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Query: UMLS:C0235394 (wasting)
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A model was developed in the rhesus monkey to determine if the marked wasting of body proteins associated with sepsis could be prevented by an intravenous supply of various nutritional substrates. All monkeys were given a basic infusion of 0.5 gm of amino acid nitrogen/kg body weight via an indwelling catheter in the jugular vein. Three groups were given diets with no added calories, 85 calories/kg from dextrose or 85 calories from lipid. In each group, six monkeys were inoculated with 3 x 10(8) Streptococcus pneumoniae and four with heatkilled organisms. In the monkeys infused with the amino acids alone, pneumococcal sepsis resulted in a fourfold increase in loss of body proteins compared with calorie-restricted controls. Addition of 85 calories/kg/day of either dextrose or lipid reduced body wasting associated with infectious disease. The calories from lipid were utilized bythe septic host as a source of energy, with a slightly reduced efficiency when compared with the isocaloric infusion of dextrose. The nitrogen sparing of the fat emulsion could not be accounted for by its glycerol content. Therefore, the septic monkey seemed to utilize fatty acids as an energy substrate. It appears that the carbohydrate calories tend to favor the synthesis of peripheral proteins (associated mainly with skeletal muscle), while lipid calories favor synthesis of visceral proteins such as plasma albumin and acute-phase proteins.
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PMID:Protein-sparing therapy during pneumococcal infection in rhesus monkeys. 10 60

Trauma and stress can cause characteristic changes in metabolism: raised lipolysis and reduced glucose tolerance as well as major renal nitrogen losses are manifestations of a postoperative or posttraumatic excess of catabolism over anabolism. Excess catabolism is caused by immobilisation and inadequate oral or parenteral nutrition. Wasting in seriously ill patients for intensive treatment. Priority must be given to the prevention of insufficiencies of organs and systems, and to the elimination of stress factors. It is only then that mobilisation and the administration of calories and nitrogen will restore a normal anabolism-catabolism balance.
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PMID:[The catabolic patient]. 29 30

Fasting energy metabolism was studied in infants to determine the rates of utilization of endogenous carbohydrate, fat, and protein in relation to length of fasting, glucose homeostasis, other circulating energy substrates and hormones, and severe depletion of energy reserves due to prior malnutrition. Five subjects about 1 yr of age were each studied before and after restoration of their energy reserves. Following 3 days of a standard maintenance intake of energy and protein, the subjects were fasted until glycogen oxidation became negligible. Total energy utilization, determined by hourly oxygen consumption, did not diminish as a result of fasting but was significantly less when malnourished than when recovered, 66 versus 79 kcal/kg/day. In all cases the major energy source shifted from oxidation of dietary carbohydrate and glycogen to oxidation of fat, determined from the respiratory quotient, until the oxidation of glycogen became negligible and fat provided 94% of energy in the malnourished subjects after 21 hr and 92% in the recovered subjects after 27 hr. Utilization of protein, determined from urinary nitrogen excretion, remained very low in the malnourished infants accounting for a maximum of 4% of energy, 103 mg N/kg/day, whereas after recovery, protein utilization doubled as a result of fasting, finally accounting for 7% of energy, 226 mg N/kg/day (p less than 0.005). Urea accounted for 60% of total urinary N in both groups and plasma urea increased correspondingly in the recovered but not in the malnourished subjects. Plasma glucose decreased to about 40 mg/100 ml in both groups as glycogen oxidation diminished. The maximum amount of glucose that could have been derived from dietary carbohydrate, glycogen, glycerol, and amino acids decreased over this time from about 6 to 1 mg/kg/min. Alanine declined in relation to glucose concentration and was not different in the two groups in spite of the difference in urea production. Glycerol free fatty acids, beta-hydroxybutyrate, and acetoacetate increased in both groups, but the latter three of these remained significantly less in the malnourished group. Insulin decreased rapidly and remained equally low in both groups. Urinary epinephrine increased in both groups and cortisol was elevated after fasting, while growth hormone did not increase significantly. It is concluded that fasting infants complete the transition from dietary carbohydrate to endogenous fat as the major energy source much faster than do adults, proportionate to relatively greater energy utilization. Severe wasting did not prevent energy homeostasis in spite of greatly depleted body fat. Oxidation of fat continued to provide virtually all of the fasting energy requirements, although ketosis was relatively less. Utilization of endogenous protein also increased as a result of fasting but, by contrast, provided only a very small fraction of total energy, and this was substantially diminished as a result of wasting, similar to what has been found in starved adults...
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PMID:Fasting metabolism in infants. I. Effect of severe undernutrition on energy and protein utilization. 41 21

The balance equation or oxygen-conservation equation in which oxygen consumption is equal to cardiac output times the maximal oxygen binding capacity times the oxygen saturation difference between arterial and mixed venous blood shows the three factors by which the oxygen supply to the tissues can be regulated according to the need. The release of oxygen to the tissues is regulated directly through the venous oxygen tension and indirectly through cardiac output, the 2,3-DPG system, and erythropoietin. Of these indirect regulation mechanisms, cardiac output has the most rapid response and erythropoietin the slowest. As the pool of oxygen in the tissues is comparatively small, the transport and the demand of oxygen under normal conditions are approximately equal over a longer period of time. The tissue oxygen tension (Fig. 21) is thus directly a result of the flows (Fig. 21), solid lines) and indirectly a result of the regulation mechanisms (Fig. 21, broken lines). Hypermetabolism, weight loss, and severe protein wasting characterize the metabolic response to thermal injury. The increased adrenergic activity following severe burns signifies a shift of flow of body substrate from storage to utilization and an increase in energy requirements. The greater the stress, the greater the response. All systems operate at maximal or near maximal levels. The critically injured patients have an accelerated glucose turnover and increased nitrogen loss; the main source of catabolized protein seems to be from skeletal muscle. The metabolic wheel has a tremendous speed. It is thus essential to feed the patient. Energy support with heat supply and nutrition must equal energy demand to avoid weight loss. Most important is to avoid loss of "lean body tissue." No hypermetabolism was found in burned patients when the patients themselves controlled the heat supply from infrared heaters. The metabolic rate corrected for rectal temperature was independent of the total body surface burned. The energy expenditure of patients with burns was studied during the daily treatment routine and showed that it is important to avoid hypovolemia, underhydration, pain, fear, and anxiety, all of which increase the metabolic demands. To prevent hypermetabolism, infrared radiation is a practical way of distributing energy from the environment to the patient. Weight loss can be essentially prevented as energy support equals energy demand (Fig. 20). Furthermore, the method has the advantages that many patients can be treated individually, the method is inexpensive, and the ambient air temperature can be kept normal. From the results of the present investigation, it may be concluded that in patients with burns treated with infrared heaters the energy intake can be predicted in an appropriate way from the calculated basal metabolism, the rectal temperature, and the activity of the patient. The effect of storage of blood on oxygen, proton, and carbon dioxide transport is mainly mediated over the concentration of 2,3-DPG...
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PMID:Transport and demand of oxygen in severe burns. 85 Feb 71

This report is a sequel to "Why Control Blood Glucose Levels?" (Arch Surg 111:229, 1976), which linked complications of diabetes mellitus to poor control. Hyperglycemia, increased gluconeogenesis, nitrogen wasting, and increased ketogenesis occur in the perioperative period, partly as a result of contrainvents are aggravated in the diabetic. Zones of levels of blood glucose control are charted, as well as the corresponding insulin needs for each of these zones. Intermediate insulins should provide basic coverage; regular insulin is recommended only as a supplement. Several blood glucose determinations per day are necessary to maintain control. The hazards of dependence on urine testing and the "sliding scale" for control are among a number of caveats discussed.
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PMID:How to control the blood glucose level in the surgical diabetic patient. 94 54

To determine if pancreatic glucoregulatory hormones can be implicated in the glucose fall of pregnancy, we have measured plasma immunoreactive insulin and glucagon (IRI and IRG) in rats. Fed rats in midgestation show a rise in IRI without a corresponding increase in IRG. In late gestation, IRG rises significantly, but only enough to keep pace with a further rise in IRI. On a molar basis, IRI remains the predominant hormone despite a marked fall in blood glucose. After a 48-h fast IRI falls to comparably low levels in pregnant and virgin rats. A small rise in IRG is seen in virgin but not in pregnant rats despite frank hypoglycemia in the latter. Thus, IRG secretion in pregnancy is diminished relative to IRI in the fed state and fails to increase in the fasted state despite the stimulus of a lower glucose in both instances. To evaluate IRG secretory reserve, the IRG response to i.v. alanine was assessed in late gestation. In fed rats a greater IRG increase is seen in pregnancy; after fasting no difference is seen between pregnant and virgin rats. These results preclude an absolute deficiency in glucagon secretion. Pancreas hormone stores were alos measured in an effort to explain the altered secretory state. We find reciprocal changes in IRI and IRG content favoring IRG in midgestation and IRI in late gestation. Thus, pancreas hormone storage is altered in pregnancy but does not account for the changes in hormone secretion. Rather, pregnancy exerts an effect on the islet secretory process itself. Release of IRI is enhanced relative to IRG regardless of the blood sugar level. These observations suggest that in the pregnant rat circulating levels of insulin and glucagon may act to limit hepatic glucose output. Available evidence from the literature supports the concept of restrained glucose production. It is proposed that a lower blood glucose production. It is proposed that a lower blood glucose in rat pregnancy may be a lesser liability teleologically than would be the obligate nitrogen wasting which accompanies gluconeogenesis.
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PMID:Plasma glucagon and insulin in rat pregnancy. Roles in glucose homeostasis. 110 77

During recovery from severe wasting, malnourished children gain weight at greatly accelerated rates. To determine if additional zinc added to their basal therapeutic diets increased the retention of lean tissue and stimulated protein metabolism, we studied three groups of children taking either the basal diet alone or the basal diet supplemented with either 76 mumol (5 mg) or 153 mumol (10 mg) Zn/kg diet. The zinc-supplemented children gained similar weight and consumed the same amount of diet as the unsupplemented children. Zinc supplementation resulted in a greater net absorption of nitrogen and a higher rate of protein turnover, as estimated from urinary ammonia 15N enrichment after oral [15N]glycine. We conclude that additional zinc affected the composition of newly synthesized tissue and intermediary nitrogen metabolism.
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PMID:Effect of zinc on lean tissue synthesis during recovery from malnutrition. 142 24

Previous work has indicated that 40-50% of glucose intake is oxidized in normal humans with protein-sparing effect. In contrast, the catabolic stressed patient is hyperglycaemic with decreased glucose oxidation and protein wasting. This study evaluated whether the plasma glucose concentration alone would be a reliable indicator of efficient glucose utilization and protein sparing in the critically ill septic cancer patients receiving glucose infusions. Glucose turnover, glucose concentration, nitrogen excretion, oxygen consumption, and glucose oxidation were measured in 8 septic cancer-bearing patients during a glucose infusion of 4.0 mg/kg/min followed by the infusion of insulin with the same glucose load. During glucose infusion without insulin the glucose concentration was 11.8 +/- 1.4 mmol/l, glucose oxidation 10 +/- 5% of glucose tissue uptake, and nitrogen excretion 9.0 +/- 1.3 mg/kg/h. During the euglycaemic clamp the glucose concentration was 3.8 +/- 0.2 mmol/l, glucose oxidation increased to 45 +/- 6% of glucose tissue uptake (p < 0.001), and nitrogen excretion dropped to 6.8 +/- 1.2 mg/kg/h (p < 0.001). The glucose concentration was greater than 10 mmol/l in 4 patients and between 6.9 and 9.3 mmol/l in 4 patients after glucose infusion alone. Despite this difference in initial glucose concentration, normalization of plasma glucose to less than 5 mmol/l with insulin resulted in the same decrease in nitrogen excretion and improvement in glucose oxidation. We conclude that, independent of the initial glucose concentration, maintenance of euglycaemia with insulin appears to be a good indicator of efficient glucose utilization and protein sparing in septic cancer-bearing patients receiving glucose as the primary mode of nutritional support.
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PMID:Lowering of plasma glucose concentration in septic cancer-bearing patients: metabolic significance. 149 99

Oliguric ARF occurred in 0.5% of battle casualties who reached the field medical care system and raised their mortality expectancy from less than 5% to nearly 90%, due primarily to fluid volume overload and/or myocardial potassium intoxication. For their effective treatment the Renal Insufficiency Center with laboratory and a Brigham-Kolff rotating drum dialyzer began operations in 1952, as depicted in a videotape prepared for this presentation from motion picture footage filmed in early 1953. Our Surgical Research Team's major findings relevant to ARF were: (1) Renal function was depressed in most battle casualties in proportion to the severity of their wounds and blood loss. (2) Among the more severely wounded some developed nonoliguric; others, oliguric ARF. (3) Oliguria lasted from 3 days to 3 weeks without a discernible peak frequency of beginning diuresis at 10 days. (4) During oliguria, posttraumatic catabolism greatly accelerated extracellular accumulations of nitrogen, potassium, phosphate, and hydrogen ion with rapid, concurrent clinical deterioration. (5) Dialysis "on indication" produced an oscillating clinical and chemical course. (6) ARF was then revealed as a wasting disease complicated by infections, poor wound healing until diuresis occurred, anemia and bleeding, and hypertension during dialyses and in early diuresis. (7) The overall mortality rate was reduced.
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PMID:Acute renal failure during the Korean War. 150 54

Severe burn injury elicits the release of catabolic hormones that contribute to negative nitrogen balance, protein wasting, and impaired wound healing. Previous studies have shown that burn patients receiving recombinant human growth hormone (rhGH) therapy have an increase in the rate of skin donor site healing and a shorter hospital stay. The mechanism by which rhGH exerts its effects, however, is not clearly understood. This study examines the effects of rhGH on circulating levels of catabolic hormones and nonesterified fatty acids in pediatric burn patients. Patients with greater than 40% total body surface area burn were randomly assigned to receive placebo (n = 8) or 0.2 mg/kg/day rhGH (n = 6) throughout their hospitalization. All patients had early morning blood samples assessed for catecholamines (CAT), cortisol, insulin, glucagon, and free fatty acid (FFA) levels during a period of hypermetabolism. No differences could be demonstrated in age, burn size, postburn day of evaluation, resting energy expenditure per kilogram, respiratory rate, heart rate, respiratory quotient, serum cortisol, and serum glucose between placebo- and rhGH-treated patients. The rhGH-treated group did show a significant elevation (p less than 0.05) in insulin-like growth factor-1 (55.9 +/- 14.5 vs. 168 +/- 23.7 mU/mL), total catecholamines (1,817 +/- 177 vs. 1,117 +/- 137 pg/mL), norepinephrine (1,257 +/- 121 vs. 867 +/- 113 pg/mL), epinephrine (385 +/- 175 vs. 147 +/- 36 pg/mL), insulin (32.8 +/- 3.3 vs. 25.0 +/- 3.0 mU/mL), glucagon (215 +/- 18 vs. 158 +/- 22 pg/mL), and free fatty acids (0.74 +/- 0.01 vs. 0.59 +/- 0.04 mEq/L) compared with the placebo group (data expressed as mean +/- SE).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of recombinant human growth hormone on catabolic hormones and free fatty acids following thermal injury. 161 29


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