SUMMARY Suspensions of isolated epithelial cells (colonocytes) from the human colon were used to assess utilisation of respiratory fuels which are normally available to the colonic mucosa in vivo. Cells were prepared from operative specimens of the ascending colon (seven) and descending colon (seven). The fuels that were used were the short chain fatty acid n-butyrate, produced only by anaerobic bacteria in the colonic lumen, together with glucose and glutamine, normally present in the circulation. The percentage oxygen consumption attributable to n-butyrate, when this was the only substrate, was 7301 in the ascending colon and 750% in the descending colon. In the presence of 10 mM glucose these proportions changed to 59%0 and 72%. Aerobic glycolysis was observed in both the ascending and descending colon. Glucose oxidation accounted for 85% of the oxygen consumption in the ascending colon and 300/ in the descending colon. In the presence of 10 mM n-butyrate these proportions decreased to 41% in the ascending colon and 16% in the descending colon. Based on the assumption that events in the isolated colonocytes reflect utilization of fuels in vivo, the hypothesis is put forward that fatty acids of anaerobic bacteria are a major source of energy for the colonic mucosa, particularly of the distal colon.The mucosa of the small and of the large bowel depend upon respiratory fuels to maintain cellular turnover and function. Respiratory fuels can either be derived from the bowel lumen or from the circulation.' The preferred respiratory fuels of the mucosa in the small bowel are glutamine and ketone bodies rather than glucose which is poorly oxidised and largely converted to lactic acid2. This lactic acid may be reconverted to glucose in the liver and is a means of conserving glucose during glucose absorption.3The respiratory fuels used by the colonic epithelial cells (colonocytes) have not been studied. In this regard, anaerobic bacteria produce short-chain fatty acids (SCFAs), mainly acetate, propionate, and butyrate, which are water soluble and readily absorbed.4 By using a method to prepare isolated surface epithelial cells5 it was possible to show that over 80% of energy needs for the colonic mucosa in the rat were obtained from the absorbed fatty acid,

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Nutrition of colonic epithelial cells is mainly from short chain fatty acids (SCFAs) produced by bacterial fermentation in the colonic lumen. n-Butyrate contributes more carbon of oxidation to epithelial cells than glucose or glutamine from the vasculature. Incomplete starvation of colonic epithelial cells through lack of luminal SCFAs leads, in the short term, to mucosal hypoplasia with either diminished absorption or diarrhea. A chronic lack of SCFAs or complete organ starvation in conjunction with other factors leads to nutritional colitis, either "diversion colitis" or "starvation colitis." Whether predominantly diarrhea or colitis develops in mucosal malnutrition appears to depend upon the severity and duration of starvation. Ulcerative colitis may be classified as a nutritional colitis in that colonic epithelial cells are unable to utilize SCFAs reflecting epithelial starvation despite abundant SCFAs.