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

Muscle protein catabolism has been evaluated using the excretion of urinary 3-methylhistidine (3-MEH) is six normal male and six normal female subjects and in four surgical patients, two of whom developed febrile episodes during the course of their study. In addition, their nutritional status was also evaluated using percentage body weight losses before hospital admittance, creatinine-height ratios, and, in two patients, serum alkaline ribonuclease levels. The results indicate that: 1) prolonged starvation may produced decreased 3-MEH excretion because of an adaptive diminution of muscle breakdown in sustained starvation, decreased 3-MEH excretion also may simply reflect diminished lean body mass, 3-MEH excretion may be increased above basal levels because of superimposed stresses such as fever, and the acute phases of starvation produce increased levels of 3-MEH excretion until adaptive mechanisms occur; 2) creatinine-height ratios are low in starvation, and increase not only with improved nutrition but in response to fever and stress of operation, even when these are superimposed on malnutrition; and 3) alkaline RNAase levels are elevated in malnutrition and decrease with improved nutrition but in response to fever and stress of operation, even when these are superimposed on malnutrition; and 3) alkaline RNAase levels are elevated in malnutrition and decrease with improved nutrition. The enzyme may also be elevated by the stress of operations.
 ...
PMID:Muscle protein catabolism in the septic patient as measured by 3-methylhistidine excretion. 88 85

Degradation rates of muscle proteins were determined in young rats allowed access to standard rat chow 12 h/day. degradation was assessed by determination of 3-methylhistidine (3MH) excretion rates. 3MH is a nonreutilized amino acid produced almost exclusively within the actin and myosin of skeletal and cardiac muscle. Because plasma levels of 3MH are low and renal clearance is high, excretion reflects myofibrillar degradative rates. Excretion of 3MH was determined for 4-h periods beginning 12 and 20 h after initiation of feeding and after 24-and 48-h fasts. Excretion of 3MH per 4-h period increased with time after the last feeding. Because creatinine excretion is a function of muscle mass dividing 3MH excretion by creatinine excretion represents myofibrillar degradation per unit muscle mass, the fractional degradative rate. Degradation rates rose from 4.6 to 14.5%/day between 12 and 16 and 60 and 64 h after the beginning of the last meal. These results support the presence of a diurnal pattern of protein degradation as well as increased muscle degradation during starvation.
 ...
PMID:Protein degradation in muscle: response to feeding and fasting in growing rats. 88 48

Carnitine is synthesized from lysine and methionine. In the rat, inadequate intake of either of these essential amino acids causes carnitine depletion. Inasmuch as protein deficiency is common in the hospital population, we have investigated the possible occurrence of nosocomial carnitine deficiency. Fasting serum carnitine concentration was measured in 16 normal and 247 patients in 16 disease groups. Normal range of carnitine was 55-103 muM. Only the cirrhotic group showed significant (P < 0.05) hypocarnitinemia. 14 of 36 hospitalized cirrhotics had subnormal values for serum carnitine. The creatinine/height index, midarm muscle circumference, and triceps skin-fold thickness indicated protein-calorie starvation in the 14 hypocarnitinemic liver patients. In six of the hypocarnitinemic cirrhotics (average serum level 50% of normal), spontaneous dietary intakes of carnitine, lysine, and methionine were measured and found to be only 5-15% as great as in six normocarnitinemic, healthy controls. When these six cirrhotic and six normal subjects were given the same lysine-rich, methionine-rich, and carnitine-free nutritional intake, the normals maintained normal serum carnitine levels and excreted 100 mumol/day, whereas the cirrhotics' serum level fell to 25% of normal, and urinary excretion declined to 15 mumol/day. Seven hypocarnitinemic cirrhotics died. Postmortem concentrations of carnitine in liver, muscle, heart, kidney, and brain averaged only one-fourth to one-third those in corresponding tissues of eight normally nourished nonhepatic patients who died after an acute illness of a 1-3-day duration. THESE DATA SHOW THAT CARNITINE DEPLETION IS COMMON IN PATIENTS HOSPITALIZED FOR ADVANCED CIRRHOSIS, AND THAT IT RESULTS FROM THREE FACTORS: substandard intake of dietary carnitine; substandard intake of lysine and methionine, the precursors for endogenous carnitine synthesis; and loss of capacity to synthesize carnitine from lysine and methionine.
 ...
PMID:Deficiency of carnitine in cachectic cirrhotic patients. 89 75

The effects of selenium (Se) deficiency on urinary ketone body excretion in starved rats were examined. Rats were fed a basal diet which was Se-deficient (Se content: 0.011 micrograms/g) or a Se-adequate diet (the basal diet supplemented with 0.1 micrograms Se/g as sodium selenite). On the 11th and 22nd week of the feeding period, Se-deficient status in rats fed the basal diet was verified by the observation that the Se content and glutathione peroxidase activity in their plasma, erythrocytes, and livers were markedly lowered. On the 4th, 6th, 11th, 15th, and 22nd week, the rats were starved for 48 h and the urinary excretion of ketone bodies (acetoacetate (AcAc) and 3-hydroxybutyrate (3-OHBA)), urea, and creatinine were examined. The urinary excretion of AcAc and 3-OHBA during the second 24 h of the 48-h starvation period were markedly higher in the Se-deficient rats than in the Se-adequate rats for all weeks examined, while the urine volume and the excretion of urea and creatinine were similar in the Se-deficient and Se-adequate rats, irrespective of the feeding period and the number of hours of starvation. On the 22nd week, the plasma ketone body levels were also determined and significantly higher plasma 3-OHBA levels were observed in the Se-deficient rats than in the Se-adequate rats 72 h after starvation began. These results indicate that Se deficiency causes an increase of urinary ketone body excretion in starved rats and that the increase is ketone-specific with no changes in major urinary profiles.
 ...
PMID:Increase of urinary ketone body excretion in selenium-deficient rats is a ketone-specific change. 176 47

Energy expenditure and substrate oxidation rate for fat, glucose and protein were evaluated by indirect calorimetry in 20 normal individuals, 35 patients with acute hepatitis and 22 patients with biopsy-proven alcoholic cirrhosis in the postabsorptive state. Measurements were done in the resting state after an overnight fast (10 to 12 hr). Oxygen consumption (ml/min/1.73 m2) in normal subjects, in patients with acute hepatitis and in patients with cirrhosis was 206.5 +/- 4.0 (mean +/- S.E.M.), 216.4 +/- 4.7 and 228.8 +/- 7.1 (p less than 0.05 vs. controls), respectively. When related to body surface area (kcal/min/1.73 m2), resting energy expenditure did not differ between normal subjects (0.98 +/- 0.02), patients with acute hepatitis (1.03 +/- 0.02) and cirrhotic patients (1.06 +/- 0.03). However, when related to 24-hr urinary creatinine excretion as an estimate of lean body mass, energy expenditure was increased in cirrhosis (p less than 0.0001). In cirrhosis an inverse association between the severity of liver disease according to Pugh and oxygen consumption and resting energy expenditure was found. In cirrhotic patients the percentages of total calories derived from fat (86% +/- 5%), carbohydrate (2% +/- 4%) and protein (12% +/- 1%) were different from those of normal controls who metabolized 45% +/- 4%, 38% +/- 4%, 17% +/- 1%, respectively. In acute hepatitis no alterations in metabolism could be found apart from a decreased protein oxidation rate. In conclusion no appreciable changes in energy metabolism exist in acute hepatitis. The pattern of fuel use in cirrhosis resembles that in starvation.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Energy metabolism in patients with acute and chronic liver disease. 210 37

The metabolic alterations, nutritional and metabolic assessment, and nutritional requirements of critically ill patients are discussed, and parenteral nutrition support therapies are reviewed. Physiological alterations in the metabolism of the injured or septic patient are mediated through the interactions of neuroendocrine, cardiovascular, toxic, and starvation responses. These responses cause mobilization of nutritional substrates in an effort to maintain vital organ function and immune defenses. A patient's nutritional status can be determined from anthropometric measurements, creatinine excretion rate, and evaluations of protein stores and immune reserves and function; body weight is a poor indicator. Nitrogen-balance calculations are also useful for determining the adequacy of nutritional intake and the degree of metabolic stress. Early assessments of nutritional status may assist in identifying those patients for whom nutritional support interventions are needed. Nutritional requirements are altered by the metabolic responses to injury and sepsis. Studies suggest that use of nutrient solutions enriched for branched-chain amino acids may enhance nitrogen retention and that energy expenditures in injured or septic patients are only moderately elevated. Most nonprotein calories in parenteral nutrient solutions are provided as glucose, but lipids are an important source of energy in the critically ill patient who has high energy requirements or carbohydrate intolerance; however, clearance of lipids may be decreased. Fluid, electrolyte, and mineral status must be evaluated frequently. Critically ill patients have unique nutritional requirements, and parenteral nutrition support therapies for these patients are being investigated and refined.
 ...
PMID:Parenteral nutrition in the critically ill patient. 250 29

To determine whole-body energy and nitrogen responses to submaximal exercise during repletion levels of intravenous feeding (IVF), five normal male volunteers were hospitalized and underwent serial changes in nutritional intake consisting of weight-maintaining oral feeding (4 d), starvation (10 d), and weight-increasing parenteral feeding (10 d). Twelve-hour aliquots for urinary nitrogen, creatinine, and 3-methylhistidine were collected during the final 36 h of oral feeding and IVF. During these experimental periods, indirect calorimetry was utilized to determine resting oxygen consumption and that occurring during a 1-h period of submaximal (40% of maximal) upright, bicycle exercise. Despite differences in the route of nutrient delivery, oxygen uptake during a fixed rate of exercise (75 W) was similar during oral (16.7 +/- 0.4 mL X kg-1 X min-1) and IVF (14.7 +/- 1.0 mL X kg-1 X min-1). When compared with basal urinary losses, submaximal exercise resulted in diminished nitrogen (p less than 0.01, oral) and 3-methylhistidine (p less than 0.05, oral; p less than 0.01, IVF) excretion during a 12-h post-exercise recovery period.
 ...
PMID:Thermogenic and nitrogen response to submaximal exercise in parenterally repleted normal man. 311 27

The effects of dietary protein, fasting, and refeeding on urinary hydroxyproline of nine captive female white-tailed deer (Odocoileus virginianus) were examined from 23 February to 3 May 1984 in northern Minnesota. In the fasted group, mean hydroxyproline:creatinine (OHP:C) was greater (P less than 0.05) at week 4 compared to baseline at week 0. Between fasted deer and deer fed high protein-high energy (HPHE) and low protein-high energy (LPHE) diets, no difference in OHP:C ratios was detected during the initial 4 wk of the study. Urinary OHP:C ratios were significantly (P less than 0.05) greater in the fasted group during refeeding, concomitant with greater feed consumption and weight gain. There was also a significant (P less than 0.02) time effect in the fasted-refed group; OHP:C ratios increased during these two phases of the study. There was no difference between the HPHE and LPHE fed deer in renal OHP excretion. However, mean OHP:C ratios in yearlings (16.8 +/- 2.2) were greater (P less than 0.001) than in the adults (7.5 +/- 1.2) of those groups, indicating a higher collagen turnover rate. Urinary OHP:C shows potential as an indicator of growth and starvation, and the data presented may serve as reference values.
 ...
PMID:Response of urinary hydroxyproline to dietary protein and fasting in white-tailed deer. 335

The effect of starvation on urinary output and biochemical indices of renal function was investigated in rats. Starvation resulted in a marked fall in water intake. Urinary output paradoxically increased during the first day following starvation, but fell dramatically thereafter. Urinary creatinine excretion and creatinine clearance fell markedly, but plasma creatinine concentration did not alter. Plasma urea concentration and urinary urea excretion fell. Plasma sodium concentration increased, whilst plasma potassium concentration did not alter; urinary sodium and potassium excretion fell. Plasma bicarbonate concentration fell marginally, but the anion gap increased to a greater extent. Following re-feeding, water intake and urine output increased, as did urinary creatinine excretion and creatinine clearance. Plasma urea and urinary urea concentrations, as well as sodium and potassium excretion, increased. Plasma bicarbonate increased and the anion gap decreased. These indices improved within 2 days of re-feeding and were restored to normal in 5 days.
 ...
PMID:Effect of starvation on biochemical indices of renal function in the rat. 342 45

Arginine levels diminished markedly in the plasma during starvation, suggesting that plasma arginine level principally depends on food intake. Organ arginine levels were relatively stable except for an extraordinary increase in the pancreas at 96 h. Guanidinoacetic acid decreased dramatically in all organs within 24 h and low level were maintained thereafter, except for the brain (and plasma). Creatinine output increased after 24h of starvation. The increased creatinine output recovered to the control level after 48 h. A small but significant amount of guanidinosuccinic acid was detected in the normal liver and decreased transitorily after 24 h and increased after 48 h starvation, corresponded with an increased output in the 24 h urine excretion. Otherwise this decrease may be related to the transitory decrease in arginine level in the liver over the same time course. Methylguanidine in the muscle and gamma-guanidinobutyric acid in the liver decreased gradually during starvation. These results suggest that guanidino compounds levels in mouse organs are principally dependent on exogenous nitrogen.
 ...
PMID:Effects of starvation on guanidino compound metabolism in mice. 379 7


1 2 3 4 5 Next >>