Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parenteral nutrition therapy was born 35 to 40 years ago when the first steps were taken to perform a protein nutrition by the intravenous supply of amino acids in man. Since that time, many efforts have been made to supply adequate amounts of energy intravenously. These efforts have resulted in the two available systems for parenteral nutrition: the lipid-carbohydrate system and the glucose system. The lipid-carbohydrate system, which corresponds to the nutrient content of normal food, may be given either in a peripheral vein or through a central vein catheter. The glucose system is administered through a central venous catheter. Many problems concerning the parenteral nutrition need to be solved and further elucidated. However, our present knowledge and technique in this field are far advanced over earlier methods. Now all patients who cannot take food in adequate amounts orally or enterally may be kept in good nutritional status by parenteral nutrition. In this way it is possible to prevent starvation and its complications in these patients.
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PMID:Parenteral nutrition. 10 10

To study the influence of cyclophosphamide and methotrexate on the function of isolated perfused liver, and the hepatoprotective effect of starvation and parenteral glucose feeding, the authors conducted 57 tests on the rabbit liver. It was established that addition of cyclophosphamide, and, especially, of methotrexate into the perfusate negatively affected the function of the isolated perfused liver. Parenteral glucose feeding produced a protective effect on the isolated liver against the detrimental action of both methotrexate and cyclophosphamide.
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PMID:[Effect of fasting and elemental carbohydrate feeding on the liver resistance to the action of cytostatics]. 211 65

1. Intravenous infusion of endotoxin into rats over 18 h caused a reduction in food intake to 20% of normal levels, weight loss, hypoalbuminaemia and a fall in rates of protein synthesis in vivo in heart and skeletal muscle. 2. Measurements of protein turnover in vitro in skeletal muscle of endotoxaemic animals, showed a 50% fall in protein synthesis rates and a 200% increase in rates of protein degradation. 3. Total parenteral nutrition was only partially able to reverse endotoxin-induced weight loss. Total parenteral nutrition did not reverse endotoxin-induced catabolism in cardiac or skeletal muscle, but was able to reverse the catabolism of protein in skeletal muscle produced by starvation. 4. Endotoxin treatment elevated rates of protein synthesis in vivo in liver. The combination of parenteral nutrition and endotoxaemia further increased the rate of protein synthesis in the liver. Parenteral nutrition did not influence endotoxin-induced hypoalbuminaemia.
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PMID:Effect of parenteral nutrition on protein turnover in endotoxaemic rats. 247 47

Parenteral nutrition associated cholestasis is a condition that challenges even the most astute clinician. The risk:benefit ratio of parenteral nutrition must be individualized for each neonate. The dilemma is based on weighing the risk of progressive cholestasis and its complications against the risk of starvation, malnutrition, and their consequences. Avoiding excessive nutrient infusion and providing even minimal enteral calories may prevent or mitigate cholestasis. Routine monitoring of hepatic function in all neonates receiving parenteral nutrition allows early detection and intervention. Affected infants must be evaluated for treatable causes of neonatal cholestasis. Parenteral nutrition related cholestasis remains a diagnosis of exclusion. Further research is needed to unravel the cause and to define the long-term consequences of parenteral nutrition associated cholestasis.
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PMID:Parenteral nutrition and hepatobiliary dysfunction. 308 61

This study set out to investigate the effect of three different parenterally administered diets on the free amino acid (AA) levels in the plasma, muscle, and liver of scalded rats. Diet I consisted of AA (1.4 g/100 g weight) and a high glucose dose (6 g/100 g weight), diet II consisted of AA and a low glucose dose (1.4 g/100 g weight) and in diet III only a low glucose dose was infused. Parenteral nutrition was started on the 3rd day posttraumatically. Sampling was performed on the 7th day posttraumatically. Nitrogen balances were significantly different in all three groups, being lowest in group III. Scalded rats fed isonitrogenously, but with different amounts of glucose showed only minor changes in AA concentrations. However scalded rats fed with a nitrogen-free diet exhibited significantly reduced total muscle and liver AA levels. These decreased AA levels were due to a drop of glycine in the muscle tissue (74%) and liver (49%). Contrary to the clinical catabolic situation in scalded and starved rats, it was not intracellular glutamine but glycine which was considerably influenced by catabolism and starvation.
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PMID:Effects of nutrition on plasma, liver and muscle amino acids in scalded rats. 309 64

The use of total parenteral nutrition (TPN) in patients with advanced, untreatable cancer is controversial. Occasionally, however, damage to bowel by tumor, radiation, or surgery renders these patients unable to eat and TPN may be indicated to prevent premature death from starvation. We have used Home Parenteral Nutrition (HPN) to support three patients with advanced, untreatable abdominal cancer and inability to eat. Morbidity was minimal and survival times were 24, 6 and 1.5 months. Payment was covered by third party agencies. All patients and their families were gratified by the ability to return home with nutritional support. HPN can be used to support terminal cancer patients with bowel obstruction and may afford them longer survival. Ideally, patients considered for this should be well motivated, with good support systems, and with survival estimated to be at least months.
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PMID:Home parenteral nutrition for patients with advanced intraperitoneal cancers and gastrointestinal dysfunction. 309 93

Experiments were performed on 94 male Sprague-Dawley rats to explore the influence of starvation and parenteral nutrition on the development of acute gastric mucosal changes under stress. Comparative assessments were made of lesions in the gastric mucosa of rats on 1- or 6-day repeated exposure to the stress consisting of restraint with immersion in water. Marked hemorrhagic lesions over the extensive area of the glandular stomach and pronounced ulcerative changes in the nonglandular stomach were observed in 6-day stress group as compared to 1-day stress group where only a few hemorrhagic lesions were observed. Thus, this model has proven to provide an excellent experimental model suitable to the purpose of the present investigation. Parenteral nutrition significantly suppressed the development of mucosal damage either in the nonglandular or glandular stomach of rats under 6-day stress. Furthermore, it has been demonstrated that lesions caused in the glandular stomach increase in severity via exposure to stress and starvation while those evoked in the nonglandular stomach rise in incidence even in the presence of starvation alone.
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PMID:Acute gastric mucosal lesions--a new experimental model and effect of parenteral nutrition. 393 Jul 64

Heme oxygenase (HO), the enzyme system catalyzing the conversion of heme to bilirubin, was studied in the liver and spleen of fed, fasted, and refed rats. Fasting up to 72 hr resulted in a threefold increase in hepatic HO activity, while starvation beyond this period led to a gradual decline in enzyme activity. Refeeding of rats fasted for 48 hr depressed hepatic HO activity to basal values within 24 hr. Splenic HO was unaffected by fasting and refeeding. Hypoglycemia induced by injections of insulin or mannose was a powerful stimulator of hepatic HO. Glucose given together with the insulin abolished the stimulatory effect of the latter. Parenteral treatment with glucagon led to a twofold, and with epinephrine to a fivefold, increase of hepatic HO activity; arginine, which releases endogenous glucagon, stimulated the enzyme fivefold. These stimulatory effects of glucagon and epinephrine could be duplicated by administration of cyclic adenosine monophosphate (AMP), while thyroxine and hydroxortisone were ineffective. Nicotinic acid, which inhibits lipolysis, failed to modify the stimulatory effect of epinephrine. None of these hormones altered HO activity in the spleen. These findings demonstrate that the enzymatic mechanism involved in the formation of bilirubin from heme in the liver is stimulated by fasting, hypoglycemia, epinephrine, glucagon, and cyclic AMP. They further suggest that the enzyme stimulation produced by fasting may be mediated by glucagon released in response to hypoglycemia. The possibility is considered that the enhanced HO activity in the liver may increase hepatic heme turnover and hence, bilirubin production, which may explain the rise of unconjugated serum bilirubin observed in fasting or hypoglycemic individuals.
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PMID:Metabolic regulation of heme catabolism and bilirubin production. I. Hormonal control of hepatic heme oxygenase activity. 433 19

Mild tail pinch (TP) in rats resulted in 72% of animals displaying ingestive behavior with 20% demonstrating gnawing behavior without food ingestion and 8% demonstrating licking behavior only. The animals ate steadily over 5 min with a maximum rate occurring at 1 min (0.5 +/- 0.2 g). There was a circadian rhythm of TP-induced behavior with the peak food ingestion occurring at 24 h. A mild increase in blood glucose occurred 120 s after commencement of TP (115 +/- 4 mg/dl). Common satiety signals such as stomach distension and glucose decreased food ingestion. Parenteral administration of glucagon, cholecystokinin-octapeptide, bombesin, and thyrotropin-releasing hormone resulted in suppression of TP-induced food ingestion. Chronic TP (12 5-min TP periods/day) resulted in a fall in spontaneous food intake with the total intake remaining similar to food intake prior to the chronic TP period. We suggest that TP serves as an excellent model for eating behavior because 1) it correlates well with starvation-induced eating; 2) it precludes the necessary deprivation of food and water to adrenalectomized animals; and 3) animals subjected to TP continue chewing in the face of decreased food intake allowing one to exclude the possibility that the effects of an anorectic are secondary to nausea.
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PMID:Stress-induced eating in rats. 719 55

Cancer anorexia/cachexia is a major clinical problem, especially in advanced cancer patients. Its pathogenesis is quite complex. Anorexia plays a central role, but cancer cachexia is more complex than pure chronic starvation. One of the key differences is the preferential mobilization of fat and the sparing of skeletal muscle in simple starvation compared with an equal mobilization of fat and skeletal muscle in cancer patients. An increase in basal energy expenditures seems to play a contributory role in many patients. Cytokines, essentially but not exclusively tumor necrosis factor alpha, play an essential role, and the syndrome can be compared with a low-grade chronic inflammatory state. As it is in most fields in medicine, prevention is more efficacious than treatment, and, to avoid the final and dramatic stages of cancer cachexia, adequate nutritional advice and support must be provided sufficiently early. Parenteral nutrition could facilitate the administration of complete doses of chemotherapy or radiotherapy, but no significant survival benefit or decrease in treatment-induced toxicity have ever been demonstrated in prospective randomized trials. The gut should always be used if at all possible. Percutaneous endoscopic gastrostomy is used increasingly in patients who cannot eat but who have functionally intact gastrointestinal tracts, especially in patients with head and neck cancer. Eight randomized, double-blind, placebo-controlled studies have demonstrated that progestational drugs can somewhat stimulate appetite, food intake, and energy level; increase weight in many patients; and often decrease nausea and vomiting severity; however, pharmacologic treatment of cancer cachexia remains disappointing, and more trials with anticytokine drugs should be conducted.
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PMID:The syndrome of anorexia-cachexia. 1041 77


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