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Fasting Prevents Experimental Murine Colitis Produced by Dextran Sulfate Sodium and Decreases Interleukin-1ß and Insulin-Like Growth Factor I Messenger Ribonucleic Acid¹

Department of Pediatrics, Division of Endocrinology (L.S., L.E.U.), and Departments of Physiology (P.K.L., K.M.H.) and Pediatrics (M.H.U.), University of North Carolina, Chapel Hill, North Carolina 27599

Address all correspondence and requests for reprints to: Dr. P. K. Lund, Department of Physiology, CB#7545 University of North Carolina, Chapel Hill, North Carolina 27599-7545. E-mail: empk{at}med.unc.edu

Cytokines and insulin-like growth factors (IGFs) are involved in the induction and/or perpetuation of inflammatory bowel disease. The effect of fasting on inflammatory bowel disease was studied in a mouse experimental model of acute colitis caused by adding dextran sulfate sodium (DSS) to drinking water. Animals were either fed ad libitum or fasted (water only) for 2 days before death. Inflammation and tissue damage, measured as a colitis activity score, were markedly reduced in fasted (2.4 ± 0.1) compared to fed (5.3 ± 0.1) DSS animals (P < 0.0001). Colon interleukin-1ß (IL-1ß), IGF-I, and tumor necrosis factor- messenger RNAs (mRNAs) were quantified by Northern blot hybridization and expressed as a percentage of mRNA abundance in fed controls. In DSS mice, IL-1ß mRNA was elevated in the fed group (954 ± 155%; P < 0.001), but was suppressed in fasted animals (71.1 ± 11%). IGF-I mRNA also was elevated in fed DSS mice (421 ± 71%; P < 0.01). This increase was attenuated in fasted DSS mice (202 ± 17%; P < 0.01 compared to fed DSS mice). Tumor necrosis factor- mRNA was increased in fed DSS mice (162 ± 15%; P < 0.01), but was not significantly lower in fasted animals. By in situ hybridization, IL-1ß mRNA was localized to the lamina propria of colonic mucosa in fed DSS animals, but was not detectable in other groups. We conclude that fasting has a protective effect on the progression of acute DSS-induced colitis. This is associated with decreased expression of IL-1ß and IGF-I mRNAs in the colon.

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