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)

Acetone oxidation in rat liver microsomes was induced 5- or 8-fold by the treatment of the animals with ethanol or acetone, respectively. The apparent Km of the reaction was 0.9 mM, a value lower than the concentration reported for plasma acetone under starvation conditions. The major acetone metabolite was identified as acetol by GC-MS. Acetone oxidation in microsomes was inhibited by typical P-450 inhibitors as well as by compounds (e.g. imidazole) known to interact with the ethanol-inducible P-450 form. Antibodies against this P-450 isozyme were inhibitory for the reaction in rabbit liver microsomes and this isozyme was the only one that showed acetone hydroxylation activity in reconstituted membranes. Imidazole inhibited the conversion of [14C]acetone into low-Mr compounds (e.g. glucose) in vivo. It is suggested that the ethanol- and acetone-inducible P-450 make use of acetone as an endogenous substrate in the utilization of the compound for, e.g. glucose production under conditions of starvation and diabetic ketoacidosis.
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PMID:Hydroxylation of acetone by ethanol- and acetone-inducible cytochrome P-450 in liver microsomes and reconstituted membranes. 394 33

The effect of starvation and glucose addition on glucuronidation was assessed in sublobular regions of the lobule in perfused livers from phenobarbital-treated rats. Fibre-optic micro-light guides were placed on periportal and pericentral areas on the surface of livers to monitor the fluorescence (excitation 366 nm, emission 450 nm) of free 7-hydroxycoumarin from the tissue surface. After infusion of 7-hydroxycoumarin (80 microM) under normoxic conditions, steady-state increases in fluorescence were reached in 6-8 min in both regions. Subsequently, the formation of non-fluorescent 7-hydroxycoumarin glucuronide was inhibited completely by perfusion with N2-saturated perfusate containing 20 mM-ethanol. The difference in fluorescence between anoxic and normoxic perfusions was due to glucuronidation under these conditions. In livers from fed rats, rates of glucuronidation in periportal and pericentral regions of the liver lobule were 8 and 19 mumol/h per g, respectively. In contrast, rates of glucuronidation were 3 and 9 mumol/h per g, respectively, in periportal and pericentral regions of livers from starved rats. Infusion of glucose (20 mM) had no effect on rates of glucuronidation in livers from fed rats; however, glucose increased rates of glucuronidation rapidly (half-time, t0.5 = 1.5 min) in periportal and pericentral regions to 7 and 17 mumol/h per g, respectively in livers from starved rats. These results indicate that the rapid synthesis of the cofactor UDP-glucuronic acid derived from glucose is an important rate-determinant for glucuronidation of 7-hydroxycoumarin in both periportal and pericentral regions of livers from starved rats.
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PMID:Effect of glucose on 7-hydroxycoumarin glucuronide production in periportal and pericentral regions of the liver lobule. 398 43

Depletion of hepatic glutathione in male rats by starvation caused a significant increase in microsomal glutathione S-transferase activity, which was not affected by acute ethanol pretreatment. An additional depletion in fasted rats by diethylmaleate (0.5 g/kg) caused a further increase in the enzyme activity, but this increase was delayed in ethanol intoxicated rats. Although ethanol caused a small increase in hepatic microsomal lipid peroxidation in control animals, this effect of ethanol was not observed in diethylmaleate treated rats and thus was apparently not responsible for the delay in enzyme activation. It is suggested that the activation of microsomal glutathione S-transferase activity towards 1-chloro-2,4-dinitrobenzene in glutathione-depleted rat liver may be produced by changes in thiol/disulfid ratio and/or some reactive oxygen species.
Alcohol
PMID:Effect of ethanol on the microsomal glutathione S-transferase activity in glutathione-depleted rat liver. 401 36

1. CoA, acetyl-CoA, long-chain acyl-CoA, carnitine, acetylcarnitine and long-chain acylcarnitine were measured in rat liver under various conditions. 2. Starvation caused an increase in the contents of these intermediates, except that of carnitine. 3. A single dose of ethanol had no effect on CoA content, whereas those of acetyl-CoA, acetylcarnitine and carnitine were increased and those of long-chain acyl-CoA and acylcarnitine were decreased. 4. Four weeks' adaptation to ethanol consumption did not change the effect of ethanol administration on these metabolites. 5. It is suggested that ethanol directly increases hepatic fatty acid synthesis and esterification. It is also suggested that this change is reversible and limited to the period of ethanol oxidation. 6. It is demonstrated that ethanol-induced triglyceride accumulation is not related to carnitine deficiency.
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PMID:The effect of acute and prolonged ethanol treatment on the contents of coenzyme A, carnitine and their derivatives in rat liver. 473 99

The effect of ethanol on the interrelationship of lactate and glucose metabolism was investigated in eight human volunteers. Lactate and glucose kinetics and intervconversion rates were determined by the sequential administration of L-(+) lactate-U-(14)C and glucose-1-(14)C over an 8 hr period. After a 12 hr fast, the glucose turnover and recycling rates were 94.0 +/-3.8 (SEM) and 13.7 +/-1.1 mg/kg per hr, respectively. Approximately 50% of the glucose turnover or 40.7 +/-2.1 mg/kg per hr was converted to lactate, accounting for 50% of the lactate turnover rate. Lactate turnover and lactate conversion to glucose were 81.8 +/-6.2 and 16.7 +/-1.1 mg/kg per hr, respectively. Approximately 20% of the glucose turnover was derived from lactate under these conditions. During the administration of ethanol, the blood lactate concentration doubled and the lactate turnover rate declined slightly. Lactate conversion to glucose was markedly inhibited, decreasing from 16 to 5 mg/kg per hr, and the per cent of the glucose turnover derived from lactate decreased from 18 to 6. Despite the marked inhibition of lactate conversion to glucose, neither the blood glucose concentration nor the glucose turnover rate changed. Both glucose recycling and glucose conversion to lactate were decreased, indicating that ethanol inhibited peripheral glucose utilization. There was no difference in the degree of inhibition of lactate incorporation into glucose produced by ethanol when nonfasted subjects were compared with two subjects who had fasted for 48-72 hr despite the presence of hypoglycemia in the latter. These results indicate that starvation is not a prerequisite for ethanol inhibition of gluconeogenesis from lactate in humans but is necessary for the development of hypoglycemia. Inhibition of lactate incorporation into glucose in nonfasted subjects is probably masked by a concomitant increase in glycogenolysis which prevents hypoglycemia. Ethanol decreases glucose conversion to lactate as well as lactate conversion to glucose, thus inhibiting the Cori cycle.
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PMID:Glucose-lactate interrelationships: effect of ethanol. 510 Dec 94

Rats preferring ethanol were distinct from water-consuming animals in a decreased level of immunoreactive insulin im blood serum as well as in glucokinase activity of liver tissue. Per oral loading with glucose, 4 g/kg of body mass, enabled to detect a difference in the sugar phosphorylation via hexokinase and glucokinase reactions as well as the dissimilar sensitivity of the insulin system to glucose in the ethanol-, water-consuming and intermediate animals. Ethanol-consuming rats were more resistant to the effect of starvation during 48 hrs. The data obtained suggest that the characteristic properties of glucose metabolism in ethanol-consuming rats appear to be responsible for increased consumption of ethanol, which is used as optimal energy source, metabolized via pathways which did not involve the glycolytic pathway.
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PMID:[Characteristics of glucose metabolism in rats with different preferences for alcohol]. 609 27

The specific activity of X-prolyl-dipeptidyl aminopeptidase in Saccharomyces cerevisiae grown on glucose-containing medium remains constant during exponential growth and increases less than twofold when cells reach the stationary phase. In cells harvested from exponential growth on glucose-containing medium the specific activity of the enzyme is found to be 20-30% lower than the specific activity observed in media without glucose, containing acetate or ethanol as the carbon source. X-Prolyl-dipeptidyl aminopeptidase is not inactivated after the addition of glucose to stationary phase cells. Growth of the yeast on poor nitrogen sources or under nitrogen-starvation results in a three- to fourfold increase in the level of the enzyme.
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PMID:Studies on the regulation of X-prolyl dipeptidyl aminopeptidase activity. 614 Dec 15

Lysine-mediated inhibition of postexponential growth in Saccharomyces cerevisiae occurred when glucose, fructose, or maltose, but not lactate, pyruvate, or ethanol, was used as the carbon source. Arginine starvation is not responsible for the inhibitory effect, since neither the intracellular pool of glucose-grown (inhibited) cells nor that of lactate-grown (noninhibited) cells contained arginine.
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PMID:Effect of carbon source on lysine-mediated inhibition of postexponential growth of Saccharomyces cerevisiae. 640 82

Energy metabolism of broiler breeders housed in groups was measured in large open-circuit respiration chambers. The design, function and calibration of the chambers are described. Each of the three chambers has a capacity for 24 pullets or adult layers, or 16 adult broiler breeders. Control of ventilation rate is by calibrated choked-flow nozzles. Before experiments were started the system was assessed by CO2 infusion and recovery and ethanol combustion studies. Percentage CO2 recoveries were greater than 98 of infused and the mean (+/- SD) quotient of CO2 produced to O2 consumed from the combusion of ethanol was 0.67 (+/- 0.02). Forty-eight broiler breeder hens in lay were placed in the respiration chambers (16 per chamber) and fed at different rates from around maintenance to about twice this value. The energy required for maintenance (MEm) was 365 kJ/kgW0.75 d and the efficiency of utilisation of metabolisable energy (ME) for production (kp) was 0.70. Starvation heat production was about 350 kJ/kgW0.75 d and was shown to affect the derived values of the energetic parameters when included in the relationship between retained energy and metabolisable energy intake. Published results were recalculated and found to support this.
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PMID:Energy metabolism of groups of broiler breeders in open-circuit respiration chambers. 642 59

A study was undertaken on the antiulcer effect of some active ingredients present in the lipid part of the fruits of M. azedarach administered p.o. to male rats. Acute gastric ulcers were induced by gipsing the rats for 22 hr preceded by 24 hr starvation to obtain the maximum stress. The free HCl, total HCl and total acidity were also measured. The total lipid (TLP), 1.0, 2.5 and 5.0 g/kg, reduced the ulcer index by 25-41.8% and 50-58% when given daily for 5 and 10 days, respectively. The saponifiable fraction (SP), 0.85, 2.0 and 4.0 g/kg, given for 10 days reduced the ulcer index by 41.8-50%, while the nonsaponifiable (NSP), 0.075, 0.150 and 0.50 g/kg, for 10 days reduced it by 50-83.5%. The 70% ethanol extract of the defatted residue showed no antiulcer effect. Analysis of the gastric juice showed a significant decrease in free HCl (P less than 0.001) induced by TLP; the total HCl and total acidity were reduced only at 5 g/kg. The results revealed the antiulcer effect of the lipid components of M. azedarach fruits which is mainly due to the phytosterol fraction.
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PMID:Effect of Melia azedarach fruits on gipsing-restraint stress-induced ulcers in rats. 654 33


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