FASTING AND REFEEDING: CELL KINETIC RESPONSE OF JEJUNUM, ILEUM AND COLON

Following a period of fasting, feeding a normal diet results in a burst of DNA synthesis in the crypts of the colonic epithelium. This is due largely to a prompt entry of cells, blocked in G₁, into S. Peak levels of S cellularity exceed 4 times the fasting, and 2 times the normal fed, control values. Refeeding a low residue diet (soluble casein, glucose and corn oil) results in a return to control levels of proliferative activity, but no hyperplasia. However, in jejunum and ileum, refeeding is followed by a return to near control levels of proliferation with only a slight overshoot in S phase cellularity. During the fasting period, the ileal crypt proliferative compartment (P_c-zone) and total crypt cellularity decline significantly. These changes are accompanied by an increase in the total cycle time, due to an equivalent lengthening of the G₁ and S phases. Following refeeding, there is a reduction in the cycle time and a gradual return to the control values for the P_c-zone size and cellularity. In the colon, fasting has no effect on the P_c-zone size or total crypt cellularity. There is an approximate doubling of the cycle time due solely to an increase in G₁. Following refeeding there is an increase in the P_c-zone size and crypt cellularity and a marked shortening of the cycle time. Evidence that a G₁ cycle blockade is induced in the colon by fasting is given by a lengthening of the G₁ period and by stathmokinetic studies employing vincristine.     

An Iron Requirement For the Synchronous Progression of Colonic Cells Following Fasting and Refeeding

Evidence is presented to show dietary iron to be a major co-factor in the colonic hyperplasia observed following fasting and refeeding. the iron component serves to remove a fasting induced colonic G₁ cycle block and produce the resultant synchronous progression of cells through the cycle. Deleting iion from the refed diet results in no colonic hyperplasia and/or synchronous progression of cells. the results are discussed from the viewpoint of colonic steady state cell renewal and as a possible tool for the study of in vivo steady state cell renewal.