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PubMed1979

Preoperative starvation and plasma glucose concentrations in children undergoing outpatient anaesthesia.

Thirty-one children aged less than 5 years were studied while attending hospital for anaesthesia as outpatients. Plasma glucose concentrations were measured after the induction of anaesthesia. The mean plasma glucose concentration was 4.70 mmol litre-1. No patients had a plasma glucose concentration less than 2.8 mmol litre-1, despite at least 8 h of starvation. This is unexplained. It is suggested that the conclusions drawn from studies made in young inpatients may not be applicable to young outpatients.

Ambulatory Care↗
PubMed2002

Nutrient control of gene expression in Drosophila: microarray analysis of starvation and sugar-dependent response.

We have identified genes regulated by starvation and sugar signals in Drosophila larvae using whole-genome microarrays. Based on expression profiles in the two nutrient conditions, they were organized into different categories that reflect distinct physiological pathways mediating sugar and fat metabolism, and cell growth. In the category of genes regulated in sugar-fed, but not in starved, animals, there is an upregulation of genes encoding key enzymes of the fat biosynthesis pathway and a downregulation of genes encoding lipases. The highest and earliest activated gene upon sugar ingestion is sugarbabe, a zinc finger protein that is induced in the gut and the fat body. Identification of potential targets using microarrays suggests that sugarbabe functions to repress genes involved in dietary fat breakdown and absorption. The current analysis provides a basis for studying the genetic mechanisms underlying nutrient signalling.

Animal Feed↗
PubMed1997

Nutritional reserves, body weight, and starvation tolerance of autogenous and anautogenous strains of Culex tarsalis (Diptera:Culicidae).

The nutritional reserves and body weight of autogenous and anautogenous strains of Culex tarsalis Coquillett were determined for 4th instars, pupae, females, and males. Starvation tolerance and survivorship of adult females and males also were studied. The autogenous individuals contained significantly greater amounts of total lipids (except the total lipids in 4th instars), total carbohydrates, glycogen, and total proteins, which resulted in a heavier mean body weight of autogenous than anautogenous mosquitoes (except the fresh weight in pupae). Results of the body fluid coefficient determination were inconclusive. Nutritional reserves in the immature stages, especially the pupal stage, were significantly greater (except the total proteins in 4th instars and female adults) than those in the adult stage. There were no significant differences in median longevity between autogenous and anautogenous females, and between autogenous and anautogenous males, provided with distilled water alone after emergence. The median longevity of females and males was significantly different in both autogenous and anautogenous strains. Our findings strongly indicate a relationship between autogenous reproduction and differences in nutritional reserves of autogenous and anautogenous strains.

Animals↗
PubMed1998

Serum composition of Aedes aegypti (Diptera: Culicidae) larvae and the production of an oviposition repellent are influenced by infection with the entomopathogenic digenean Plagiorchis elegans (Trematoda: Plagiorchiidae), starvation, and crowding.

Subjecting Aedes aegypti (L.) larvae to conditions that induced the production of oviposition repellency also reduced their wet and dry weights and the concentration of total serum carbohydrates, amino acids, and proteins. Thus, infection with metacercariae of the entomopathogenic digenean Plagiorchis elegans (Rudolphi), starvation for 7 d, or crowding for 2 d reduced larval dry weights by as much as 32, 20, and 23%, respectively, and wet weights by 20, 14, and 11%, respectively. Total serum carbohydrates declined by as much as 36, 21, and 29% for infected, starved, and crowded larvae, respectively, amino acids by 39, 48, and 44%, and protein concentrations by 72, 63, and 62%, respectively. Repellency dilution titers were correlated inversely with movement of the mouth parts and gut. Incubation of infected, starved, and crowded larvae in 0.01 g/liter glucose greatly reduced the level of repellency of their waters, whereas adding glucose to repellent waters had only minor effects. Results indicate that the induction of repellency is associated strongly with nutritional depletion effects.

Aedes↗
PubMed1998

Oviposition attraction and repellency of Aedes aegypti (Diptera: Culicidae) to waters from conspecific larvae subjected to crowding, confinement, starvation, or infection.

As the biomass of Aedes aegypti (L.) larvae increased in relation to the volume of rearing waters, oviposition attraction of these waters to conspecific, gravid females first rose to a peak and then declined. Further increases in biomass rendered waters strongly repellent. Comparable responses were elicited by a decrease in the volume of rearing waters or an increase in the relative size or number of mosquito larvae. Low volumes of water reduced oviposition attraction and increased repellency, whereas larger volumes increased attraction. Excessively large volumes diluted attraction to neutrality. Constraints imposed by the physical dimensions of the larval environment which interfered with the normal postural movements and behaviors of the larvae also induced repellency, independent of rearing volume. Titration of repellent waters revealed that infection with the digenean Plagiorchis elegans (Rudolphi) generated the most powerful repellent effect, whereas crowding or starvation induced significantly weaker responses. At no time did dilution of repellent waters restore attractive properties. Repellents, even at minute concentrations, overrode attractants. The density-dependent action of oviposition attractants and repellents may help to maintain larval populations near optimal levels through their influence on recruitment. Oviposition repellency induced by sublethal infections with P. elegans may maintain population levels below the carrying capacity of the environment. Persistence of oviposition attraction and repellency varied inversely with temperature. The magnitude of the repellent effect induced by larvae appears to be a good indicator of their probability of survival and may be of selective significance. Repellency may deflect ovipositing females away from sites close to human habitation and may lead to new, and perhaps more effective, method, to control mosquitoes and the diseases they transmit.

Aedes↗
PubMed1976

Assessment of effect of starvation, glucose, fatty acids and hormones on alpha-decarboxylation of leucine in skeletal muscle of rat.

The present investigations of rates of oxidation of [U-14C] or [1-14C]leucine by homogenates of gastrocnemius muscle of fed and starved rats have indicated that 14CO2 production is mainly the result of alpha-decarboxylation of leucine in this tissue. This incomplete oxidation was not the result of imparied tricarboxylic acid cycle since the oxidation of palmitate proceeded to completion within the experimental conditions. In the subsequent studies, the effect of altered nutrition and metabolic factors on alpha-decarboxylation of leucine by gastrocnemius muscle homogenates was investigated. Starvation increased the rate of alpha-decarboxylation of leucine. Glucose or palmitate (C16) added in physiological concentrations to the incubation medium were without effect on decarboxylation of leucine, but this reaction was stimulated by addition of 1 mM hexanoate (C6) or octanoate (C8) to the incubation medium. However, when fatty acid chain length was elongated to C10 (decanoate), the stimulatory effect was not only abolished, but this fatty acid significantly inhibited the rate of leucine decarboxylation. Addition of insulin, epinephrine, glucagon and cyclic AMP within a wide range of concentrations to the incubation medium did not significantly affect the rate of decarboxylation of leucine. These studies indicate a complex interrelationship between the metabolism of leucine and that of fatty acids.

Animals↗
PubMed1978

Effects of prolonged starvation on cardiac energy metabolism in the rat.

Experiments were carried out on two series of adult male rats (ad libitum-fed control and starved) for 7 days, at the end of which time components of the glycolytic, citric acid cycle, and associated metabolic pathways in the heart were examined. Levels of myocardial and arterial plasma metabolites in vivo were determined by fluoroenzymatic assays. Activities of enzymes in heart extracts and isolated mitochondria were measured in vitro spectrophotometrically. In starved rats, decreases were observed in heart tissue glucose, fructose-1,6-diphosphate, lactate, alanine, glutamate, and ADP; increases occurred in fructose-6-phosphate, beta-hydroxybutyrate, acetoacetate, and ATP. Slight to moderate elevations were noted in citric acid cycle metabolites. States of marked hypoglycemia, hyperketonemia, and hypocitricemia also developed. Evidence indicates that flux through the glycolytic pathway is diminished in prolonged starvation as a result of PFK inhibition. Elevated ATP and decreased AMP are suggested as possible factors in PFK inhibition; citrate is believed to have little effect. It is also postulated that amino acid utilization in the heart increases and that dependence on lipids as fuels of oxidation decreases. The latter occurs despite the high levels of circulating ketone bodies. There is little indication from a profile of citric acid cycle metabolites and analyses of mitochondrial enzyme activities that regulation of cycle activity is significantly altered.

Adenine Nucleotides↗
PubMed1980

Effect of starvation and refeeding a high-protein or high-carbohydrate diet on lipid composition and glycogen content of rat livers in relation to age.

Rats of two different ages (72 and 490 days) were subjected to a 3-day fast and then refed for the same period a high-protein (89%) or high-carbohydrate (99%) diet. This experimental model served to study whether alterations occur in the content of the main lipid components, triacylglycerol, phospholipids and cholesterol in liver. It also examined whether the aging process itself has any effect on the lipid pattern. With the high-protein diet the content of all lipids returned to or nearly to the control level regardless of age. Refeeding the 72-day-old rats the high-carbohydrate diet led to a 2.4-fold overshoot in the triacylglycerol content, while the phospholipids and the cholesterol remained far below their control levels. In the 490-day-old rats the total lipids, phospholipids and cholesterol remained at the starvation level. With aging, the total cholesterol content showed a marked increase of about four-fold when corrected for growth.

Aging↗
PubMed1981

Starvation-induced changes of hepatic glucose metabolism in hypo- and hyperthyroid rats in vivo.

The role of thyroid hormones in the metabolic adaptation to starvation was investigated in vivo. Glucose production, measured by tracer technique, was enhanced in hyperthyroid (185%) and reduced in hypothyroid (39%) 48-hour starved rats (euthyroid control = 100%). Urinary nitrogen excretion was increased in hyperthyroidism (132%) and decreased in hypothyroidism (70%). Compared with euthyroid controls (=100%) significant alterations for the following regulatory parameters of hepatic gluconeogenesis were observed: 1) tissue cAMP (124%/91%) and protein kinase activation (132%/90%), with a corresponding crossover between pyruvate and P-enolpyruvate (-/+/+/-); 2) pyruvate carboxylase (165%/60%), P-enolpyruvate carboxykinase (140%/82%) and fructose-1.6-bis-P-phosphatase activity (99%/61%), and 3) tissue content of the glucogenic amino acids: alanine (187%/66%) and glutamate (187%/88%), aspartate (179%/68%) and glutamate (137%/75%), as well as of oxaloacetate (254%/66%) and malate (164%/104%). The observed alterations in hepatic oligomycine-sensitive oxygen consumption in hyper- (161%) and hypothyroidism (51%) were related to the measured concentration of the intermediates of the citric acid cycle, the energy state and the mitochondrial redox state. In summary, the different rates of hepatic glucose production in hyper- and hypothyroid starved rats observed in vivo can be ascribed to 1) cAMP content, 2) gluconeogenic key enzyme activities, 3) glucogenic precursor supply and 4) cofactor (ATP) availability.

Animals↗
PubMed1981

Effects of estrogen on the responses of male and female rats to starvation-refeeding.

The effects of sex, castration and estrogen treatment of castrated rats subjected to starvation-refeeding were studied. Food intakes, liver lipid levels and the activities of glucose 6-phosphate dehydrogenase and malic enzyme in ad libitum-fed, starved and starved-refed rats were determined. Sex differences observed in the intact ad libitum-fed rats could be explained in part by the differences in estrogen levels. Sex differences were obliterated in the starved-refed intact rats but were observed when castrated female starved-refed rats were compared to castrated male starved-refed rats. The differences could not be erased with the administration of estrogen. Estrogen significantly reduced food intake of castrated rats. Results of this study suggest that the characteristically higher liver lipid level and enzyme activity in the female, compared to the male, may reflect the female's tendency to undereat when circulating estrogen levels are high and to compensate (by overeating) for this undereating when estrogen levels are low.

Alcohol Oxidoreductases↗
PubMed1982

Effect of starvation and diet composition on two pathways of L-serine metabolism in isolated rat hepatocytes.

This study examined the effects of starvation and of feeding to rats diets that contain varying protein, carbohydrate and fat levels on serine metabolism in isolated hepatocytes. The conversion of [14C]serine and [14C]lactate to 14CO2 and [14C]glucose was measured in the presence and absence of 5 mM quinolinic acid (QA) or 1 mM 3-mercaptopicolinic acid (MPA), inhibitors of phosphoenolpyruvate carboxykinase. Inclusion of MPA eliminated the contribution of the serine dehydratase-mediated pathway of serine metabolism to glucose production, allowing estimation of serine aminotransferase-mediated metabolism. Addition of MPA reduced [14C]glucose formation from [14C]serine to between 3 and 47% of control values in all dietary treatments. Addition of 10 mM threonine or 10 mM pyruvate depressed [14C]glucose production in hepatocytes from the groups fed 80% protein. Differences in serine metabolism were observed within each protein group, depending on the carbohydrate and fat ratio of the diet. These results suggest the following: 1) MPA is a more potent gluconeogenic inhibitor than QA, permitting estimation of relative flux through two pathways of serine metabolism; 2) serine metabolism occurs primarily via serine dehydratase, although the contribution of serine aminotransferase varies depending upon the nutritional state of the rat, and 3) changing a single dietary component at the expense of another may mask the intricacies of metabolic homeostasis.

Animals↗
PubMed1983

Effects of bone fracture and starvation-refeeding on lipogenesis in rats.

The effects of trauma and/or starvation-refeeding on lipogenesis in rats was studied. Male Sprague-Dawley rats were subjected to fracture of the right femur and either ad libitum fed or starved for 48 hours and refed a 65% glucose diet for 48 hours. Lipogenesis was assessed in terms of glucose-6-phosphate dehydrogenase activity or the incorporation of 3HOH into lipids by liver and adipose tissue. Traumatized rats differed little from control rats in their lipogenic activity, whereas starved-refed and starved-refed-traumatized rats had greatly increased lipogenic activities. These results suggest that the fatty liver that frequently develops as a consequence of trauma in humans may be due to their decreased food intake rather than to the trauma itself.

Animals↗
PubMed1984

Effect of prolonged starvation on glycogen synthase and glycogen synthase phosphatase activity in rat heart.

Rats were fasted 24, 48 or 72 hours to determine the effect of several days without food on glycogen synthase and synthase phosphatase activity in heart. The basal percentage of synthase I decreased gradually from approximately 20% in fed animals to approximately 6% in rats starved for 72 hours. Glycogen increased progressively from 4.6 mg/g wet weight in fed rats to 7.6 mg/g wet weight in 72-hour starved rats. Thus, there was an inverse relationship between the glycogen concentration and the basal percentage of synthase I. The total synthase phosphatase activity measured at a standardized glycogen concentration decreased 50% by 24 hours of starvation and then was unchanged up to 72 hours. The 50% decrease in phosphatase activity correlated directly with insulin concentration in rats fasted 24-72 hours. The rapid stimulatory effect of insulin on synthase activity observed in fed rats was delayed in rats starved 24 and 48 hours. This correlated with a progressively slower synthase phosphatase response to insulin. The stimulatory effect of insulin was lost completely in 72-hour fasted rats. The proposed mechanism for the delayed response in rats starved 24 and 48 hours and lack of response in rats starved 72 hours is insulin resistance. The mechanism remains to be elucidated.

Animals↗
PubMed1986

Hepatic mitochondrial and peroxisomal oxidative capacity in riboflavin deficiency: effect of age, dietary fat and starvation in rats.

The effects of riboflavin deficiency on mitochondrial and peroxisomal substrate oxidation were examined in young (treatment begun at weaning) and adult Sprague-Dawley rats that were fed diets low and high in fat. State 3 respiration rates (ADP-stimulated) were used as an estimate of mitochondrial oxidation rates. The oxidation of palmitoyl-CoA and palmitoylcarnitine, and to a lesser extent, glutamate, pyruvate and succinate, by hepatic mitochondria isolated from the young rats was depressed with riboflavin deficiency. There was no effect of dietary fat level on mitochondrial substrate oxidation. Carnitine palmitoyltransferase-A (CPT-A) Vmax was increased with riboflavin deficiency and with increasing dietary fat. Cyanide-insensitive palmitoyl-CoA oxidation was used to estimate peroxisomal palmitate oxidation. Expressed as total hepatic capacity, peroxisomal palmitate oxidation was depressed with riboflavin deficiency. This effect was the result of the reduced feed intake rather than riboflavin deficiency per se. Increasing dietary fat resulted in increased peroxisomal palmitate oxidation. Starvation of young rats did not change mitochondrial oxidation rates, although riboflavin-deficient starved rats exhibited increased rates of palmitoyl-CoA oxidation as well as increased CPT-A Vmax. In adult rats, after 5 wk of deficiency, only palmitoyl-CoA and palmitoylcarnitine oxidation rates were depressed. Dietary fat level did not interact with riboflavin deficiency. However, CPT-A Vmax was increased with riboflavin deficiency and with increased dietary fat level. Further, depressed hepatic fatty acid oxidation can occur in adult rats as a sequel to the feeding of riboflavin-deficient diets.

Aging↗
PubMed1986

Dynamics of recovery of body composition after overfeeding, food restriction or starvation of mature female rats.

In this study we examined the body composition of rats recovering from overfeeding, underfeeding or starvation. Female rats (220 g) were fed 160%, 100% or 40% of control intake, by stomach tube, until the 40% rats had lost 50 g. Other rats were starved to lose 50 g. Carcass composition was measured on one group from each treatment. The remaining rats returned to ad libitum feeding. The 160% rats were hypophagic and lost weight. Starved and 40% rats were hyperphagic and gained weight. Serum insulin increased with increased food intake. T4 was depressed by food restriction. T3 and T4 increased during weight loss in 160% rats. Carcass composition of rats from each treatment was determined at progressive stages of recovery. Overfed rats had gained 7 g of protein and 43 g of fat. Protein was soon lost but fat was still significantly increased after 44 d of recovery. Starved and restricted rats had lost 11 g of protein and 28 g of fat. Starved rats regained protein earlier than body fat. Restricted rats recovered body fat much earlier than body protein or weight. Body protein and fat may have individual regulatory mechanisms that work together to control body weight.

Animals↗
PubMed1987

Development of gluconeogenesis from various precursors in isolated rat hepatocytes during starvation or after feeding a high protein, carbohydrate-free diet.

Gluconeogenesis from dihydroxyacetone (DHA), glycerol, lactate, pyruvate or alanine was studied in the absence or in the presence of glucagon in hepatocytes isolated from starved rats or from rats fed a high protein diet for 2-48 h. In both groups, gluconeogenesis from DHA, glycerol, lactate and pyruvate exhibited similar changes over 48 h; the rates of glucose production increased progressively until 24 h and then plateaued. During the early phase (2-11 h), gluconeogenesis from DHA and glycerol were higher than gluconeogenesis from lactate and pyruvate. During the first 24 h of the experiment, gluconeogenesis from alanine displays a kinetic similar to that from lactate or pyruvate. After feeding a high protein diet for 24 to 48 h, gluconeogenesis from alanine was slightly higher than that in starved rats and paralleled the increase in alanine aminotransferase activity. Glucagon stimulated gluconeogenesis from DHA up to 48 h, but with glycerol this effect occurred only during the early phase (2-11 h). Glucagon stimulated gluconeogenesis from lactate, pyruvate or alanine by 1.35-fold throughout the experimental period. These findings suggest that the development of gluconeogenesis during starvation or after feeding a high protein diet displays different kinetics, depending on the substrate used and on the level of entry in the gluconeogenic pathway: triose phosphates or pyruvate.

Animals↗
PubMed1994

Hepatic CCAAT/enhancer binding protein (C/EBP-alpha and C/EBP-beta) expression changes with riboflavin deficiency, diet restriction and starvation in rats.

To study the role of nuclear regulatory proteins in mediating dietary effects, hepatic CCAAT/enhancer binding protein (C/EBP), mRNA and transcription rate were measured for C/EBP-alpha and C/EBP-beta in nutritional states that profoundly alter energy metabolism and growth. Weanling male Sprague-Dawley rats were fed riboflavin-sufficient (R+) or deficient (R-) diets for 4 wk. A diet-restricted, pair-fed (RP) group was maintained concurrently, because riboflavin-deficient rats voluntarily decrease food consumption by approximately 50% compared with controls. Half of each group was deprived of food for 48 h. The 4-wk treatment altered hepatic levels of both proteins (P < 0.05). C/EBP-alpha protein levels were increased -twofold by diet restriction. C/ EBP-beta protein levels were increased nearly threefold by riboflavin deficiency. Starvation had no significant effect on the expression of either protein. We investigated the mechanism responsible for increased protein by measuring steady-state mRNA levels and transcription rates for C/EBP-alpha and C/EBP-beta. In both isoforms, increases in mRNA were parallel to increases in transcription rates. The nutrient-induced changes in protein, mRNA and transcription rates could not be attributed only to alterations in serum glucagon or insulin concentrations. We conclude that 1) C/EBP-alpha and C/EBP-beta expression responds to diet but may involve different dietary signals for diet restriction vs. riboflavin deficiency; 2) the dietary regulation of C/EBP-alpha and C/EBP-beta expression seems to be controlled in part at the level of gene transcription; and 3) C/EBP-alpha and C/EBP-beta nuclear proteins, by virtue of their increased quantities, may participate in regulating altered energy metabolism and growth by influencing hepatic transcription of key metabolic enzymes.

Animals↗
PubMed1994

Transcriptional control of rat hepatic glutaminase expression by dietary protein level and starvation.

Mammalian liver possesses a unique isozyme of phosphate-activated glutaminase that is subject to long-term regulation. In rats during starvation or after consumption of diets containing high amounts of protein (60%), hepatic glutaminase activity was 100% higher than in rats fed a 20% protein diet. Conversely, rats fed low protein diets (0 and 5%) had lower hepatic glutaminase activity when compared with rats fed the 20% protein diet. Differences in activity with different dietary protein levels were not due to differences in the amount of food consumed. The relative abundance of mRNA encoding hepatic glutaminase was lower in rats fed 0% protein and higher in those starved or fed 60% protein diet when compared with rats fed the 20% protein diet. The mRNA elongation assay in hepatic nuclei isolated from these animals demonstrated that the rate of transcription of the glutaminase gene was also different in rats starved or fed different levels of dietary protein. Overall, the results indicate that differences in hepatic glutaminase activity in rats starved or fed different levels of protein are mainly due to differences in the rate of transcription of the gene. In this way the regulation of hepatic glutaminase expression is similar to that seen for other enzymes involved in hepatic amino acid catabolism but differs markedly from that of renal glutaminase, in which changes in transcription rate are not observed and alterations of mRNA turnover are the principle mechanism of long-term regulation.

Animals↗