Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stripped duodenal mucosa of rabbits was mounted in Ussing chambers containing a Ringer solution gassed with 100% O2. The disappearance of acid or alkali from the mucosal solution of short-circuited tissue was measured with a pH stat while the serosal pH was kept at 7.4. The duodenum rapidly disposed of both acid and alkali; neither property was altered by gassing with N2 while iodoacetate was in the perfusing solutions. Prevention of release of CO2 from the mucosal chamber obliterated the early rapid phase of acid disposal by the mucosa while a similar maneuver in the serosal chamber increased the appearance of serosal acid without altering the rate of acid disposal. Gut sacs of rabbit duodenum in vitro and in vivo showed a positive correlation between acid disposal and the rate of luminal CO2 production. While acid disposal progressively decreased with time for the in vitro gut sacs, the in vivo gut sac showed no fatigue in this respect. Luminal acidification in the Ussing chamber was associated with a profound reduction in short-circuit current (Isc), partially reversible by elevation of the mucosal pH but not by luminal glucose. Our data suggest that acid disposal occurs in part by intraluminal neutralization and in part by diffusion into the mucosa.
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PMID:Mechanisms of disposal of acid and alkali in rabbit duodenum. 0 19

The metabolic effects of 60-min exposure to 250-2000 mg gamma-hydroxybutyrate (GHB) per kilogram or 150-1200 mg gamma-butyrolactone (GBL) per kilogram were studied in rats by measurement of the cerebral hemisphere contents of energy phosphates and glycolytic-Krebs' cycle metabolites. A general pattern of increased glycogen and glucose with decreased pyruvate, lactate, alpha-ketoglutarate, and malate was observed. This pattern in association with unchanged adenylates and decreased energy phosphate utilization was consistent with a metabolic adaptation to a state of cerebral depression. The major qualitative difference between the two drugs was that higher doses of GBL were associated with additional decreases of citrate and glutamate. Since these doses of GBL were also associated with acute increases of arterial CO2 tension, it is proposed that these differences were secondary to hypercapnia and not due to a distinctive primary action of GBL. Derivation of the cytoplasmic NAD(P)H:NAD(P)+ ratios indicated that GHB and GBL were not associated with consistent alterations of the cytoplasmic redox state.
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PMID:A comparison of the effects of gamma-hydroxybutyrate and gamma-butyrolactone on cerebral carbohydrate metabolism. 4 Jun 77

A 3-yr-old boy was investigated for numerous episodes of fatigue, irritability, pallor, and sweating, which began at 11 mo of age, when he had an episode of symptomatic hypoglycemia with ketonuria. He had euphoria, mental confusion, drowsiness, nausea, and vomiting 1-5 hr after oral administration of glycerol in doses of 0.5-1.0gm/kg. Orally administered MCT (1 gm/kg) had similar effects. On one occasion, oral glycerol also provoked hypoglycemia, as had a 16 1/2 hr fast. Intravenously administered glycerol (0.09 gm/kg) induced an immediate loss of consciousness from which he recovered spontaneously after 30 min; there were no changes in blood glucose values. Intravenously administered fructose (0.25 gm/kg) was tolerated normally. Leukocytes showed normal activities for FDPase, glycerol kinase, and glycerol phosphate dehydrogenase. The restriction of dietary intake of fat has been associated with a marked improvement in physical and mental activities. These observations suggest a unique, yet undifined intolerance to glycerol, which suggest caution in the diagnostic use of glycerol in the investigation of hypoglycemia as well as in the therapy of increased intracranial or intraocular pressure.
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PMID:Glycerol intolerance in a child with intermittent hypoglycemia. 16 54

[3H]adenine was taken up by a crude hypothalamic synaptosomal fraction and incorporated into mainly nucleotides. The synaptosomes were superfused and after the initial washout a steady fractional release rate of 0.5-1% of the content/min was found. Electrical pulses (2 ms, 50 Hz, 10-20 mA, 4 min) and veratridine (10 microM, 4 min) induced a Ca++-dependent increase in purine release rate. K+ (30 mM, 4 min) caused a largely Ca++-independent increase. Most of the released material co-chromatographed with adenosine, inosine and hypoxanthine, while little or no nucleotide material was detected. Release of endogenous adenosine, inosine and hypoxanthine was detected by high performance liquid chromatography. However, following hypo-osmotic shock most of the released material was in nucleotides. The removal of glucose from the medium increased the fractional release rate 2-3 fold. Histamine, acetylcholine and glutamate were without effect. High amounts of noradrenaline caused an EGTA-inhibited release of purines, which was un-affected by propranolol or phentolamine. It is suggested that purines are released from neuronal structures and that the release reflects increased energy consumption and/or decreased energy production.
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PMID:Release of 3H-nucleosides from 3H-adenine labelled hypothalamic synaptosomes. 22 29

1 The accumulation of glucose in the brain produced by the administration of phosphatidylserine liposomes into mice has been studied by measurement of the cerebral contents of glycolytic intermediates and high-energy compounds. 2 With a normal supply of oxygen to the brain, inhibition of glycolysis is indicated mainly at the phosphofructokinase step. The ratio of glucose-6-phosphate to fructose-1,6-diphosphate increased, whereas the levels of pyruvate and especially lactate decreased. 3 Under conditions of cerebral ischaemia, the administration of phosphatidylserine delays glycogen mobilization and ATP use. As a consequence of decreased energy utilization, the brain adenylate energy charge remains at a high level. 4 It is concluded that the phosphatidylserine-induced glucose accumulation in the brain is due to reduced energy expenditure and therefore to a decrease in carbohydrate consumption. The inhibition of glycolysis by the high level of adenylate energy charge is probably the control mechanism explaining the decreased carbohydrate utilization.
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PMID:Pharmacological effects of phosphatidylserine liposomes: regulation of gylcolysis and energy level in brain. 46 67

Nine trained cyclists were studied to determine the effects of caffeine (CAF), and glucose polymer (GP) feedings on work production (kpm) during two hr of isokinetic cycling exercise (80 rpm). Ingestion of 250 mg of CAF 60 min prior to the ride was followed by ingestion of an additional 250 mg fed at 15 min intervals over the first 90 min of the exercise. This treatment significantly increased work production by 7.4% and Vo2 by 7.3% as compared to control (C) while the subjects' perception of exertion remained unchanged. Ingestion of approximately 90 g of GP during the first 90 min (12.8 g/15 min) of the exercise had no effect on total work production or Vo2. It was, however, effective in reducing the rate of fatigue over the last 30 min of cycling. Although GP maintained blood glucose and insulin levels (P less than or equal to 0.05) above those of the C and CAF trials, total CHO utilization did not differ between treatments. During the last 70 min of the CAF trial, however, fat oxidation was elevated 31% and appeared to provide the substrate needed for the increased work production during this period of exercise. These data, therefore, demonstrate an enhanced rate of lipid catabolism and work production following the ingestion of caffeine.
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PMID:Influence of caffeine and carbohydrate feedings on endurance performance. 48 Nov 58

During studies of the regulation of phosphorylase activity and glycogenolysis in contracting muscle, it was found that conversion of phosphorlyase beta to alpha is transient. Reversal of phosphorylase activation during both continuous and intermittent stimulation in the plantaris might, in part, have been due to development of fatigue. However, a complete reversal of phosphorylase activation was also evident within 5 min in the absence of fatigue in soleus muscles stimulated tetanically with 100-ms-long trains at a rate of 60/min. These muscles showed no significant decline in contractile force. Glycogen breakdown stopped in the soleus when phosphorylase reverted to the beta form, providing evidence that phosphorylase beta was not active. This lack of activity is probably explained by the finding that ATP and AMP concentrations changed little, while glucose 6-phosphate increased. Reversal of phosphorlyase activation soon after the onset of steady-state work may be a mechanism for conserving glycogen when the supply of other substrates is adequate to meet the muscles' energy needs.
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PMID:Reversal of phosphorylase activation in muscle despite continued contractile activity. 49 77

10 patients entered a controlled 4-week study to evaluate the effect of a glucose-enriched dialysate (400 mg/100 ml) on hemodialysis tolerance. Headache during and after dialysis and post-dialysis fatigue decreased in a statistically significant manner. The average glycemia was only moderately increased with an adequate insulin response. Blood cholesterol and triglycerides did not vary signifcantly during this short study period.
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PMID:Glucose-enriched dialysate and tolerance to maintenance hemodialysis. 51 25

Chronic stimulation of fast rabbit muscles (tibialis anterior, extensor digitorum longus and the peroneal muscle group) at a frequency naturally occurring in nerves to slow muscles increased their ability to withstand fatigue. Isometric tension decreased during a 10-min period of contractions at 4 Hz by 75% in control muscles, but only 55% in muscles chronically stimulated for 4 days, and 23% in muscles stimulated for 28 days. Chronic stimulation had little effect on resting blood flow, oxygen or glucose consumption. The output or consumption of lactate and free fatty acids (FFA) at rest were also unaffected. The glycogen content was regularly increased, and was apparent after only 2 days of stimulation. The activity of fatty acid activating enzyme was increased after 28 days. During a 10-min period of isometric contractions at 4 Hz, there was a markedly greater increase in blood flow and oxygen consumption in muscles stimulated for 14-28 days than in control muscles; lactic acid output was lower in muscles stimulated for 28 days, and the uptake of FFA was significantly higher. It is therefore suggested that muscles chronically stimulated for 14-28 days use fats as the main source of energy during isometric contractions. The predominantly oxidative metabolism is probably facilitated by the higher density of capillaries. The latter also enables more efficient delivery of oxygen, and therefore smaller fatiguability, already after 4 days of chronic stimulation.
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PMID:The effect of long-term stimulation of fast muscles on their blood flow, metabolism and ability to withstand fatigue. 56 Jun 75

A 10-year old girl (34.5 kg) being treated at our clinic for osteomyelitis erroneously received an overdose of lincomycin. On a single day she was given 2 infusions containing 6 g of lincomycin each, which corresponds to a dose of 343 mg/kg of body weight. There was an interval of 10 h between infusions. Apart from fatigue and unpleasant taste sensation, she demonstrated no signs of intoxication. None of the laboratory parameters (GOT, GPT, gamma-GT, LDH, G-LDH, LAP, alkaline phosphatase and CK; furthermore, the concentrations of glucose, BUN, creatinine, uric acid and bilirubin) offered any evidence of toxic organ damage. Osteomyelitis in children demands extremely high doses of antibiotics. In view of this fact, the therapeutic range of a substance is of utmost clinical interest.
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PMID:[The toxicity of lincomycin. Two i.v. applications of 6 g. each to a 10 year old girl without toxic symptoms]. 58 12


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