Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020505 (hyperphagia)
6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects on food intake and body weight in lean and obese Zucker rats were evaluated following substitution in the diet with either 1) poorly absorbable lipid (hydrogenated soybean oil) for corn oil, or 2) nonabsorbable carbohydrate (fiber) for glucose. Lean Zucker rats compensated for the reduced caloric availability of the high-fiber and hydrogenated oil diets by increasing food consumption. In contrast, obese rats did not respond significantly to these dietary alterations and failed to attain caloric balance during the 16-day study. These differences in caloric compensatory responses were reflected in body weight gains. There were no differences in the amount of weight gained by lean rats fed either the high-or low-fiber diets because of compensatory hyperphagia in the high-fiber group. Lean rats fed the hydrogented oil diets gained less weight than controls fed corn oil diets, even in the presence of compensatory hyperphagia, because of the enhanced fecal excretion of water and metabolites caused by the poorly absorbed fat diet. As a result of a delayed and incomplete response to reduced caloric availability, obese rats fed the high-fiber and hydrogenated oil diets gained significantly less weight than the obese rats fed low-fiber and corn oil diets.
...
PMID:Caloric compensatory responses to diets containing either nonabsorbable carbohydrate or lipid by obese and lean Zucker rats. 70 86

Intravenous hyperalimentation was done in 11 underweight adults whose body weight (body wt) was less than 85 percent of ideal. For the first 6 days, "complete formula" was infused furnishing per kilogram ideal body wt per day: 15 g glucose, 0.40 g N, 0.018 g P, 2.4 meq K, 3.0 meq Na, 2.3 meq C1, 0.5 meq Mg, 0.45 meq Ca, and 50 ml H20. Patients gained weight at an average rate of 9.0 g/kg ideal body wt/day and showed average balances/kilogram ideal body wt/day as follows: plus 0.14 g N; plus 0.012 g P; plus 0.43 meq K; plus 0.49 meq Na; plus 0.37 meq Cl; and plus 0.085 meq Ca. Application of standard equations to the elemental balances indicated weight gain consisted of 35-50 percent protoplasm, 35-50 percent extracellular fluid, 5-25 percent adipose tissus, and less than 1 percent bone. Withdrawas of N, P, Na, or K impaired or abolished retention of other elements. Removal of N halted retention P, K, Na and C1; withdrawal of K stopped retention of N and P; and removal of Na or P interrupted retention of all other elements. Weight gain continued at a rate of 1.4-3.1 g/kg ideal body wt/day despite zero or negative elemental balances of N, K, P, and sometimes Na and C1. Calculations showed that weight gain during infusion of fluids lacking N, P, K, or Na consisted largely of adipose tissue, with little or no contribution by protoplasm or extracellular fluid. Data show that repletion of protoplasm and extracellular fluid of wasted adults by intravenous hyperalimentation is retarded or abolished if N, P, Na, or K is lacking. Repletion of bone mineral does not occur in absence of Na or P but proceeds in absence of N, P, K, or Na. Thus, quality of weight gained by underfed adult patients during hyperalimentation depends on elemental composition of the infusate.
...
PMID:Elemental balances during intravenous hyperalimentation of underweight adult subjects. 80 19

Glucose tolerance and insulin responses have been examined over extended periods in severely obese, but otherwise healthy, subjects. Three significant points emerge from this study. First, it was shown that obese, supposedly ketosis resistant, subjects may deteriorate in a brief time span from a state of normal glucose disposal and adequate or increased insulin responses to insulin-deficient diabetes, culminating in ketoacidosis. Unusually high blood glucose levels complicating the ketoacidosis in two patients suggest hyperosmolarity obesity and added risk factor in severely obese diabetics. It appears that, after long-standing obesity and after years of hyperinsulinemia, a large weight gain due to prolonged overeating may impose an excessive challenge to islet cells of marginal competence. Such an event by itself or a superimposed stress or both may then cause acute insulin deficiency and/or insulin resistance leading to diabetic ketoacidosis. Hyperosmolarity may be exacerbated in the obese with cessation of food intake due to large losses of salt and water. Second, many symptoms and manifestations of hyperphagic obesity are similar to the early functional abnormalities of decompensated diabetes. The advent of the critical phase of uncontrolled diabetes, therefore, fails to alarm the obese patient and may escape timely recognition by the physician. Third, technical and mechanical difficulties due to severe obesity are apt to cause critical delays in therapy. These factors, when added to coexisting hyperosmolarity and ketoacidosis, probably account for the high mortality in these patients.
...
PMID:Evolution of diabetic ketoacidosis in gross obesity. 80 48

Hepatic fatty infiltration complicating jejunoileal bypass can be massive and may require restoration of gastrointestinal continuity. This fatty infiltration appears to be caused by protein depletion associated with adequate or high carbohydrate intake. The present study has shown that calorie-free amino acid alimentation can reverse these changes. In three of thirteen patients who underwent 12 inch to 6 inch jejunoileal bypass procedures, symptomatic hepatomegaly developed with near total replacement of hepatocytes by massive fatty infiltration. After undergoing liver scan, liver biopsy, and liver function tests, the patients were started on a peripheral infusion of 2L per day of a 4.25 per cent crystalline amino acid solution, allowing for fat mobilization while preserving body protein stores. All oral intake was withheld except for water. At the end of a fourteen to twenty-one day infusion period, serum albumin levels increased by 1 gm in all patients. Decreases in liver volume of 83, 45, and 40 per cent occurred. During the infusion period ketonuria was 4 plus in all patients indicating active lipolysis. Weight loss was impressive (17, 19, and 40 pounds). All patients showed marked symptomatic improvement, and postinfusion liver biopsy specimens showed a return to near normal architecture. Maintenance of normal liver size by a high-protein, low-carbohydrate diet was observed in a five to seven month follow-up period. In contrast to previous studies using standard hyperalimentation solutions, the use of calorie-free amino acid solutions reverses the hepatic fatty infiltration seen after intestinal bypass by mobilization of fat. This fat mobilization does not occur as readily in the presence of large amounts of glucose.
...
PMID:Reversal of severe fatty hepatic infiltration after intestinal bypass for morbid obesity by calorie-free amino acid infusion. 80 74

The hypothesis that clinical and biochemical essential fatty acid deficiency (EFA) might occur from the feeding of eucaloric, fat-free diets was tested in two experiments in healthy men. In Study I, eight men were given fat-free, eucaloric diets containing 80% of calories as glucose and 20% as amino acid hydrolysates by a constant drip over a 24-h period. The diets were fed in succession for periods of 2 wk each, either through a superior vena cava catheter or via a nasogastric tube. EFA deficiency was detected by decreases in linoleic acid and by the appearance of 5, 8, 11-eicosatrienoic acid in lipid fractions of plasma. Linoleic acid decreased significantly during 2 wk of the fat-free diet given intravenously from 48.8 to 9.8% (percent of total fatty acids) in cholesterol esters, from 21.2 to 3.2% in phospholipids, from 9.6 to 2.0% in free fatty acids, and from 14.1 to 2.6% in triglycerides. Eicosatrienoic acid, normally undetectable, appeared 0.6% in cholesterol esters, 2.5% in phospholipids, 0.2% in free fatty acids, and 2.3% in triglycerides. EFA deficiency occurred similarly during the nasogastric feeding. In Study II a subject received the same diet continuously by the nasogastric route for 10 days followed by a 24-h fast. He was then given the fat-free diet intermittently in three meals per day for 3 days. Finally, he was repleted with a diet containing 2.6% linoleic acid. By the 3rd day of the continuous nasogastric feeding, linoleic acid had fallen significantly and eicosatrienoic acid had appeared in plasma lipid fractions as in Study I. These findings were accentuated by day 10. Adipose tissue fatty acid composition did not change. Free fatty acid outflow from adipose tissue was presumably suppressed during the 10 days of continuous feeding. With increased free fatty acid outflow during fasting and intermittent feeding, linoleic acid rose and eicosatrienoic acid decreased. After 13 days of repletion with dietary linoleic acid, the EFA deficiency readily develops when fat-free diets containing glucose are given intravenously or orally as constant 24-h infusions. These diets are similar to the hyperalimentation formulas now being used clinically.
...
PMID:The development of essential fatty acid deficiency in healthy men fed fat-free diets intravenously and orally. 80 9

The effects of semistarvation and parenteral nutrition on the gastric mucosa were studied in 24 Wistar rats (250 to 350 grams). The animals were divided into three dietary regimens: Group I-standard rat chow ad libitum; Group II-50 cc. per day of a hyperalimentation solution containing 30% glucose + 5% amino acids; Group III-50 cc. per day of 5% glucose. The animals were fed for a period of 7 days. Gastric mucosal fluxes of Na+, Li+, and H+ then were measured after the gastric instillation of two gastric wash solutions, one primarily an HC1 solution, the other a solution of HC1 plus sodium taurocholate. Gross examination of the gastric mucosal surfaces were recorded. Compared to Group I (oral diet), Groups II and III demonstrated a decrease in volume in gastric secretion during the test period (p less than 0.005); and an increase in net negative hydrogen flux (p less than 0.005). Compared to Group II (hyperalimented), Group III (semistarved) demonstrated an increased net negative H+ flux (p less than 0.01), but no difference in volume of secretion. Only Group III demonstrated a difference in H+ flux after the addition of sodium taurocholate (p less than 0.05). Gastric lesions were significantly increased in Group III, as compared to Groups I and II. Semistarvation renders the gastric mucosa of the rat more susceptible to injury. Adequate intravenous nutrition alone protected against these effects.
...
PMID:The effects of semistarvation and parenteral nutrition on the gastric mucosa of rats. 81 25

The effect of a deficiency of calories and/or nitrogen on protein metabolism in the rat was investigated. During the 5 days of the study, the rats received all nutrients except water via intravenous hyperalimentation. Four diets were used: I) 1.25 g amino acids, 12.5 g glucose/day; II) 1.25 g amino acids/day; III) 1.25 g glucose/day; and IV) 12.5 glucose/day. The rate of protein synthesis in heart, lung, muscle, kidney, and liver was estimated by a modification of the technique of Garlick et al. (The diurnal response of muscles and liver protein synthesis in vivo in meal-fed rats. Biochem. J. 136: 935-945, 1973) except that [15N]glycine was used as the tracer. Heart and lung protein synthesis was depressed by both caloric and nitrogen restriction. Muscle protein synthesis was only significantly affected by omission of calories from the diet. Kidney nitrogen content increased with the amino acid diets and decreased with the nitrogen-deficient diets. The major response of the liver to a dietary deficiency was to lose nitrogen via an increase in the rate of liver protein catabolism.
...
PMID:Effect of nitrogen and calorie restriction on protein synthesis in the rat. 81 8

Influence of the infusion of amino acid solutions on metabolic changes caused by parenteral nutrition with fructose. In eleven unconscious polytraumatized patients of the intensive care station, intravenous infusions with fructose (0.5 g/kg bodyweight and hour) were performed. During the last 24 hours of the 72 hours infusion period, amino acid solutions (1.0 g/kg bodyweight and 24 hours) were given in addition to fructose. The investigations were initiated after an eight hour "starvation period" preinfusion. During this time only electrolytes were given. For comparison 48 hours intravenous infusions with fructose (0.5 g/kg B.W. and hour) were performed with six healthy volunteers. In both groups of subjects the intravenous fructose was metabolized very well, renal losses were less than 2% of the whole amount given. Considering the metabolic healthy volunteers, the blood glucose concentration remained unaltered despite the high dosage carbohydrate infusion. The patients of the intensive care station showed a slight increase of blood glucose values which were elevated already before infusion. Additionally, during fructose infusions, the increase in blood lactate concentration was more pronounced in the intensive care patients than in healthy volunteers. However, in contrast to the healthy volunteers, no increase in serum bilirubin concentration and only a slight increase in serum uric acid concentration was observed in the intensive care patients, despite the high-dose fructose infusion for 72 hours. Additionally, the fructose-induced hypertriglyceridemia was of a minor degree in the intensive care patients. In volunteers the increase in triglyceride concentration was 200% in 48 hours, whereas only a 50% increase was observed in intensive care patients during 72 hours. The pronounced nitrogen sparing effect of fructose in healthy volunteers was not seen in the intensive care patients to the same degree. The most prominent side effect of the fructose infusions in intensive care patients was the strong decrease in serum phosphate concentration seen in some patients. The additional infusion of amino acid solutions lead to a further diminution of the slight alterations caused by fructose infusions. In conclusion, it can be stated that total parenteral nutrition with fructose and amino acid solutions is possible in intensive care patients without danger of side effects. However, it should be mnetioned that hyperalimentation can cause fatty liver.
...
PMID:[Effect of amino acid infusions on fructose-induced chemical blood changes in intensive care patients]. 82 61

Forty patients with a mean age of 56 yrs, all of whom required hemodialysis therapy, for mean of 32 days, were treated with a minimum of 2000 kilocalories of I.V. glucose, potassium orthophosphate with mulit-vitamins and 25 Gm of I.V. albumin. Patients were initially dialyzed daily and then every other day or 3 times/wk. Complications including pneumonia, GI bleeding, gram negative septicemia, shock, the need for tracheostomy and ventialtory assist were high. Overall survival rate was 33%. This survival rate we beleive to be high considering the complicated type of illness these patients had as well as our clinical experience prior to the use of total parenteral nutrition in the manner described in this report. Essential L-amino acids were not used based on our experience in 3 patients with hepatic and renal failure who developed worsening neurological findings with the use of this substance. We believe further that I.V. glucose and albumin may be preferred mode of hyperalimentation.
...
PMID:Total parenteral nutrition in acute renal failure. 82 19

The present paper described the technique of intravenous hyperalimentation applied to a group of 100 surgical patients. A specially prepared diet supplying a high amount of calories, using hypertonic glucose and supplying nitrogen, using polypeptides or aminoacid solutions, was infused into the superior vena cava. The inhibition of digestive secretions, during the period of hyperalimentation, was used in the management of 19 patients with intestinal and pancreatic fistulae. The general conclusion reached after wide clinical experience was that by supplying energy and nitrogen to a patient in a severe catabolic state, a significant and sometimes dramatic capacity could be developed which allowed him to overcome difficult conditions and even initiated a reversal of the metabolic balance in the direction of anabolism. The regimen should be adopted in the preoperative preparation of debilitated patients; in hypercatabolic states (post-trauma, post-surgery or burns); in gastrointestinal, granulomatous or infectious diseases; in acute pancreatitis; in digestive fistulae; in oncological conditions, and so on. The metabolic and infective complications can be pregressively decreased and eventually prevented by proper handling and strict metabolic monitoring. The use of this hyperalimentation was extremely encouraging, and on many occasions we had the impression that it was life saving.
...
PMID:Intravenous hyperalimentation in the management of the critically ill patient, with special reference to abdominal fistulae. 82 16


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>