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PubMed1977

Electrolytes in surgical patients: the effect of pre-operative starvation and environmental temperature.

Serum sodium, potassium and chloride values were measured before and after pre-operative starvation and after premedication in healthy subjects under going routine surgery, during both temperate and hot weather. No significant change in serum electrolytes occurred during temperate weather either after starvation or after premedication. In hot weather, when the subjects were sweating, a rise in serum electrolytes occurred, indicating fluid deficit of about 1-8 litres after a mean period of starvation of 11 hours; premedication with atropine and diazepam in these subjects was followed by a significant decrease in the serum electrolytes from the previous raised level after pre-operative starvation.

Adolescent↗
PubMed2004

A suf operon requirement for Fe-S cluster assembly during iron starvation in Escherichia coli.

The suf and isc operons of Escherichia coli have been implicated in Fe-S cluster assembly. However, it has been unclear why E. coli has two systems for Fe-S cluster biosynthesis. We have examined the regulatory characteristics and mutant phenotypes of both operons to discern if the two operons have redundant functions or if their cellular roles are divergent. Both operons are similarly induced by hydrogen peroxide and the iron chelator 2,2'-dipyridyl, although by different mechanisms. Regulation of the isc operon is mediated by IscR, whereas the suf operon requires OxyR and IHF for the response to oxidative stress and Fur for induction by iron starvation. Simultaneous deletion of iscS and most suf genes is synthetically lethal. However, although the suf and isc operons have overlapping functions, they act as distinct complexes because the SufS desulphurase alone cannot substitute for the IscS enzyme. In addition, suf deletion mutants are more sensitive to iron starvation than isc mutants, and the activity of the Fe-S enzyme gluconate dehydratase is diminished in the suf mutant during iron starvation. These findings are consistent with the model that the isc operon encodes the housekeeping Fe-S cluster assembly system in E. coli, whereas the suf operon is specifically adapted to synthesize Fe-S clusters when iron or sulphur metabolism is disrupted by iron starvation or oxidative stress.

Base Sequence↗
PubMed1982

Permeability of Dictyostelium discoideum to fucose and uracil following growth-arrest induced by starvation, hadacidin, and cerulenin.

The uptake of fucose and uracil by Dictyostelium discoideum in either a starvation or drug-induced growth-arrest state was studied. For both nutrients, the uptake was an energy-dependent process. The rate of fucose uptake remained constant for over four hours, while the uracil rate declined after about one hour, in starvation-induced growth-arrest. Under these conditions, fucose was found to be incorporated into membrane-associated glycoproteins and glycolipids, while uracil was incorporated into RNA. The rate of fucose uptake was the same for starvation or hadacidin-induced growth-arrest, but significantly lower for cerulenin-treated cells. In contrast, uracil uptake was slower in hadacidin-treated cells as opposed to starvation or cerulenin-induced growth-arrest cells. Further experiments showed that the incorporation rate of uracil into RNA was faster in hadacidin-treated cells than controls, and the cerulenin-treated cells were slower. The data suggest that the cells arrested in growth by nutrient deprivation retain the capacity to take-up and incorporate nutrients such as fucose and uracil and that pinocytosis is probably the process responsible for uptake.

Antifungal Agents↗
PubMed1994

Does Drosophila melanogaster use ethanol as an energy source during starvation?

The influence of starvation on activities of three enzymes (ADH, ODH and alpha GPDH) was studied in Drosophila melanogaster. The changes were compared in two inbred lines which had different allelic combinations at the Odh and Aldox loci. We also studied the effect of ethanol on media which contained no sucrose ("starvation conditions"). The results show that there are large differences in the larval and adult alcohol utilization. The alcohol content of the medium, in the absence of sugar, appeared to be toxic for the larvae, while the adults appeared to utilize it as an energy source. The two strains differed little in their responses to starvation or to the ethanol treatment applied under starvation conditions. We conclude that the degree of toxicity of ethanol is highly dependent on the presence of sucrose.

Alcohol Dehydrogenase↗
PubMed1982

The effects of alanine, glucose and starch ingestion on the ketosis produced by exercise and by starvation.

1. Several investigators have found that the development of post-exercise ketosis is not counteracted by glucose ingestion. Post-exercise ketosis might therefore have more in common with diabetic ketoacidosis than with starvation ketosis. 2. The effects of ingesting 100 g of glucose, alanine or starch were therefore studied in subjects rendered hyperketonaemic by prolonged running on a low carbohydrate diet, or by 65 h of starvation. These substances were also ingested by normal post-prandial subjects. 3. The runners developed post-exercise ketosis (1.81 +/- S.D. 0.81 mmol/l), which was counteracted by alanine and glucose, but only minimally by starch. 4. Fasting caused a variable ketosis (2.19 +/- S.D. 1.63 mmol/l), also counteracted by glucose and less by starch, but alanine caused vomiting. 5. Glucose and alanine lowered the blood ketone body levels of the post-prandial subjects. 6. The rising ketone body levels in starvation and after exercise were accompanied by simultaneous increases in the plasma insulin/glucagon ratios; in both, glucose ingestion increased the ratio further, while alanine decreased it. 7. It is concluded that there is no essential difference between established post-exercise and starvation ketosis, and that the blood fuel-hormone changes do not correlate with the changes in blood ketone body concentrations.

Adolescent↗
PubMed2006

Differential regulation of metabolic genes in skeletal muscle during starvation and refeeding in humans.

This study investigated the molecular alterations underlying the physiological adaptations to starvation and refeeding in human skeletal muscle. Forty-eight hours' starvation reduced whole-body insulin sensitivity by 42% and produced marked changes in expression of key carbohydrate (CHO) regulatory genes and proteins: SREBP1c and hexokinase II (HKII) were downregulated 2.5- and 5-fold, respectively, whereas the pyruvate dehydrogenase kinase 4 (PDK4) was upregulated 4-fold. These responses were not dependent on the phosphorylation status of Akt and FOXO1. On the other hand, starvation and the concomitant increase in circulating free fatty acids did not upregulate the expression of transcription factors and genes involved in fat metabolism. Twenty-four hours' refeeding with a CHO-rich diet completely reversed the changes in PDK4, HKII and SREBP1c expression in human skeletal muscle but failed to fully restore whole-body insulin sensitivity. Thus, during starvation in healthy humans, unlike rodents, regulation of fat metabolism does not require an adaptive response at transcriptional level, but adaptive changes in gene expression are required to switch off oxidative glucose disposal. Lack of effect on key proteins in the insulin-signalling pathway may indicate that changes in intracellular substrate availability/flux may be responsible for these adaptive changes in glucose metabolism. This may represent an important aspect of the molecular basis of the development of insulin resistance in metabolic conditions characterized by energy restriction.

Adaptation, Physiological↗
PubMed1978

Effect of starvation on initiation of protein synthesis in skeletal muscle and heart.

Psoas muscle of rats starved for 2 or 4 days contained increased levels of ribosomal subunits and exhibited reduced rates of protein synthesis in vitro, demonstrating a starvation-induced inhibition of peptide-chain initiation. The activity of an eIF-2-like initiation factor, assayed in postribosomal supernatants, decreased in psoas during starvation, parallel to a 25% reduction in the RNA level. Reduced eIF-2 activity did not result from nucleotide depletion or increased deacylation of initiator tRNA, nor was it abolished by extensive dialysis. Perfusion of psoas muscle in the presence of insulin reversed the starvation-induced block in peptide-chain initiation, but did not alter the activity of eIF-2 or level of RNA. Furthermore, heart muscle did not manifest a starvation-induced block in peptide-chain initiation even though the activity of eIF-2 and the level of RNA decreased as a result of food deprivation. Thus loss of eIF 2 activity in psoas and heart did not parallel changes in peptide-chain initiation but was associated with a reduction in tissue RNA. These results indicate that the level of eIF-2 is not rate-limiting for peptide-chain initiation under the conditions tested in this study.

Amino Acids↗
PubMed1981

Insulin binding and sensitivity in rat skeletal muscle: effect of starvation.

In contrast to adipose tissue and heart, the in vitro sensitivity of skeletal muscle to insulin is enhanced by starvation. To determine the basis for this, insulin binding and its ability to stimulate glucose metabolism were examined in the incubated rat soleus. In solei from 50-g rats, starvation for 48 h enhanced insulin binding by 50-100% at concentrations of 100 ng/ml or less. Starvation also resulted in higher basal and insulin-stimulated rates of glycogen synthesis, glycolysis, and glucose uptake. The enhanced effect of insulin only occurred at concentrations less than 50-75 ng/ml, in keeping with the increased binding of insulin in this concentration range. On the other hand, under conditions in which binding at equilibrium was the same, glucose uptake was still higher in the starved group, suggesting that some postreceptor event may have been more sensitive to insulin. These studies confirm that the in vitro sensitivity of rat skeletal muscle to insulin is enhanced by 48 h of starvation. They suggest that this is due at least partially to an increase in insulin binding at physiological concentrations.

Animals↗
PubMed1986

Regional ketone body utilization by rat brain in starvation and diabetes.

The rate of ketone body (beta-hydroxybutyrate and acetoacetate) metabolism was measured in individual cerebral structures of fed, starved, and diabetic rats. This was done by infusing beta-[3-14C]hydroxybutyrate intravenously and measuring the incorporation of 14C into brain by quantitative autoradiography. The capacity of the brain to use ketone bodies, expressed as plasma clearance, increased in starvation and diabetes by approximately 50-60%. Plasma clearance was near maximal after 2 days starvation and was not significantly increased after 4 days starvation, 6 days of diabetes or 28 days of diabetes. In all situations the ketone bodies provided only a modest amount of fuel for brain energy metabolism; 3.2% after 2 days starvation and 6.5 and 9.9% after 6 and 28 days of diabetes. The fraction of their energy requirement which the various structures could derive from the ketone bodies differed widely. In general the telencephalon made greatest use of ketone bodies, whereas the hindbrain used least. There was no correlation between the energy requirement of structures (estimated from glucose use in fed rats) and the fraction of energy they could derive from ketone bodies.

3-Hydroxybutyric Acid↗
PubMed1989

Fetal glucose utilization in response to maternal starvation and acute hyperketonemia.

The effects of maternal hypoglycemia and/or hyperketonemia on glucose utilization by individual fetal rat tissues have been studied in vivo. To decrease blood glucose and to raise fetal blood ketone body concentrations, 19-day pregnant rats were submitted to 48 or 96 h of starvation. To differentiate between the effects of decreased blood glucose and increased ketone body concentrations, fed pregnant rats were infused for 2 h with DL-beta-hydroxybutyrate. After 96 h of maternal starvation, fetal 2-deoxy-D-glucose (2DG) uptake decreased from 13.6 +/- 0.5 to 8.6 +/- 1.15 micrograms.min-1.g-1. This was mainly due to a decrease in 2DG uptake by fetal hindlimb muscles and heart. By contrast, 2DG uptake in fetal liver and brain was not affected by maternal starvation. Acute hyperketonemia in fed pregnant rats induced a 23% decrease in 2DG uptake by the whole fetus mainly as the result of a lowered 2DG uptake in fetal hindlimb muscles. These data suggest that fetal 2DG uptake does not simply depend on lowered blood glucose level during maternal starvation but that other hormonal, cardiovascular, or metabolic adaptations are implicated. In the rat, most of the fetal tissues including brain are protected against maternal hypoglycemia.

3-Hydroxybutyric Acid↗
PubMed1983

Different effect of starvation on activity of sucrase and lactase in rat jejunoileum.

Activities of lactase and sucrase were determined in proximal, middle, and distal thirds of the jejunoileum of 15-wk-old male rats starved for 1, 2, and 3 days and in rats fed a high-sucrose diet for 24 h after 3 days of starvation. Sucrase activity (expressed per tissue protein or DNA as well as per intestinal segment) showed a progressive decrease during starvation in proximal and middle segments but not in the distal segment. Lactase activity expressed per tissue protein or DNA in all segments increased significantly. This was obviously due to the loss of tissue protein and DNA because total lactase activity per segment did not change. Refeeding the sucrose diet produced an increase of sucrase activity without influencing lactase activity. In serial tissue homogenate of jejunal villus-crypt columns prepared using cryostat sectioning, it was shown that, during starvation, activity of lactase (specific and total) increased in the upper and middle villus. Sucrase activity (specific and total) during starvation decreased and after refeeding increased in the lower and middle villus.

Animals↗
PubMed1981

Rabbit cardiac immunoreactive cathepsin D content during starvation-induced atrophy.

To determine whether the increased activity of cathepsin D observed during starvation-induced cardiac atrophy results from activation of preexisting enzyme or synthesis of new enzyme, a solid phase double-antibody radioimmunoassay was developed for measurement of immunoreactive cathepsin D in extracts of rabbit myocardium. Cathepsin D activity was significantly increased in the hearts of animals starved for 3, 7, and 14 days (82.6 +/- 0.8, 87.2 +/- 3.8, and 95.3 +/- 3.5 U/g wet wt, respectively) compared to controls (65.5 +/- 1.4 U/g wet wt; P less than 0.001). Immunoreactive cathepsin D was increased to a greater extent (168 +/- 7, 179 +/- 16, 200 +/- 17, and 104 +/- 5 micrograms/g wet wt for 3-, 7-, and 14-day starvation and controls, respectively; P less than 0.001) than that expected on the basis of the observed increase in enzyme activity. Sephadex G100 gel filtration of cardiac lysosomal extracts from starved and control animals revealed no evidence of high or low molecular weight forms of cathepsin D. The results suggest the observed increase in cathepsin D activity during starvation-induced cardiac atrophy is accompanied by an increased synthesis and/or decreased degradation of cathepsin D protein, rather than activation of preexisting enzyme. The lower activity levels observed during starvation possibly result from alterations in the concentrations of endogenous inhibitors or activators of cathepsin D.

Acid Phosphatase↗
PubMed1975

Induction processes in blood-brain transfer of ketone bodies during starvation.

Fed and starved rats were studied on successive days during a 5-day starvation period. The ability of ketone bodies to pass the blood-brain barrier was estimated by single common carotid injections of labeled ketone bodies and water, and results were expressed as the ratio between the normalized activities of tracers in tissue and blood, the brain uptake index (BUI). BUI of D-3-hydroxybutyrate and acetoacetate decreased as their total concentrations increased in the injectate bolus: BUI of D-3-hydroxybutyrate decreased significantly from 8% at 0.2 mM to 3--4% at 20.2 mM in fed rats and from 11.5% at 0.2 mM to 6% at 20.2 mM in starved rats, indicating saturation of the uptake mechanism. The BUI of both ketone bodies increased significantly with increasing duration of starvation, indicating adaptation to ketonemia. Enzymatic kinetics explained the uptake behavior of D-3-hydroxybutyrate in both fed and starved rats and involved a rise of Km and Vmax during starvation consistent with a doubling of the transport rate at the degree of ketonemia found in starved rats. The uptake of glucose was not influenced by starvation or ketonemia.

Acetoacetates↗
PubMed1988

Effects of exercise, detraining, starvation, and refeeding on lipogenic capacity of Osborne-Mendel rat.

Both starvation and refeeding and exercise and detraining are procedures that result in lowered lipid stores followed by their refilling. Rats subjected to these procedures were evaluated for their ability to produce hepatic biosynthetic reducing equivalents. Five-week-old male Osborne-Mendel rats were exercised on a motorized treadmill for 6 wk (final speed 27 m/min, 60 min/day, 6 day/wk) or kept sedentary. Exercised and sedentary rats were starved for 48 h or fed ad libitum. After treatments, some rats in each group were killed. Remaining exercised animals were detrained or detrained and refed. Remaining sedentary rats were refed. Activities of hepatic glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, and malic enzyme were evaluated. Plasma glucose, triglyceride, insulin, liver triglyceride, and body composition were determined. Results indicate that changes in lipids stores associated with starvation and refeeding and exercise and detraining are not associated with similar changes in enzyme activity. Starvation resulted in lowered plasma glucose, triglyceride, and insulin. Starvation and all exercise treatments resulted in lowered carcass fat. Exercised rats who were starved for 48 h and then detrained and refed for 72 h had the greatest liver weights and percent liver triglycerides. This was not associated with similar changes in enzyme activity. Increased liver lipid and decreased carcass fat may indicate a redistribution of lipid stores in these animals.

Animals↗
PubMed2001

Lack of decrease in hypothalamic and hippocampal glucocorticoid receptor mRNA during starvation.

We have shown in a previous study that high corticosterone levels during repeated immobilization stress result in a reduction of glucocorticoid receptor (GR) mRNA in the hypothalamic paraventricular nucleus (PVN) and the hippocampus. The reduction of GR presumably accounts for loss of or decrease in glucocorticoid-negative feedback, and thus hyperfunction of the hypothalamic-pituitary-adrenocortical (HPA) axis persists during chronic stress. Starvation is a stress state in which the counterregulatory responses against the loss of food occur in the central nervous system. We explored the impact of starvation on the HPA axis, GR and mineralocorticoid receptor (MR) mRNAs in the hippocampus, the PVN, and the anterior pituitary (AP) of rats. Rats were starved for 4 days and sacrificed in the morning. Starved rats showed high levels of plasma corticosterone, whereas neither plasma corticotropin (ACTH), AP proopiomelanocortin (POMC) mRNA nor AP type-1 corticotropin-releasing hormone (CRH) receptor mRNA was altered in the starved rats. In the presence of high corticosterone, starvation resulted in a decrease in both CRH mRNA and type-1 CRH receptor mRNA in the PVN. Consistently, the starved rats did not show any changes in GR mRNA in the hippocampus (CA1-2, CA3, and dentate gyrus), the PVN or the AP despite the elevation of plasma corticosterone. A significant decrease in MR mRNA was seen in the dentate gyrus and the AP, but not in CA1-2, CA3 or PVN. The lack of reduction of GR may be one of the organism's counterregulatory responses during starvation, which allows an intact glucocorticoid negative feedback, thereby resulting in decreased anorectic neuropeptide levels, namely CRH, in the PVN. The results also indicate that GR mRNA in the hippocampus and other brain regions is not solely regulated by circulating glucocorticoids. The mechanism underlying the regulation of GR mRNA in the central nervous system remains to be clarified.

Adrenocorticotropic Hormone↗
PubMed1998

Inhibition of protein synthesis by acid in L6 skeletal muscle cells: analogies with the acute starvation response.

Impaired protein synthesis (PS) occurs in skeletal muscle during acute starvation. Even though it is well established that uraemic metabolic acidosis (MA) stimulates protein degradation (PD) and is a major contributor to skeletal muscle wasting in chronic renal failure, the accompanying effects of MA on PS are much less clear. Previous work has shown that, in cultured L6 skeletal muscle cells, PD and leucine oxidation are stimulated by acid. The aim of the present study was to determine whether acid (like acute starvation) can also inhibit PS. PS (14C-phenylalanine incorporation) was measured in L6 cells in MEM + 2% serum at acid pH (7.1) or control pH (7.5). After 24 h, acid inhibited PS (7.7 +/- 0.2 vs. 8.9 +/- 0.1 nmol Phe/4 h/35-mm culture well in controls, p = 0.01) and this was maintained at 72 h. In vitro this could arise because acid only inhibits the rapid PS occurring in dividing cells. However, when division was abolished with 10(-5) mol/l cytosine arabinoside, PS inhibition by acid still occurred (6.9 +/- 0.1 vs. 8.3 +/- 0.2 at control pH, p < 0.05). Acid also had no effect on the specific radioactivity of cellular phenylalanine, suggesting that the impaired PS was not a consequence of inadequate labelling of this pool. Elevated PD and impaired PS together led to loss of 7% of the total protein in only 28 h (-21 +/- 3 microg/well, p = 0.004). This combination of impaired PS with increased PD and increased leucine oxidation in response to acid resembles the response of skeletal muscle to acute starvation. These superficial similarities between the starvation state and MA suggest that fundamental metabolic signals may occur which are common to both states.

Animals↗
PubMed1992

Short-term starvation decreases POMC mRNA but does not alter GnRH mRNA in the brain of adult male rats.

Dietary restriction reduces circulating gonadotropin and testosterone levels in male rats, an effect thought to be mediated through reduced gonadotropin-releasing hormone (GnRH) secretion; however, the cellular mechanisms subserving this response are still unknown. We reasoned that if dietary restriction reduces GnRH secretion, this would be reflected by a decrease in GnRH synthesis and likewise cellular GnRH mRNA levels. We tested this hypothesis by comparing cellular levels of GnRH mRNA between ad libitum fed (n = 4) and starved (n = 4) adult male rats. Five days of starvation resulted in a 21% decrease in body weight and an 85% decline in serum testosterone levels (fed: 13.9 +/- 2.00 vs. starved: 2.1 +/- 0.70 nmol/l; p < 0.01). In situ hybridization and image analysis demonstrated that short-term starvation influenced neither GnRH cell number (fed: 148 +/- 16 vs. starved: 157 +/- 13 cells) nor cellular GnRH mRNA signal level (fed: 177 +/- 5 vs. starved: 160 +/- 7 grains/cell) in any region of the basal forebrain. Endogenous opioid peptides are known to exert an inhibitory effect on GnRH secretion and have been implicated in having a role in the starvation-induced effects on the reproductive system. We therefore also tested the hypothesis that alterations in proopiomelanocortin (POMC) gene expression are involved in the neuroendocrine response to starvation, by comparing cellular POMC mRNA levels in individual neurons (approximately 160 neurons/animal) of the arcuate and periarcuate nuclei between fed control (n = 4) and starved (n = 4) adult male rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Interactions of starvation and selective phosphorus depletion on renal phosphate reabsorption.

Renal phosphate (Pi) wastage following 7 days of starvation was investigated in normal rats (HI-P) and others previously stabilized on a low phosphorus (LO-P)diet. In LO-P animals, Pi excretion increased after starvation, but was significantly less than in starved HI-P rats. After thyroparathyroidectomy, the increase in Pi excretion after parathyroid hormone (PTH) was significantly greater in nonacidotic starved HI-P rats than in LO-P animals. However, PTH elicited a 31-fold increase in Pi excretion in both of these groups. Starved LO-P and HI-P rats responded equivalently to dibutyryl cyclic AMP. The renal response to phosphate depletion normally promotes Pi conservation, but is attenuated markedly by 7 days of subsequent starvation. This results from at least partial restoration of phosphaturic responsiveness to PTH during starvation.

Animals↗