Protein Chow Research Articles

Effect of Low Protein Diet on Bone Structure of Young Wistar Mice.

<b>Background and Objective:</b> Malnutrition and stunting are major unresolved problems in Indonesia. Protein deficiency can cause stunted growth, as well as make physical and cognitive abilities cannot reach their maximum potential. During childhood the need for protein must be fulfilled so that the peak of bone formation during adolescence can be perfect. In malnourished children, a low protein diet will lead to thinning of the bone cortex. Due to the high rate of stunting and malnutrition in children due to protein deficiency, a study was conducted on the effects of feeding low protein diet on rat bones. <b>Materials and Methods:</b> Male Wistar rats (n = 10) at 6-8 weeks old (body weight around 250 g), control groups were fed a normal chow diet and low protein diet groups were given low protein chow diet (protein 5%) for 18 weeks, then the rats were sacrificed and the femoral bones were isolated. Body weight, femur weight, femur length were checked and bone density was examined using X-ray. <b>Results:</b> The body proportions of the low protein group rats were smaller and thinner than those of the control group. This difference is supported by the significant weight loss starting from the sixth week after low protein feeding. There are significant differences in body weight and femur weight between the control and low protein diet groups. Bone density decreases significantly in low protein diet group. Macroscopically, the femur length of the low protein group was shorter than the control group, however the femur length did not show significant differences statistically between the two groups. <b>Conclusion:</b> A low protein diet decreased the body weight of the rats, also causing impaired bone growth characterized by decreasing femur weight. The low protein diet also caused osteoporosis in the bones.

Effects of Dietary Protein Intake on Cutaneous and Systemic Inflammation in Mice with Acute Experimental Psoriasis.

Background: Psoriasis is a systemic inflammatory disorder, primarily characterized by skin plaques. It is linked to co-morbidities including cardiovascular disease and metabolic syndrome. Several studies demonstrate that dietary habits can influence psoriasis development and severity. However, the effect of different dietary protein levels on psoriasis development and severity is poorly understood. In this study, we examine the influence of dietary protein on psoriasis-like skin disease in mice. Methods: We fed male C57BL/6J mice with regular, low protein and high protein chow for 4 weeks. Afterwards, we induced psoriasis-like skin disease by topical imiquimod (IMQ)-treatment on ear and back skin. The local cutaneous and systemic inflammatory response was investigated using flow cytometry analysis, histology and quantitative rt-PCR. Results: After 5 days of IMQ-treatment, both diets reduced bodyweight in mice, whereas only the high protein diet slightly aggravated IMQ-induced skin inflammation. IMQ-treatment induced infiltration of myeloid cells, neutrophils, and monocytes/macrophages into skin and spleen independently of diet. After IMQ-treatment, circulating neutrophils and reactive oxygen species were increased in mice on low and high protein diets. Conclusion: Different dietary protein levels had no striking effect on IMQ-induced psoriasis but aggravated the systemic pro-inflammatory phenotype.

Malnourishment during early lactation disrupts the ontogenetic distribution of the CART and α-MSH anorexigenic molecules in the arcuate/paraventricular pathway and lateral hypothalamus in male rats

Developmental malnourishment impacts the energetic metabolism control throughout life. In rat offspring, a 0% protein diet during the first 10 days of lactation results in leptin resistance and in alterations in: feeding behavior, serum leptin and neuropeptide Y (NPY) levels in the hypothalamic arcuate nucleus (ARC)/paraventricular (PVN) pathway. Here, the distributions of alpha-melanocyte stimulating hormone (α-MSH) and cocaine and amphetamine regulated transcript (CART), anorexigenic molecules, were immunohistochemically assessed in the ARC, PVN and lateral hypothalamus (LH) nuclei. Rat dams were subjected to one of the following diet protocols from postnatal day (P) 1–10: 1) Protein-free (PFG, 0% protein chow); 2) Pair-fed (UFG, normoprotein chow); 3) Control group (CG, normoprotein chow). PFG, UFG and CG male offspring were analyzed at different time points, from P5 to P180. In the ARC, PFG α-MSH and CART were increased from P10 to P45 when compared to CG and UFG. In the PVN, α-MSH and CART peaks in PFG animals were delayed from P20 to P30 when compared to CG. In the LH, CART was more intense in PFG animals than in UFG and CG ones by P20, and, by P30, UFG immunostaining became less intense than in CG. In conclusion, aproteic diet altered the ontogenetic distribution of both anorexigenic molecules. In the PVN, the peak was delayed to P30, which coincides with the leptin peak and follows the previously described NPY (orexigenic) peak in this model. The permanent LH CART and α-MSH increase may be associated with the previously observed PFG hypophagia.

Food restriction followed by refeeding with a casein- or whey-based diet differentially affects the gut microbiota of pre-pubertal male rats

Researchers are gaining an increasing understanding of host–gut microbiota interactions, but studies of the role of gut microbiota in linear growth are scarce. The aim of this study was to investigate the effect of food restriction and refeeding with different diets on gut microbiota composition in fast-growing rats. Young male Sprague–Dawley rats were fed regular rat chow ad libitum (control group) or subjected to 40% food restriction for 36 days followed by continued restriction or ad libitum refeeding for 24 days. Three different diets were used for refeeding: regular vegetarian protein chow or chow in which the sole source of protein was casein or whey. In the control group, the composition of the microbiota remained stable. Food restriction for 60 days led to a significant change in the gut microbiota at the phylum level, with a reduction in the abundance of Firmicutes and an increase in Bacteroidetes and Proteobacteria. Rats refed with the vegetarian protein diet had a different microbiota composition than rats refed the casein- or whey-based diet. Similarities in the bacterial population were found between rats refed vegetarian protein or a whey-based diet and control rats, and between rats refed a casein-based diet and rats on continued restriction. There was a significant strong correlation between the gut microbiota and growth parameters: humerus length, epiphyseal growth plate height, and levels of insulin-like growth factor 1 and leptin. In conclusion, the type of protein in the diet significantly affects the gut microbiota and, thereby, may affect animal's health.

Atrofia de neurônios do plexo mientérico do íleo de ratos submetidos à intensa carência de proteínas

The effects of a 4%-protein diet in adult rats with respect to the morphometric aspects of the myenteric plexus in the ileum were assessed. Twenty animals were randomly divided into two groups: Control Group (n = 10), which received 26%-protein chow, and Experimental Group (n = 10), which received 4%-protein chow for 90 days. Neurons in the myenteric plexus in the ileum in whole mount were evidenced through Giemsa and NADH-diaphorase techniques. The overall neuronal population as well as the subpopulation positive for NADH diaphorase presented atrophy, with a reduction of the perikaryon, nucleus and cytoplasm.

Quantitative analysis of the neurons from the myenteric plexus in the ileum of rats submitted to severe protein deficiency

The effects of protein malnutrition on the quantitative aspects of the myenteric plexus in the ileum of adult Rattus norvegicus were assessed. Thirty 90-day-old rats were divided into two groups: Control Group (CG, n=15) and Experimental Group (EG, n=15). The CG received 26% protein chow and the EG received 4% protein chow for 90 days. At the end of the experiment, the animals from the CG weighed 369.63+/-26.33, and the ones from the EG 215.34+/-56.31. The ileum was submitted to Giemsa, NADH- and NADPH-diaphorase technique in order to evidence nervous cells in the whole-mount preparations. Animals from the EG presented a 41.75% body weight loss in relation to the CG as well as 17.6% length reduction for the ileum-jejunum. Moreover, the organ was 41% lighter for the EG. Giemsa-stained neurons were 17.02% more concentrated in the EG (p>0.05). NADH-diaphorase-stained neurons were 26.6% more concentrated in the EG (p<0.05), while the NADPH-diaphorase were 26.28% more concentrated in this group (p<0.05).

Hypertension and renal disease in Dahl salt‐sensitive (SS/Mcwi) rats are dependent on dietary protein intake

We previously observed that the source of dietary protein influences the severity of sodium-sensitive hypertension in Dahl SS/Mcwi rats; the present study evaluated the influence of the amount of protein consumed on Dahl SS/Mcwi hypertension and renal disease. Rats (6–9/group) were fed isocaloric diets with low (6%), normal (18%), or high (30%) amounts of protein (casein) and 0.4% NaCl from 5 to 12 weeks of age; the NaCl content was increased to 4.0% NaCl for the final 3 weeks of the study. Mean arterial blood pressure (MAP) increased when the rats were fed the elevated NaCl diet; moreover, it was observed that rats fed the high protein diet developed the highest level of MAP when fed the 4.0% NaCl diet (MAP=153±7 mmHg) compared to rats fed normal (132±3 mmHg) or low protein diets (132±6mmHg). Urinary albumin excretion, an index of kidney damage, significantly and progressively increased during the course of the study in the rats fed the high protein diet. A minimal sodium-dependent increase in albumin excretion was observed in rats fed the low protein chow when NaCl intake was increased (4±1 mg/day), but albumin excretion further increased to 26±6 mg/day and 114±37 mg/day in rats fed the normal and high protein diets, respectively. The level of sodium intake and the plasma concentration of creatinine, albumin and protein were not different between the groups. A histological analysis demonstrated significantly greater glomerular and tubular damage in the kidneys of rats fed the high protein diet. These results indicate that long-term restriction of protein intake protects the Dahl SS/Mcwi from sodium-sensitive hypertension and kidney disease. Moreover, these data demonstrate that hypertension in Dahl SS/Mcwi rats is sensitive to both NaCl and protein intake. Supported by DK-62803 and HL-29587.

Estudo morfoquantitativo do plexo mioentérico do duodeno de ratos submetidos a carência de proteínas e vitaminas do complexo B

This study aims to evaluate the effects of protein and vitamin deficiency on the neurons of the duodenum myenteric plexus of rats. 24 90-day old animals were divided in two groups: control (n=12) and experimental (n=12). During 120 days, the control group received chow with 22% protein level, vitamins and minerals; the experimental group was fed with 8%-protein chow, without vitamin supplementation. After the experimental period, the animals’ blood was collected and the duodenum was removed for ultrastructural and morphoquantitative analyses (NADH-d; NADPH-d). The experimental group had reduced total protein, plasma albumin and body weight lower than the control group. The density (NADPH-d) was higher and significant for the experimental group; with the NADH-d technique the neuronal profile differed between the groups. The ultrastructural aspects were similar in both groups. The results allow the conclusion that the diet caused a moderate deficiency, not leading to quantitative alterations, but changed the neuronal profile

Growth Hormone Effects on Wound Healing in Malnourished Animals: A Histological Study

Systemic growth hormone (GH) markedly improves celiotomy wound strength in protein malnourished (PM) animals. This study was undertaken to analyze the effect of GH as a basis for anatomically understanding. Adult female Spraque-Dawley rats were divided into normally nourished controls, PM and GH-treated PM groups. Protein malnutrition was achieved by feeding 5.5% protein restricted chow every other day for eight weeks before surgery. Controls were fed 23.4% protein chow. All animals were fed 23.4% protein chow postoperatively. Rat-GH was injected subcutaneously twice daily (1.0 mg/day) for three days prior to and five days after 5 cm midline celiotomy. Bursting strength of the wound was measured at 3, 6 and 14 days postoperatively. Histologic wound specimens (hematoxylin and eosin) were obtained from each group. Wound strength of malnourished rats was significantly less than that of normal controls at six days after operation (p < 0.001). With administration of growth hormone, the wound strength was significantly improved. Histologically, there was no difference between groups on day 3. On day 6 the normal control group showed a decrease in the early inflammatory cell infiltrate with concurrent development of granulation tissue and a dense proliferation of fibroblasts. The PM wound showed fatty infiltration, a very narrow band of poorly formed granulation tissue and a sparse fibroblastic proliferation. The GH-treated PM group showed a combination of histologic findings. Fatty infiltration, similar to that in malnourished non-treated animals, was still evident but there was also a dense proliferation of capillary channels and fibroblasts comparable to normal animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of growth hormone on wound healing in protein-malnourished rats treated with corticosteroids

This study was designed to evaluate the efficacy of human growth hormone (GH) in improving the tensile strength of wounds weakened by chronic protein malnourishment and corticosteroid (CS) administration. Eighty-six female Sprague-Dawley rats, weighing 80 to 100 g, were divided into five groups. Group 1 (control) received 23.4% protein chow for 8 weeks before surgery. Groups 2, 3, 4, and 5 received nonprotein chow on alternate days for the same duration. Groups 3 and 5 received prednisolone (2 mg/kg/d intramuscularly) for 3 weeks preoperatively and for 5 days postoperatively. Groups 4 and 5 were given GH (somatotropin, 1 IU/d) for 5 days postoperatively. All the animals underwent a precise 4-cm midline celiotomy. Wound testing was performed on the sixth postoperative day, after removal of the sutures. The bursting strength (BS, mean ± SD) for group 1 was 145 ± 16 mm Hg. The BS for groups 4 (137 ± 13 mm Hg) and 5 (134 ± 7 mm Hg) were significantly stronger than those for groups 2 (115 ± 15 mm Hg) and 3 (91 ± 16 mm Hg). The authors conclude that postoperative systemic GH restored the wound BS in protein-malnourished animals treated with CS, to the level of the normally nourished controls.

Mechanisms of adaptation to proteinuria in adriamycin nephrosis.

To evaluate the impact of urinary protein losses on whole body protein turnover (WBPT) independent of acidosis or uremia, we utilized a model of unilateral adriamycin nephrosis. Control rats were matched by weight to nephrotic rats and pair fed 22% protein chow for 14-18 days; urinary urea nitrogen (UUN) was measured on day 12, and leucine turnover measurement was performed on the final day. Growth rates of nephrotic and pair-fed control rats did not differ during the first 2 wk of pair feeding; thereafter, a small difference in growth could be detected. Despite an identical intake of dietary protein, UUN excretion was 29% less in the nephrotic rats (P < or = 0.02). Fasting whole body protein synthesis and degradation did not differ between nephrotic and control rats; in contrast, leucine oxidation decreased by 21% in nephrosis (P < 0.05). On the basis of near normal growth and normal rates of WBPT, we conclude that nephrotic rats fed ad libitum can adapt to the stress of continuous protein losses. A reduction in amino acid oxidation and UUN excretion were the primary mechanisms responsible for protein conservation in experimental nephrosis.

Growth hormone reverses impaired wound healing in protein-malnourished rats treated with corticosteroids

Corticosteroid (CS) administration amplifies the inhibitory effect of protein malnutrition (PM) on wound healing. Abdominal surgery in protein malnourished patients receiving corticosteroids (eg, advanced malignancy, transplant recipients) may be complicated by wound dehiscence or anastomotic breakdown. Although preoperative parenteral nutrition can reduce the incidence of these complications, this is not possible in patients requiring urgent surgical intervention. In a previous report we demonstrated that postoperative growth hormone (GH) administration could restore normal wound healing in PM rats. This study evaluates the effect of GH on wound healing in PM rats treated with CS. Forty-eight female Sprague-Dawley rats weighing 180 to 210 g were divided into four groups: (1) normally nourished; (2) PM only; (3) PM + CS; and (4) PM + CS + GH. PM rats (groups 2 to 4) received 5.5% protein chow every other day for 8 weeks. Control rats (group 1) received 23.4% protein chow for the same duration. Group 3 and 4 rats received prednisolone (2 mg/kg, intramuscularly) during the last 3 weeks of PM. All animals underwent precise 5-cm midline celiotomies. Postoperatively, rats in all groups were given 23.4% protein chow. Group 3 and 4 rats continued to receive CS postoperatively. Group 4 rats were given GH (0.5 mg/d, intraperitoneally) postoperatively for 5 days. Wound testing was performed on the 6th postoperative day after removal of the sutures. A balloon inserted into the peritoneal cavity through the vagina was gradually inflated. The pressure at which the wound disrupted was recorded as the wound bursting strength. The results of this study suggest that (1) postoperative GH restored the wound bursting strength in PM animals treated with CS to that seen in normally nourished controls, and (2) the wound healing enhancement of GH occurs at an early stage when compromised abdominal wounds are most likely to dehisce.

Influence of nutrition on anti-tumor activity

Nutritionally supporting the malnourished tumor bearing host may not benefit the disease outcome, but, rather, may preferentially "feed the cancer". We hypothesized that repletion is beneficial only when it augments an anti-tumor immune response. To support this hypothesis, 240 A/J mice were assigned to isocaloric dietary groups (24%, 5%, or 2.5% protein). On day 14 the mice received either immunogenic C1300- neuroblastoma (NB) or non-immunizing TBJ-NB. On day 21 half of the restricted animals were repleted with 24% protein chow. At day 35, chromium-release cell-mediated cytotoxicity was measured. In the group of mice that received 2.5% protein chow, nutritional repletion specifically augmented anti-tumor activity for C1300-NB which elicits a host immune response (33.78 L.U. (repleted) vs 3.47 L.U. (depleted) p less than 0.01), in contrast, nutritional repletion was detrimental for non-immunizing TBJ-NB, where further depression of cytotoxicity was seen (1.37 L.U. (repleted) vs 2.06 L.U. (depleted) 0 less than 0.01). This suggests that the influence of nutritional repletion in tumor nearing animals is dependent on the integrity of host's anti-tumor immunity.

Effect of phenylalanine, p-chlorophenylalanine and α-methylphenylalanine on glucose uptake in vitro by the brain of young rats

Phenylketonuria (PKU) is an inherited metabolic disease caused by a deficiency of phenylalanine hydroxylase (phenylalaninc 4-mono-oxygenase EC; 1.14.16.1 ) activity. Phenylalanine (Phe) and its metabolites accumulate in tissues of affected children. It is clinically manifested by neurological abnormalities and mental retardation, which can be prevented by early treatment with a low-Phe diet [I]. Experimental models of PKU have been developed for biochemical and behavioural studies in mice and in rats. In most of these models p-chlorophenylalanine (CIPhe) or amethylphenylalanine (MePhe) are used for phenylalanine hydroxylase inhibition [2]. ClPhe is said to be more toxic to the animals than MePhe, but the mechanisms underlying this toxicity are poorly understood [ 31. Since glucosc is the main source of energy production in brain, we studied the effect of Phc, ClPhe and MePhe on glucose uptake in vitro by the brain of IS-day-old rats, in thc hope that we might contribute to the clarification of this point. Wistar rats bred in our laboratory were used in this study. A mother and eight pups were kept per cage. Free water and a 20% (w/w) protein chow were provided. The rats were killed by decapitation at 15 days of age. The brain was rapidly removed and olfactory bulbs, cerebellum and pons were dissected out over a Petri dish placed on ice. The rest of brain was cut into two perpendicular directions, with a Mcllwain chopper, into prisms of 40 pn width. About 100 mg of prisms were incubated in 1.0 ml of Krebs-Ringer bicarbonate buffer (pH 7.0) containing 5.0 mM-glucose at 37°C for 30 min under O,/COz ( 10: 1) mixture. Phe, CiPhe or McPhc were added to a final concentrations of 2.0 or 10.0 mM, corresponding to the range observed in the serum of rats submitted to experimental PKU. The control experiments did not contain any added substance in the incubation medium. Glucose was measured at the beginning and at the end of incubation by the glucose oxidase method 141. Glucose uptake was determined by subtracting the amount of glucose found after the incubation from the amount found before the incubation, and was expressed as nmol/min per mg of brain. Data were analysed by one-way analysis of variance followed by Duncan’s multiple range test. It can be seen from Table 1 that MePhe had no effect on glucose uptake by rat brain prisms. However, ClPhe and Phe Abbreviations used: PKU. phenylketonuria; Phe, phenylalanine;

Effect of protein intake on the autoregulation of renal blood flow

Autoregulatory ability was evaluated in male Sprague-Dawley rats (200-250 g) fed either low protein (LP, 6%), high protein (HP, 50%), or standard rat chow (CON) for 2 wk. Renal perfusion pressure (RPP) was first raised above normal by bilateral ligation of the carotid arteries. LP rats exhibited normal autoregulatory behavior between 130 and 100 mmHg, whereas autoregulation in HP rats was impaired (autoregulation factor 100-130; HP 0.86 +/- 0.16, LP 0.38 +/- 0.07, and CON 0.39 +/- 0.04). Autoregulation studies were repeated in HP- and LP-fed rats after administration of the cyclooxygenase inhibitors, meclofenamate and piroxicam. Cyclooxygenase inhibition did not significantly affect base-line hemodynamics but did restore the ability of the HP rat to autoregulate renal blood flow (RBF) at high RPP. (Autoregulation factor between 100 and 130 mmHg; HP 0.29 +/- 0.10, LP 0.19 +/- 0.07, P, NS). Thus an HP diet resulted in impaired autoregulation of RBF at high RPP, an effect that appears to be mediated by excessive production of vasodilatory prostaglandins.

Effect of protein intake and urea on sodium excretion during inappropriate antidiuresis in rats

Administration of urea to patients with the syndrome of inappropriate antidiuresis (SIAD) is thought to ameliorate hyponatremia by both producing an osmotic diuresis and diminishing ongoing natriuresis. The present study evaluated these effects in a rat model of SIAD utilizing dilutional hyponatremia induced by continuous infusion of 1-deamino[8- d-arginine] vasopressin. Following 48 hours of sustained hyponatremia, separate groups of rats were then refed with either: (1) 5% dextrose alone, (2) a 20% protein chow, (3) an isocaloric protein deficient (0%) chow, or (4) the isocaloric protein-deficient chow supplemented with oral urea. Our results demonstrate that rats refed a 20% protein diet significantly improved their plasma [Na +] as compared to rats refed protein deficient diets, and this improvement was accompanied by decreases in natriuresis despite an increased glomerular filtration rate and an unchanged negative free water clearance. Identical effects were observed in rats refed a protein deficient diet but supplemented with oral urea, suggesting that urea generation from catabolism of dietary protein is responsible for the effect of protein refeeding to decrease urinary sodium excretion. Both the protein and urea refed rats had significantly higher inner medullary urea contents and concentrations compared to rats refed protein-deficient diets and also to rats studied immediately before protein refeeding, supporting the hypothesis that urea and dietary protein decrease natriuresis in patients with SIAD in association with increased inner medullary urea concentrations.

Chronic effects of dietary protein in the rat with intact and reduced renal mass

The chronic effects of dietary protein on renal structure and function were studied in rats with normal and reduced renal mass. Control rats with two kidneys were compared with unilaterally nephrectomized rats, and with one and one-third nephrectomized rats obtained by unilateral nephrectomy and infarction of one-third of the remaining kidney. Rats at each level of renal mass were maintained on chow containing either 6% or 40% protein content. Separate cohorts of rats were studied four and eight months after ablation and institution of these dietary regimens. At both time intervals and at all levels of renal mass, rats fed the high protein diet had higher average values for GFR than comparable animals fed the low protein chow. Within each of the dietary regimens the animals with loss of renal mass developed greater prevalences of sclerotic glomeruli by eight months. Furthermore, at each level of initial renal mass, rats eating the high protein diet had a greater prevalence of sclerotic glomeruli than those on the low protein diet. Similarly, rats on the high protein diet had greater rates of protein excretion than those on the low protein diet at each degree of ablation. The prevalence of sclerosed glomeruli increased between four and eight months in each group. Thus, the extent of renal injury as manifested by proteinuria and glomerular sclerosis was directly related to the degree of initial loss of renal mass, and dietary protein restriction retarded these manifestations of injury across a wide range of initial renal mass.(ABSTRACT TRUNCATED AT 250 WORDS)

Neuroblastoma and nutritional support: Influence on the host-tumor relationship

The nutritional sequelae of neuroblastoma are secondary to tumor burden, tumor-host influenced metabolism, and antitumor operative, pharmacologic, and radiation therapy. Nutritional support and its influence on the outcome of clinical cancer is confusing; but in a defined murine system, we hypothesized that whether or not nutritional repletion favors the host-tumor relationship is dependent on a nutritional augmentation of host antitumor immunity. C1300 murine neuroblastoma (NB) elicits a host antitumor immune response as determined by in vivo and in vitro testing; but the TBJ clone of the same tumor is nonimmunogenic. After receiving two weeks of either regular 24% protein or protein restricted 2.5% protein chow, normal and malnourished mice received either C1300-NB or TBJ-NB and were serially followed to animal death. The median survival time (MST) of TBJ recipients was shorter in this more aggressive tumor, but the MST of 27.5 days was equal for normal and malnourished mice. Contrasting with these data were an MST of 38 days for malnourished C1300 NB recipients and an MST of 64.5 days for normally nourished C1300 NB recipients, values that are significantly different (P less than 0.02). These data suggest that nutritional support influencing host antitumor immunity may be of benefit only in that circumstance where the tumor elicits an antitumor immune response.

Tumor immunogenicity--the prime determinant of the nutritional influence on the host-tumor relationship.

The influence which malnutrition plays on the host-tumor relationship is controversial because of the disparity of human and rodent tumors, a critical difference being the minimal immunogenicity of human tumors and the variable antigenicity of rodent tumors. The hypothesis we tested is that the influence of malnutrition on tumor growth is a result of the immunogenicity of the host's tumor. C-1300 neuroblastoma (NB) is an immunogenic tumor by in vivo and in vitro assessment while the histologically identical TBJ-NB clone is non-immunizing. Isogeneic A/J mice were malnourished with 2.5% protein chow and were inoculated with C-1300-NB or TBJ-NB; either serial tumor volumes were assessed by three-dimensional measurement or animals were serially killed and tumor weight/carcass weight ratios (TW/CW) were calculated. Non-immunogenic TBJ-NB grew more rapidly than C-1300-NB in both control and malnourished groups, but there was no difference in either tumor size or TW/CW ratios between the two TBJ-NB nutritional groups. Contrasting with these data were immunogenic C-1300-NB in that the tumor grew significantly better in malnourished mice (tumor volume p less than 0.05 day 12 and 14; TW/CW p less than 0.026 by day 21). Prior whole-body irradiation abrogated this difference. These data demonstrate that for tumors differing only in antigenicity the influence of malnutrition is on that tumor which induces an immunologic antitumor response.