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)

About 90 per cent of morbidly obese patients show histological abnormalities of the liver. One third of patients have fatty change involving more than 50 per cent of hepatocytes. Fatty liver disease can be divided into four histological groups: Fatty liver, fatty hepatitis, fatty liver with portal fibrosis, and cirrhosis. Most patients show only fatty change. Alcohol, drugs, diabetes, poor nutrition, and weight-reducing surgery contribute to progressive liver damage, but morbid obesity alone may lead to severe disease showing all the features of alcoholic hepatitis and may end in cirrhosis and liver failure. The accumulation of fat alone is unlikely to be the stimulus to inflammation and fibrosis. Only one fifth of patients have complaints that arise from the liver. The development of severe fatty liver disease may also be asymptomatic and rarely shows the florid picture associated with alcoholic hepatitis. There is poor correlation of liver function test results with morphology in obesity. ALT levels exceeding twice the normal limit have some predictive value for histological grades of severity, but they are present in few patients. Pericentral and pericellular fibrosis in prebypass liver biopsies may be an important prognostic lesion for the development of fatty hepatitis and cirrhosis. In contrast with the frequent progression to massive fatty change, inflammation and fibrosis after bypass surgery, weight loss by low-calorie dieting, or starvation is accompanied by improvement in fatty change and return of liver function tests to normal.
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PMID:Fatty liver disease in morbid obesity. 331 4

Effects of starvation (24 and 48 h), dexamethasone, sodium thiosulfate, atropine, and ethanol on the toxicity of methyl isocyanate (MIC) vapor, which escaped during the Bhopal accident of December 3, 1984, were studied in male Swiss-Webster mice. Toxicity to MIC appeared to be biphasic; majority of animals died between 1 and 2 d or between 7 and 21 d after exposure to 40 ppm MIC. Starvation (24 or 48 h) or an injection of 2 mg dexamethasone/kg prior to exposure inhibited the toxicity of MIC, especially during the first 6-7 d; administrations of sodium thiosulfate, alcohol, and atropine before or of dexamethasone after the exposure to MIC were ineffective. Starvation increased serum corticosterone levels. The antidotal effects of both starvation and dexamethasone might be due to suppression of the inflammatory response to MIC.
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PMID:Inhibition of methyl isocyanate toxicity in mice by starvation and dexamethasone but not by sodium thiosulfate, atropine, and ethanol. 337 66

Two major forms of hepatic microsomal cytochrome P-450 were purified from starved and acetone-treated rats. On the basis of amino acid sequence analysis, they were identified as P-450j and P-450b. Ethanol or acetone treatment of rats caused a 9-fold increase in the amount of P-450j in liver microsomes accompanied by similar increases in the rate of NADPH-dependent metabolism of carbon tetrachloride, acetone, and benzene. Immunological experiments indicated that P-450j constitutes the major catalyst of the microsomal metabolism of the latter agents and contributes by about 50% to microsomal P-450-dependent ethanol oxidation under the conditions used. The P-450j-dependent catalytic activities had a high rate of turnover. In contrast, this was not the case for the immunodetectable P-450j, indicating the occurrence of inactive forms of this protein in microsomes. Starvation or ethanol or acetone treatment caused 10-30-fold increases in the amount of both mRNA and apoprotein of P-450b,e compared to control. Run-on experiments and the concomitant increases of the P-450b,e gene products at the mRNA and protein levels indicated the appearance of mainly a transcriptional activation by acetone, ethanol, or starvation. Fasting exerted, in addition, a pronounced synergistic effect on acetone-dependent induction of P-450b,e mRNA (3-fold), apo-P-450b,e (4.3-fold), P-450j mRNA (2-fold), and apo-P-450j (2-fold). No increase of mRNA coding for P-450j, compared to control, was seen after acetone or ethanol treatment alone. The results indicate that effects of ethanol, acetone, and/or starvation on drug and xenobiotic metabolism are caused by the induction of P-450 forms belonging to at least two gene subfamilies.
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PMID:Ethanol-, fasting-, and acetone-inducible cytochromes P-450 in rat liver: regulation and characteristics of enzymes belonging to the IIB and IIE gene subfamilies. 337 38

Rats preferring ethanol differ from those preferring water in a lowered blood serum IRI level in the presence of the same level of glycemia. Ethanol preferring animals are characterized by raised function of the adrenal cortex revealed in an elevated II-oxycordicosteroid content in these glands and a lowered cholesterol level. The glucose tolerance test (4 g/kg by intragastric administration) shows a faster depletion of beta-cells of langerhans islets in ethanol preferring animals which is suggestive of a prediabetic state. A different sensitivity of the insular apparatus to glucose is noted in the study group, too. As for glycemia, rats preferring ethanol demonstrate greater resistance to 48-hour starvation as compared to rats preferring water.
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PMID:[Characteristics of the hormonal regulation of glycemia in rats with varying alcoholic motivation]. 351 59

Ethanol is constantly formed endogenously from acetaldehyde, and level of the former can be measured in both human beings and animals. Acetaldehyde can be generated in situ from the metabolism of pyruvate, threonine, deoxyribose-5-phosphate, phosphoethanolamine, alanine and presumably from other substrates. The levels of blood and tissue endogenous ethanol change as a function of various physiologic and experimental conditions such as starvation, aging, stress, cooling, adrenalectomy, etc. and are regulated by many exogenous compounds such as antimetabolites, derivatives of amino acids, lithium salts, disulfiram, cyanamide, etc. Under free choice alcohol selection situations, the levels of endogenous ethanol in rat blood and alcohol preference by the animals are negatively correlated. Similar negative correlations have been found between the levels of blood endogenous ethanol and the frequency of delirium in alcoholic patients undergoing alcohol withdrawal. Endogenous ethanol and acetaldehyde can therefore be regarded as compounds which fulfil substrate, regulatory and modulator functions.
Alcohol
PMID:Endogenous ethanol--its metabolic, behavioral and biomedical significance. 353 Feb 79

The phosphorylated proteins of Escherichia coli, radioactively labeled with [32P]orthophosphate, have been analyzed by the O'Farrell gel technique and autoradiography. The effects of various culture conditions on the pattern of protein phosphorylation have been studied, including growth on different carbon sources in either exponential or stationary phase, treatment of cells with ethanol, heat shock and amino acid starvation. A total number of 128 different phosphoproteins, labeled to a varying extent, have been detected and each of them has been characterized by both its molecular mass and isoelectric point. These proteins are located mainly in the cytosolic fraction of cells, none of them being present within either ribosomes or nucleoids, and only three being associated with membranes. Analysis of their phosphoamino acid content has shown that they are phosphorylated mostly at serine residues and, less frequently, at threonine and tyrosine residues.
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PMID:Characterization of the phosphoproteins of Escherichia coli cells by electrophoretic analysis. 353 Jul 54

We prospectively studied 23 episodes of suspected alcoholic ketosis in order to learn whether there was objective evidence of the patients having stopped drinking ethanol a few days before admission, and of being starved. Eight patients had moderate ketosis (plasma 3-hydroxybutyrate 4.1-7.8 mmol/liter); seven patients had mild ketosis (2-4 mmol/liter); and eight had little or no ketosis (less than 2 mmol/liter). The latter eight patients had mainly lactic acidosis (plasma lactate 2.0-13.3 mmol/liter). Most of the ketotic patients did not have ethanol detected in their blood. The presence of starvation was supported by the finding of subnormal plasma triiodothyronine levels (less than 90 micrograms/dl) in six of seven ketotic patients (average 60 micrograms/dl for all seven). The ketotic patients usually had low-normal plasma insulin levels (3- 16 microU/ml), as is common in starvation. Our findings support the previously undocumented belief that most patients with alcoholic ketosis did stop drinking ethanol some time before admission, and that starvation is a major pathogenetic factor in the disorder.
Alcohol Clin Exp Res 1986 Dec
PMID:Alcoholic ketosis. 354 13

Yeast tRNA nucleotidyl transferase rapidly inactivates (half life c. 2 hr) upon nitrogen starvation of exponentially growing cells. The inactivation does not occur when glucose together with the nitrogen source is removed or when glucose is replaced by ethanol. The transferase activity reappears shortly after replenishment of the nitrogen source and this appearance of the enzymatic activity is blocked by cycloheximide, indicating the need for protein biosynthesis during the process. The nucleotidyl transferase activity is also very low in stationary phase yeast cells. A ten fold decrease in the transferase activity is not paralleled by loss of the integrity of the 3' end of the tRNA chains. It seems that there is a large excess of enzymatic activity over that needed to keep the tRNA chains complete. The observed lack of the 3' end of tRNAs from late stationary phase yeast cannot be accounted for by the observed drop in transferase activity in these cells.
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PMID:Inactivation of yeast nucleotidyl transferase and its effect on the integrity of the aminoacid acceptor end of transfer RNA. 355 80

Severely ill patients often do not eat or cannot retain ingested food. Malnutrition occurs frequently in hospitalized individuals and is known to be associated with substantial changes in the pharmacokinetics of certain drugs. On the other hand, little is known about the effect of acute starvation or malnutrition on the pharmacodynamics (concentration-effect relationship) of drugs. To explore the effects of acute starvation on the pharmacodynamics of drugs that depress or stimulate the central nervous system, adult male Sprague-Dawley rats were deprived of food (but not water) for 3 days, whereas control animals had free access to food and water. Slow i.v. infusion of phenobarbital to onset of loss of righting reflex showed that the starved animals required a larger body weight normalized dose and that they had higher phenobarbital concentrations in serum, serum water, brain and cerebrospinal fluid at the pharmacologic endpoint. Refeeding of the rats for 2 or 7 days did not normalize the decreased body weight and serum total protein concentration. The starvation-associated decrease in the sensitivity of the central nervous system to the hypnotic effect of phenobarbital was only reversed slightly by refeeding for 2 days and persisted even after 7 days of refeeding. Acute starvation had no apparent effect on the dose of i.v. infused ethanol required to cause loss of righting reflex and on ethanol concentrations in serum, brain and cerebrospinal fluid at that time. The infused dose and the concentrations of pentylenetetrazol in serum, brain and cerebrospinal fluid at onset of maximal seizures did not differ significantly between starved and control (fed) rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kinetics of drug action in disease states. XX. Effects of acute starvation on the pharmacodynamics of phenobarbital, ethanol and pentylenetetrazol in rats and effects of refeeding and diet composition. 361 21

Pyruvate formate-lyase (PFL) (formate acetyltransferase; EC 2.3.1.54) of oral streptococci is essential for metabolizing sugar into volatile compounds (formate, acetate, and ethanol). This enzyme is extremely sensitive to oxygen, and its activity is irreversibly inactivated by oxygen. When Streptococcus sanguis was anaerobically starved, a part of the active form of PFL was converted into a reversible inactive form that was tolerant of oxygen. This reversible inactive enzyme could be reactivated to the active enzyme by anaerobic sugar metabolism, with the recovery of volatile compound production. The PFL in Streptococcus mutans was not converted into an oxygen-tolerant inactive form by anaerobic starvation, and after exposure of the cells to oxygen the PFL could not be reactivated. These findings suggest that S. mutans can produce acids rapidly under anaerobic conditions because of its capacity to keep PFL active and that S. sanguis can protect its sugar metabolism from oxygen impairment because of its interconversion of PFL.
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PMID:Oxygen sensitivity of sugar metabolism and interconversion of pyruvate formate-lyase in intact cells of Streptococcus mutans and Streptococcus sanguis. 381 89


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