Nutritional repletion of malnourished tumor-bearing and nontumor-bearing rats: Effects on body weight, liver, muscle, and tumor

Abstract

Effects of nutritional repletion were evaluated in malnourished rats with either no tumor (NTB), small tumor burdens (TB), or large tumor burdens (TB). One hundred and four Sprague-Dawley rats were inoculated with Walker-256 carcinosarcoma and were fed regular diet (RD) for 5 days in Study A. At this time, one group was maintained on RD while the remaining rats were fed a high carbohydrate, protein-free diet (PFD). On Day 15, one PFD group was switched to RD; one PFD group continued on PFD. Eighty-nine NTB rats received an identical dietary protocol. Animals were killed on Days 15, 21, and 33. Mean food intake and carcass weight changes were similar in corresponding groups of TB and NTB rats in Study A. After Day 15, mean carcass weight and liver and muscle protein content increased rapidly in PFD → RD TB and NTB rats, becoming similar to the RD group by Day 33. By Day 33, mean tumor weights and mean total tumor protein content in the PFD group were significantly less than the RD or PFD → RD groups. In Study B, tumor-bearing animals were fed regular diet for 20 days after tumor inoculation to produce a larger tumor burden prior to nutritional depletion. Twelve rats were given PFD; six rats continued on the RD. On Day 30, one PFD group ( n = 6) was switched to RD while the other PFD group ( n = 6) continued on PFD. On Day 36, all rats were sacrificed. Mean carcass weight, liver, and muscle protein levels at sacrifice were significantly less in the PFD → RD group compared with the RD group, but mean serum protein levels were similar in the two groups. Animals co$tinued on PFD lost significant carcass weight, liver, and muscle protein. The presence of a small tumor (5% carcass weight) did not affect protein repletion in host liver or muscle when an adequate diet was provided, although tumor growth was increased. The presence of a larger tumor burden (>25% carcass weight) significantly inhibited host nutritional repletion.