It has long been known that butyrate manages oxidative stress and inflammation in the colon. Butyrate is absorbed in the colon and transported into colonocytes by monocarboxylate transporter isoform 1 (MCT1) and sodium-coupled monocarboxylate transporter (SMCT1). Butyrate is the major energy source for colonocytes and is produced by fermentation of carbohydrates by resident microbiota. Ulcerative colitis (UC) and Crohn’s disease (CD) are two forms of idiopathic inflammatory bowel disease (IBD). Their exact etiologies are unknown, but a decrease in butyrate metabolism in colonocytes has been suggested to be a possible contributing factor. A transport deficiency of butyrate can possibly be a major contributing factor for the decreased butyrate metabolism. AIM: To analyse and compare SMCT1 and MCT1 levels in colon biopsy samples of normal (n=19), ulcerative colitis (n=9) and Crohn’s disease (n=8) patients. METHOD: Colon biopsies were obtained with consent from normal, UC and CD patients. RNA was extracted from these samples and prepared for analyses using RT-qPCR. ALUSq, ALUSx and SF3A1 were used as reference genes. RESULTS: The results of the RT-qPCR were analysed using one-way ANOVA and a Mann-Whitney test. SMCT1 is less expressed than MCT1 in the colon of all patients. MCT1 is significantly down regulated in colon samples of both UC and CD’s patients when compared to normal patients with no colon pathology. MCT1 is also significantly less expressed in UC compared to CD patients. CONCLUSION: MCT1 is the most important butyrate transporter in the colon. Lower butyrate transport expression can contribute to a less inflammatory inhibition in the colon. The lower expression of MCT1 in UC patients compared to CD patients could explain the higher incidence of developing colorectal cancer in UC patients.