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Query: UMLS:C0038187 (starvation)
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Carbon dioxide production in free living animals and humans can be measured using tracer techniques, but the prediction of energy expenditure also requires an estimate of the energy equivalents of CO2 (energy expended/CO2 produced; EeqCO2). This work is concerned with assessing the variation in EeqCO2 with the use of dietary information, indirect calorimetry, and theoretical concepts. The EeqCO2 for diets (EeqCO2 diet) ingested by 63 individuals living in a Cambridgeshire village, UK, was found to vary by less than 10%. The EeqCO2 diet for different populations varied by greater than 10% and for artificial enteral feeds by approximately 20%. Alcohol increases this variability because it has a particularly high EeqCO2. Variation in the nitrogenous end products of metabolism may also have a substantial effect on the EeqCO2 for a subject (EeqCO2 body), especially when a large proportion of energy expenditure is derived from protein oxidation, as in strict carnivores. Nutrient/energy imbalances such as those associated with growth, hypercaloric feeding, or starvation may also have major effects on EeqCO2 body. It is concluded that the calculation of energy expenditure from CO2 production should not employ a universal value for EeqCO2 body. The value should take into account the physiological and clinical state under investigation. Practical recommendations are suggested.
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PMID:Energy equivalents of CO2 and their importance in assessing energy expenditure when using tracer techniques. 189 5

Food restriction, combined with access to a running wheel, produces "activity anorexia" (self-starvation) in rats. The relative effects of ethanol and propylene glycol on activity-maintained self-starvation were examined. Young male rats were provided with access to a running wheel while on a 22.5-h food deprivation schedule. One-third were concurrently provided with a 7% solution of ethanol, one-third with a (pharmacologically weak) 7% solution of propylene glycol, and one-third with water. Results indicated that neither survival rate nor running activity were affected significantly by ethanol consumption, relative to water-drinking controls. However, increased survival rates and decreased activity were observed for those animals which consumed propylene glycol. Antagonistic effects of ethanol on energy metabolism, stress responses, and the preservation of body weight are considered in light of these findings.
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PMID:Caloric vs. pharmacologic effects of ethanol consumption on activity anorexia in rats. 192 17

Simultaneous treatment of rats with ethanol (EtOH) and methylmercury (MeHg) increases the frequency of lesions in the rat kidney. Therefore, it was of interest to us to study the effects of simultaneous treatment of rats with MeHg and EtOH on kidney metallothionein (MT) and mercury residues levels in kidneys of rats maintained on 70% of ad libitum diet. Treatment with MeHg alone induced kidney MT the most (twice) compared to its pair-fed control. Simultaneous treatment with MeHg and EtOH also induced kidney MT but to a lesser degree than treatment with MeHg alone (by about 30%). Ethanol by itself caused a slight increase in kidney MT although starvation resulting from pair-feeding with mercury-treated animals may have contributed to this observation. Simultaneous treatment with MeHg and 2 g/kg EtOH caused a significant reduction in inorganic mercury levels in the kidney (P less than 0.05) compared to treatment with MeHg alone or in combination with 1 g/kg EtOH. Corresponding with the decrease in kidney inorganic mercury levels was a significant increase in urine inorganic mercury levels in this group compared to treatment with 1 g/kg ethanol + MeHg.
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PMID:Combined effects of methylmercury and ethanol on renal metallothionein and mercury residues in rats fed restricted amounts of a liquid diet. 200 70

Incubation of rat liver microsomes with 1-propanol and 1-butanol in the presence of NADPH and of the spin trapping agent 4-pyridyl-1-oxide-t-butyl nitrone (4-POBN) allowed the detection of free radical intermediates tentatively identified as 1-hydroxypropyl and 1-hydroxybutyl radical, respectively. Microsomes isolated from rats treated chronically with ethanol (EtOH) or with the combination of starvation and acetone treatment (SA), exhibited a two-fold increase in the ESR signal intensity as compared to untreated controls, whereas no increase was observed in phenobarbital-induced (PB) microsomes. Consistently, in reconstituted membrane vesicles, ethanol-inducible cytochrome P450IIE1 was twice as active as phenobarbital-inducible P450IIB1 in producing 1-butanol free radicals. In the microsomal preparations from EtOH and SA pretreated rats the addition of antibodies against cytochrome P450IIE1, but not of preimmune IgGs, lowered the ESR signal of 1-butanol radicals by more than 50%. The same antibodies decreased the free radical production by untreated microsomes by 35-40%, but were ineffective on microsomes from PB-treated animals. This indicated that cytochrome P450IIE1 is the major enzyme responsible for the free radical activation of alcohols in control and ethanol-fed rats. The generation of 1-hydroxybutyl radicals by EtOH microsomes was inhibited by 40, 48 and 68%, respectively, by the addition of isoniazid, tryptamine and octylamine, compounds known to specifically affect the NADPH oxidase activity of this isoenzyme. This effect was not due to the scavenging of the alcohol radical since none of these compounds affected the ESR signals originated from 1-butanol in a xanthine-xanthine oxidase system. When added to reconstituted membrane vesicles isoniazid, tryptamine and octylamine also decreased 1-butanol radical formation by P450IIE1 by 54, 38 and 66%, respectively. Such an inhibition corresponded to the effect exerted by the same compounds on O2- release from P450IIE1 containing vesicles. These results indicate that the capacity of cytochrome P450IIE1 to reduce oxygen is related to its ability to generate alcohol free radicals and suggest that ferric cytochrome P450-oxygen complex might act as oxidizing species toward alcohols.
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PMID:Role of ethanol-inducible cytochrome P450 (P450IIE1) in catalysing the free radical activation of aliphatic alcohols. 203 43

Recent clinical studies have shown the presence of two short chain diols, meso-2,3-butanediol and D/L-2,3-butanediol, and in most cases 1,2-propanediol in either serum or urine collected from humans in several apparently unrelated disease states: congenital propionic and methylmalonic acidemia, premature infants, and alcoholics both in the presence and absence of ethanol. In addition 1,2-propanediol has been shown in patients during prolonged starvation, and in patients with diabetic keto-acidosis. No common defect is known to exist in these metabolic states. Understanding how these compounds are produced in clinically well-defined diseases such as methyl malonic and propionic aciduria, however, may help explain how and why these compounds are produced in alcoholics.
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PMID:Short chain diol metabolism in human disease states. 210 13

WHI2 mRNA levels were followed through the growth cycle in WHI2 mutant and wild-type cells of Saccharomyces cerevisiae. Levels were high during the first (glucose) phase of growth, and were reduced sharply during the second (ethanol) phase of growth. Transcript levels of the glycolytic genes PDC1 and PYK1 were also measured; they each showed a pattern similar to that of WHI2, whereas transcript levels of the CDC7 gene remained constant throughout the cycle, showing that a decrease in transcription is not a general feature of genes. These results make it unlikely that the WHI2 product acts as an inhibitor of cell proliferation which is activated upon carbon starvation. No difference was observed between the pattern of expression of mutant and wild-type strains, showing that the mutant phenotype was not the result of a change in regulation at the transcriptional level.
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PMID:Regulation of the Saccharomyces cerevisiae WHI2 gene. 220 79

The purpose of this review is to describe the diagnosis, emergency treatment and further observation and complications. Alcohol poisoning and complications are underdiagnosed problems. Intoxication in young children is accidental and due to lack of experience in older children. Strong spirits are usually involved. The speed of elimination is greater than in adults and presumably 3-8 mmol/l/h. Fatal cases with alcohol concentrations less than 3.0% have been reported. The lethal dose is presumably 3 g/kg. Symptoms are as in adults but appear at lower concentrations. Infants do not reach a stage of exitation. Children are more prone to develop complications such as hypothermia, acidosis, electrolyte disturbance and trauma. Hypoglycaemia develops in 24-50% of cases, more frequently in infants and after starvation. The treatment is aspiration, admission to hospital, close observation, determination of core temperature, alcohol concentration, blood glucose-concentration and determination of serum-electrolytes. Blood glucose should be monitored. Treatment is conservative but severely intoxicated children may require dialysis.
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PMID:[Acute alcohol intoxication in children. Diagnosis, treatment and complications]. 221 77

Previous data indicate that the CYP2E1 gene is transcriptionally activated after birth, but that the expression of ethanol-inducible CYP2E1 protein, hereafter, is regulated by post-transcriptional mechanisms. The constitutive expression of CYP2E1 protein is restricted to the perivenous region of the liver lobule. Here we present results from in situ hybridization and run off experiments indicating that this regioselectivity is caused by a higher rate of gene transcription in the perivenous hepatocytes. We also show that transcription of the CYP2E1 gene is activated by starvation, indicating that also this P450 gene is under transcriptional control under certain physiological conditions.
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PMID:Transcriptional control of CYP2E1 in the perivenous liver region and during starvation. 225 23

Insulin-like growth factor-I (IGF-I) has been purified from chicken serum and sequenced. The peptide has eight amino acid substitutions when compared with human IGF-I: serine26, leucine38, histidine39, histidine40, lysine41, glutamine50, isoleucine64, and proline67. Chicken IGF-I (cIGF-I) has been measured using a radioimmunoassay with a human IGF-I (hIGF-I) standard and an antibody raised against hIGF-I. In this assay the cross-reactivity of cIGF-I was approximately 50% with respect to hIGF-I and the cross-reactivity of chicken IGF-II was 1.7% with respect to chicken IGF-I. To determine whether binding proteins in chicken plasma can artifactually interfere with IGF-I measurements as they do in mammals, chicken plasma was fractionated by molecular sieve chromatography at acid pH. When the fractions corresponding to the binding protein region were included in the IGF-I radioimmunoassay, essentially no apparent IGF-I was detected, indicating that the binding proteins did not interfere. This result, together with the finding that IGF-I in acid-ethanol extracts of chicken plasma produced parallel dose-response curves to pure cIGF-I and hIGF-I, allows the reliable measurement of cIGF-I in such extracts. The concentrations of IGF-I in plasma from male birds increased two- to threefold between 1 and 7 weeks after hatching to achieve 30-45 ng/ml. Smaller increases were found in female chickens from a higher value at 1 week. No diurnal pattern of IGF-I levels could be detected. In 4-week-old birds, the plasma concentration of the peptide fell from nearly 40 to 15 ng/ml after 24 hr of starvation and to 9 ng/ml 20 hr later. These effects are very similar to those described for mammals and strongly suggest that the regulation of IGF-I is conserved during evolution, notwithstanding the lower plasma concentrations of the growth factor in chickens.
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PMID:Chicken insulin-like growth factor-I: amino acid sequence, radioimmunoassay, and plasma levels between strains and during growth. 227 67

Previously we found that Drosophila melanogaster lines selected for increased desiccation resistance have lowered metabolic rate and behavioral activity levels, and show correlated responses for resistance to starvation and a toxic ethanol level. These results were consistent with a prediction that increased resistance to many environmental stresses may be genetically correlated because of a reduction in metabolic energy expenditure. Here we present experiments on the genetic basis of the selection response and extend the study of correlated responses to other stresses. The response to selection was not sex-specific and involved X-linked and autosomal genes acting additively. Activity differences contributed little to differences in desiccation resistance between selected and control lines. Selected lines had lower metabolic rates than controls in darkness when activity was inhibited. Adults from selected lines showed increased resistance to a heat shock, 60Co-gamma-radiation, and acute ethanol and acetic acid stress. The desiccation, ethanol and starvation resistance of isofemale lines set up from the F2s of a cross between one of the selected and one of the control lines were correlated. Selected and control lines did not differ in ether-extractable lipid content or in resistance to acetone, ether or a cold shock.
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PMID:Selection for increased desiccation resistance in Drosophila melanogaster: additive genetic control and correlated responses for other stresses. 250 23


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