. Erzik7, O. Sirikci6, B. Yeğen1, N. Imeryüz1,3

1. Physiology, Marmara University, Istanbul, Turkey. 2. School of Medicine, Marmara University, Istanbul, Turkey. 3. Internal Medicine, Gastroenterology, Marmara University, Istanbul, Turkey. 4. Vocational School of Health Services,, Marmara University, Istanbul, Turkey. 5. Microbiology, Marmara University, Istanbul, Turkey. 6. Biochemistry, Marmara University, Istanbul, United Kingdom. 7. Medical Biology, Marmara University, Istanbul, Turkey. 8. Histology, Marmara University, Istanbul, Turkey.

Chondroitin sulphate (CS) controls weight gain1 induced high fat diet (HFD) in mice by restricting fat absorption and increasing incretin hormone secretion2, alleviates intestinal inflammation in chronic mild stress models. It is unknown whether anti-inflammatory action of CS has a role in the control of weight gain induced by HFD. Sprague-Dawley rats (10 week old, male, n=6 each) treated with either saline (S, 0.1 ml/100g/rat) or CS (80 mg/kg/day,oral), were fed daily and isocalorically for 4 weeks with chow ND (fat 2.7%) or HFD (45% fat). Rats in ND+S, ND+CS, HFD+S and HFD+CS groups were weighed weekly. Fecal samples were taken at 0-2-4 weeks under sterile conditions to detect Desulphovibrio piger (D. piger) by qPCR. Instestinal and colonic motility was recorded at the end of the experiments. Rats were decapitated and trunk blood was obtained for biochemical analysis. Epididymal fat was weighted and myeloperoxidase (MPO) activity studied in the ileal, colonic and gastric samples. Histopathological evaluation and scoring of inflammation were done in H&E stained samples. Data were stated as mean±standard error or median (range), compared with 2-way ANOVA; p<0.05 were considered significant. Daily caloric intake of ND group was found higher than HFD group (F7.21=5.02 diet, F2.3=19.8 time, p<0.05). CS has decreased the amount of weight gain (F1.24=7.658, p<0.05) and also decreased the HFD induced increment of epididymal fat weight (F1.20=36.4 diet, F1.20=4.4 treatment, p<0.05). In ND group triglyceride levels significantly decreased with CS treatment (F1.2=5.25, p<0.05). HFD groups resulted in increased MPO levels, indicating neutrophil infiltration to the tissues, as compared to ND groups in gastric and ileal tissues (F1.14=21.3 and F1.17=11.57 respectively, p<0.05). Histopathological inflammation score worsened by HFD while ameliorated by CS treatment in ileal (F1.21=22.52, diet, p<0.001, F1.21=6.56 CS, p<0.05) and gastric (F1.20=36.4 diet, F1.20=4.4 CS p<0.05) tissue samples. HFD has increased small intestinal transit (F1.20=5.7, p<0.05) while decreasing pellet output (F1.20=15.12, p<0.001). Time dependent increase was recorded in D. piger bacterial population with HFD (F2.32=33, p<0.001). Also D. piger population significantly increased in ND group dependent to time and CS treatment (F2.30=40.7, F15.30=2.7 respectively, p<0.01). In conclusion, the most likely reason for decreasing levels of weight gain in CS treated rats might be the recovery from intestinal inflammation. Changes in intestinal microbiota by means of CS treatment might be another reason which requires further elucidation. Current study demonstrates that HFD promotes visceral fat deposition, inflammation in the gastrointestinal tract, triggers changes in gut motility and has a role in the maintenance of microbiota while CS regulates this interaction.

Where applicable, experiments conform with Society ethical requirements