BACKGROUND

Protein calorie malnutrition remains endemic in hospitalized patients with both acute and chronic inflammation secondary to either cancer, chronic infectious processes, surgical injury, trauma, or burns. For the patients who cannot support themselves by enteral feeding, total parenteral nutrition remains an essential tool to minimize nitrogen losses and replete the depleted patient. However, in patients with active inflammation, nitrogen retention and lean tissue accretion are often impaired during total parenteral nutrition. Production of humoral factors, including proinflammatory cytokines, regulates many of the anabolic and catabolic processes that accompany inflammation.



METHODS

The investigators' experience with total parenteral nutrition and proinflammatory cytokines is reviewed.



RESULTS

Cytokines such as interleukin-1, tumor necrosis factor-α, and, in particular, interleukin-6 appear to play central roles in both the loss of skeletal muscle protein and the initiation of the acute phase response to inflammation, as well as in modulating the utilization of exogenously administered nutrients.



CONCLUSIONS

Although innovative second- and third-generation nutritional formulations for the acutely ill patient may represent one approach for improving the effectiveness of total parenteral nutrition, understanding the humoral response to inflammation and modifying cytokine actions pharmacologically may prove equally effective in improving the utility of exogenously administered nutrients. Future studies need to determine whether the effectiveness of exogenously administered nutrients in the patient with inflammation can be improved by efforts to modulate the proinflammatory cytokine response through cytokine inhibitors or antagonists. Cancer 1997; 79:1828-39. © 1997 American Cancer Society.

Proinflammatory cytokines, nutritional support, and the cachexia syndrome : Interactions and therapeutic options

Nutritional support of the pediatric oncology patient.

Measurement and significance of protein turnover.

The objective of this study was to investigate protein and glucose metabolism in ambulatory, asymptomatic acquired immunodeficiency syndrome (AIDS) patients. Nine asymptomatic AIDS patients were compared against 13 controls. We measured whole-body protein synthesis (PSRM), breakdown (PBRM), and the fractional fibrinogen synthesis rate with 15N glycine, glucose cycling from the difference between the glucose appearance rates as measured with 2-d (Ra2-d)- and 6,6-d2 (Ra6,6-d)-labeled glucose. All of these parameters are increased with hypermetabolism and decreased with undernutrition. In addition, we also determined the plasma aminogram. The principal findings were (1) whole-body protein synthesis and breakdown and the fibrinogen fractional synthesis rate were significantly lower in the AIDS patients; (2) glucose cycling was markedly lower in the AIDS patients, and most of this effect was due to a decrease in Ra2-d; there was no difference in the endogenous glucose production rate, Ra6,6d; and (3) the plasma aminogram showed decreased total amino acids and a reduced ratio of essential to nonessential amino acids in the AIDS group. We concluded that the AIDS patients showed a starvation-type response. While the depressed protein synthesis and energy substrate cycling are not likely to be the primary cause of immunodeficiency, they may represent an important facilitating factors contributing to the decreased ability of the patient to respond effectively to opportunistic infections.

Protein and energy substrate metabolism in AIDS patients

Patients with cirrhosis of the liver require an increased amount of protein to achieve N balance. However, the utilization of protein with increased protein intake, i.e. the slope from regression analysis of N balance v. intake, is highly efficient (Nielsen et al. 1995). In the present study, protein requirement and protein utilization were investigated further by measuring protein synthesis and degradation. In two separate studies, five or six patients with cirrhosis of the liver were refed on a balanced diet for an average of 2 or 4 weeks. Protein and energy intakes were doubled in both studies. Initial and final whole-body protein metabolism was measured in the fed state by primed continous [ 15 N]glycine infusion. Refeeding caused a statistically significant increase of about 30 % in protein synthesis in both studies while protein degradation was only slightly affected. The increase in protein synthesis was associated with significant increases in plasma concentrations of total amino acids (25 %), leucine (58 %), isoleucine (82 %), valine (72 %), proline (48 %) and triiodothyronine (27 %) while insulin, growth hormone, insulin-like growth factor (IGF)-I and IGF-binding protein-3 were not changed significantly. The results indicate that the efficient protein utilization is due to increased protein synthesis, rather than decreased protein degradation, and suggest that Increases in plasma amino acids may be responsible for the increased protein synthesis. A comparison of the patients who had a normal protein requirement with the patients who had an increased protein requirement suggests that the increased protein requirement is due to a primary increase in protein degradation. It is speculated that this is due to low levels of IGF-I secondary to impaired liver function, since initial plasma concentration of IGF-I was about 25 % of control values and remained low during refeeding.

/pdf/effect-of-long-term-refeeding-on-protein-metabolism-in-2aai7dywnn.pdf

Effect of long-term refeeding on protein metabolism in patients with cirrhosis of the liver

The metabolic effects of total parenteral nutrition on malnourished cancer and noncancer patients were investigated by determining whole-body protein metabolism before and during intravenous nutritional support. The results were compared to similar studies reported in normal subjects. Primed-continuous infusion of 15N glycine was used and the isotopic enrichments in urinary urea and ammonia were measured. The end product average values were used in the calculation of whole body protein turnover. After 10 days of nutritional support in cancer and noncancer patients whole body protein breakdown decreased by 50% (p = 0.01), and 59% (p = 0.001), whereas protein synthesis decreased by 21% (p = 0.005) and 33% (p = 0.025), respectively. Protein turnover did not change in noncancer patients but increased by 15% (p = 0.005) in cancer patients. The efficiency of utilization of the endogenous supply of amino acids from the breakdown of body proteins for synthetic purposes was 77% in this group of subjects. The utili...

Effect of total parenteral nutrition on whole body protein kinetics in cachectic patients with benign or malignant disease.

Tracer priming in human protein turnover studies with [15N]glycine.

Influence of increasing dietary intake on whole body protein kinetics in normal man

The kinetics of whole body protein metabolism in eight patients with benign disease were evaluated during perioperative isocaloric and isonitrogenous intravenous feedings. A prime infusion of 15N-glycine with determination of urinary end product enrichment and stochastic analysis was used to determine protein kinetics. Surgically induced increases in body protein turnover, synthesis and breakdown were evident on the fifth postoperative day. Abdominal operation was associated with a rise in urinary 3-methylhistidine (3MH) excretion. The postoperative alteration in the relationship between 3MH excretion and body protein breakdown suggests that even mild to moderate surgical injury induces tissue specific changes in protein metabolism. Resting energy expenditure remained unchanged from that of the preoperative levels on the fifth postoperative day. Despite significant changes in body and tissue specific protein kinetics, there is no change in the apparent efficiency of oxygen use for protein homeostasis postoperatively. The failure to observe a relationship between energy expenditure and protein metabolism suggests that only a small proportion of body oxygen uptake is directed toward protein homeostasis after elective surgical procedures. A comparison of perioperative complete intravenous feeding to hypocaloric regimens will be necessary to evaluate more fully the impact of protein and energy balance upon cellular and body protein homeostasis after injury.

Body protein kinetics during perioperative intravenous nutritional support.

Many high-grade malignant tumors in man show enzymatic activities strongly in favor of anaerobic glycolysis’** and may be sensitive to acute glucose depri~ation.’*~ The hypoglycemic agent, 3-mercaptopicolinic acid (3MP) blocks the key gluconeogenic enzyme, phosphoenolpyruvate carboxykinase’ thereby preventing the conversion of oxaloacetate to glucose. In a glycogen-depleted state, hypoglycemia should rapidly ensue. We sought to document the efficacy of 3MP in lowering plasma glucose and to demonstrate the safety of this agent in man under specific conditions. The rate of whole body glucose utilization and disposal was examined after 3MP administration.

The Metabolic Impact of Gluconeogenic Blockade in Tumor-Bearing Man

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