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Identification and characterization of amino acid starvation-induced CD24 gene in MCF-7 human breast cancer cells.

Amino acid starvation is a pathophysiological condition that results in protein deprivation due to cancer cachexia. Using the method of differential display of reverse transcription PCR (DDRT-PCR), we isolated a cDNA fragment in MCF-7 human breast cancer cells in response to amino acid starvation, which was identical with human CD24 gene. Northern blot results showed that CD24 mRNA in MCF-7 cells was constitutively expressed and significantly upregulated upon amino acid starvation. This stimulation was time-dependent and the maximal response was at 24 h. The expression of the amino acid starvation-induced CD24 mRNA decreased when starved cells were returned to a medium supplemented with amino acids. This repressive response was also time-dependent. Amino acid starvation-induced CD24 mRNA expression in MCF-7 cells was completely blocked by actinomycin D, which suggested that the regulation of CD24 mRNA by amino acid availability occurred at transcriptional level. When amino acid-starved cells were refed with amino acids for 8 h, the expression of CD24 mRNA declined to the basal levels confirming that CD24 mRNA expression could be stimulated by amino acid starvation. Interestingly, CD24 mRNA was poorly detected in MCF-10 cells, a benign human breast epithelial cell line. In conclusion, CD24 mRNA expression in MCF-7 cells was upregulated upon amino acid starvation. This amino acid starvation-induced upregulation of CD24 mRNA occurred at transcriptional level. The regulation of CD24 mRNA in MCF-7 cells by amino acid availability may play an important role in the progression and metastasis of human breast cancer.

Amino Acids↗

Effects of starvation on haemolymphatic glucose levels, glycogen contents and nucleotidase activities in different tissues of Helix aspersa (Müller, 1774) (Mollusca, Gastropoda).

In the present study, the glucose concentration in the haemolymph and glycogen levels were determined in the various body parts of the Helix aspersa snail after feeding lettuce ad libitum and after various periods of starvation. To characterize the effect of starvation on nucleotidase activity, enzyme assays were performed on membranes of the nervous ganglia and digestive gland. Results demonstrated the maintenance of the haemolymph glucose concentration for up to 30 days of starvation, probably due to the consumption of glycogen from the mantle. In the nervous ganglia, depletion of glycogen occurs progressively during the different periods of starvation. No significant changes were observed on ATP and ADP hydrolysis in the membranes of nervous ganglia and no alterations in Ca2+ -ATPase and Mg2+ -ATPase occurred in the membranes of the digestive gland of H. aspersa during the different periods of starvation. Although there were no changes in the enzyme activities during starvation, they could be modulated by effectors in situ with concomitant changes in products/reactants during starvation.

Adenosine Triphosphatases↗

Starvation increases the amount of pyruvate dehydrogenase kinase in several mammalian tissues.

Covalent modification of the pyruvate dehydrogenase complex provides an important regulatory mechanism for controlling the disposal of glucose and other compounds metabolized to pyruvate. Regulation of the complex by this mechanism is achieved in part by tissue-specific expression of the genes encoding isoenzymes of pyruvate dehydrogenase kinase (PDK). Starvation is known from our previous work to increase PDK activity of heart and skeletal muscle by increasing the amount of PDK isoenzyme 4 (PDK4) present in these tissues. This study demonstrates that increased expression of both PDK4 and PDK2 occurs in rat liver, kidney, and lactating mammary gland in response to starvation. PDK4 and PDK2 message levels were also increased by starvation in the two tissues examined (liver and kidney), suggesting enhancement of gene transcription. Changes in PDK2 message and protein were of similar magnitude, but changes in PDK4 message were greater than those in PDK4 protein, suggesting regulation at the level of translation. In contrast to these tissues, starvation had little or no effect on PDK2 and PDK4 protein in brain, white adipose tissue, and brown adipose tissue. Nevertheless, PDK4 message levels were significantly increased in brain and white adipose tissue by starvation. The findings of this study indicate that increased expression of PDK isoenzymes is an important mechanism for bringing about inactivation of the pyruvate dehydrogenase complex during starvation in many but not all tissues of the body. The absence of this mechanism preserves the capacity of neuronal tissue to utilize glucose for energy during starvation.

Animals↗

Effect of auxotrophic starvation of mitochondrial marker transmission in the cdc8 mutant of Saccharomyces cerevisiae.

Crosses were made using strains of S. cerevisiae which carried mitochondrial markers conferring resistance to erythromycin and chloramphenicol. The effect of auxotrophic starvation of one parent prior to mating on the transmission of its mitochondrial markers was studied in different crosses relative to the presence of the cdc8 nuclear mutation (a temperature-sensitive DNA replication). In crosses between two cdc8 mutant strains, auxotrophic starvation of one of the haploid parental stains prior to mating caused a marked decrease of its mitochondrial marker transmission to the diploid progeny of the cross. The transmission decreased as a function of the time of starvation. This effect was not observed in the cross between two wild type strains and in crosses of starved cdc8 phenotypic revertants with cdc8 mutant strains. Only a small, if any, effect of starvation on mitochondrial marker transmission was observed when starved cdc8 mutant strains were crossed either with their phenotypic revertants or with the wild-type strains. In one of the haploid parental strains the starvation increased the frequency of petites as a function of starvation time, while in the other this effect was not observed. In the progeny of cdc8 X cdc8 crosses (both in starvation experiments and in control crosses) an increased frequency of diploid petite cells accompanied by a decreased frequency of recombination between mitochondrial markers was noticed. The influence of the cdc8 mutation on the transmission of mitochondrial markers is discussed in terms of high frequency of p- molecule formation in cdc8 strains.

Chloramphenicol↗

Effect of starvation on neutral amino acid transport in isolated small-intestinal cells from guinea pigs.

The effects of starvation on neutral amino acid transport were examined in isolated enterocytes. Starvation stimulated L-alanine transport by the Na(+)-dependent system A and the Na(+)-independent system L without producing any changes in either the Na(+)-dependent systems ASC or the passive non-mediated uptake. Starvation produces a twofold increase in Vmax of system A without any change in Kt. Starvation produces an increase in Vmax of system L of 1.7 times without any change in Kt. Activation of systems A and L by starvation was reversible with subsequent refeeding. The effects of a series of amino acids on systems A and L were evaluated. A different inhibition pattern was found in starved animals as compared to controls. Starvation increases Na(+)-dependent L-alanine uptake and Na(+)-independent cycloleucine uptake by small-intestinal brush-border membrane vesicles. These results suggest that starvation stimulates amino acid transport across the apical plasma membrane of the enterocytes by inducing specific carrier units.

Alanine↗

Plasma fibronectin metabolism during hemorrhagic shock and starvation.

In this report we characterize the response of the plasma protein fibronectin to hemorrhagic shock and starvation, conditions associated with decreased function of mononuclear phagocyte system (MPS). Rats were starved for 3 days, then half of the animals were subjected to fixed-volume hemorrhagic shock by removing an estimated 35% of their blood volumes for 20 min. After volume replacement, animals were injected iv with [14C]valine. At time points up to 10 hr after hemorrhage, plasma fibronectin concentrations and fibronectin synthesis were quantitated. In additional rats treated identically, fibronectin clearance was assessed by measuring the disappearance of 125I-fibronectin from the plasma. When compared to control animals, either starvation or hemorrhagic shock produced similar perturbations in plasma fibronectin metabolism; fibronectin concentrations were reduced from 241.3 +/- 34.6 micrograms/ml (mean +/- SEM) (controls) to 123 +/- 32.6 micrograms/ml (starvation) or 150.0 +/- 13.0 micrograms/ml (hemorrhage). Plasma [14C]fibronectin specific radioactivities, indicative of fibronectin synthesis, were also significantly reduced. Hemorrhagic shock in rats that previously had been starved did not depress fibronectin concentrations or synthesis to a greater extent than starvation alone. The rates of 125I-fibronectin clearance were increased in starvation and hemorrhagic shock (t1/2 = 233.0 +/- 13.0 min, controls; 174.6 +/- 10.7 min, starvation; 167.4 +/- 13.6 min, hemorrhage). In contrast to changes observed in fibronectin metabolism, total plasma protein concentrations were not significantly altered in any experimental groups. Furthermore, total plasma protein synthesis increased in rats subjected to either starvation or hemorrhagic shock, but decreased in starved rats that were subsequently shocked.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Starvation activates MAP kinase through the muscarinic acetylcholine pathway in Caenorhabditis elegans pharynx.

Starvation activates MAPK in the pharyngeal muscles of C. elegans through a muscarinic acetylcholine receptor, Gqalpha, and nPKC as shown by the following results: (1) Starvation causes phosphorylation of MAPK in pharyngeal muscle. (2) In a sensitized genetic background in which Gqalpha signaling cannot be downregulated, activation of the pathway by a muscarinic agonist causes lethal changes in pharyngeal muscle function. Starvation has identical effects. (3) A muscarinic antagonist blocks the effects of starvation on sensitized muscle. (4) Mutations and drugs that block any step of signaling from the muscarinic receptor to MAPK also block the effects of starvation on sensitized muscle. (5) Overexpression of MAPK in wild-type pharyngeal muscle mimics the effects of muscarinic agonist and of starvation on sensitized muscle. We suggest that, during starvation, the muscarinic pathway to MAPK is activated to change the pharyngeal muscle physiology to enhance ingestion of food when food becomes available.

Acetylcholine↗

Starvation induced stress and the susceptibility of the Colorado potato beetle, Leptinotarsa decemlineata, to infection by Beauveria bassiana.

Starvation of second instar Colorado potato beetle larvae for 24h immediately after treatment with Beauveria bassiana conidia increased susceptibility to the pathogen and subsequent sporulation of cadavers but decreased time to larval death. In feeding studies, B. bassiana-treatment had no effect on subsequent larval development, and mortality occurred 5-6 days after treatment. Twenty-four hours of starvation alone retarded subsequent larval development but did not affect mortality. Mortality of B. bassiana-treated starvation stressed larvae occurred 4-5 days after treatment. Both B. bassiana treatment and 24h starvation significantly reduced total foliage consumption and daily weight gains. On the day of treatment, B. bassiana had no effect on the efficiency with which food was converted to biomass (ECI). ECI was not affected by B. bassiana or starvation alone on the day following treatment but was significantly affected by a combination of both. When larvae were exposed to a range of limited food quantities, ECI decreased with decreasing food availability but only extreme stress (starvation for 24h) increased susceptibility to B. bassiana. Topical application of Dacryodes excelsa resin (an antifeedant) to potato leaves caused a concentration dependent reduction in foliage consumption and weight gain by second instar larvae but did not affect larval mortality. When larvae were exposed to a fixed concentration of B. bassiana and a range of antifeedant concentrations there were significant linear relationships between 24h larval weight gain and mortality and 24h larval weight gain and sporulation. The interaction between starvation stress and the susceptibility to B. bassiana infection is discussed and its possible implications in pest management considered.

Animals↗

Effects of starvation on liver microsomal P450 activity in juvenile Pleuronectes americanus.

Recent work has produced evidence to support the existence of a cytochrome P450 CYP2E1-like isoform in the marine fish, Pleuronectes americanus (winter flounder) (Wall K, Crivello JF. Toxicol Appl Pharmacol 1998;151:98-104). Starvation has been previously demonstrated to induce CYP2E1 activity (assayed as chlorzozazone-6-hydroxylase activity) in mammals and this study was undertaken to determine the effects of starvation on liver chlorzozaxone-6-hydroxylase and ethoxy-resorufin-O-deethylase activity (a CYP1A1 activity) in juvenile winter flounder liver microsomes. A 2-week starvation period resulted in a statistically significant increase in liver microsomal protein, and a decrease in liver lipid and liver glycogen. Ethoxy-resorufin-O-deethylase activity (pmol/min/mg microsomal protein) was reduced with starvation, chlorzoxazone 6-hydroxylase activity (pmol/min per mg microsomal protein) initially decreased but then increased over controls. When these activities were expressed per gm/liver (to account for the starvation-induced changes in liver microsomal protein), chlorzoxazone 6-hydroxylase activity doubled over control during starvation but ethoxy-resorufin-O-deethylase was not significantly changed. The effects of starvation on liver microsomal chlorzoxazone 6-hydroxylase and ethoxy-resorufin-O-deethylase activities are discussed in the context of the impact of physiological states on the ability of fish to detoxify marine xenobiotics.

Animals↗

Metabolic depression and whole-body response to enforced starvation by Crassostrea gigas postlarvae.

Physiological and biochemical measurements were performed on six oyster (Crassostrea gigas) cohorts, in order to: (a) investigate the whole-body response (growth, energy content, metabolic and excretion rates) of 2-week-old postlarvae (spat) to enforced (0-8 days) starvation, and (b) test the potential use of three aerobic enzyme systems as indices of physiological condition. Starvation resulted in exponential reduction of postlarval metabolic and excretion rates, as well as a linear decrease in enzyme activity. These response mechanisms effectively limited the loss of endogenous reserves after 2 days of starvation and maintained the oyster's functional integrity over prolonged (8 days) starvation. Proteins appeared to be selectively conserved during short-term (2 days) starvation, as suggested by a decrease in total protein content, while maintaining constant weight-specific enzyme activity. Postlarvae starved for 2 days exhibited relatively higher lipid losses, lower mortality and lower metabolism than metamorphosing stages, thus suggesting a greater buffering capacity to starvation in the former. The activity of the electron transport system may be a useful indicator of long-term stress or developmental condition of oyster postlarvae, while citrate synthase and cytochrome oxidase could be used as indicators of growth rate. None of these enzyme systems is recommended as an index of aerobic metabolism during short-term starvation.

Animals↗

The control of partitioning between protein and fat during human starvation: its internal determinants and biological significance.

Human subjects vary in the extent to which their body's protein and fat compartments are mobilized for fuel during starvation. Although an inverse association between the initial adiposity and the contribution of protein as fuel during starvation has been known for nearly a century, interest in the quantitative importance and functional significance of the initial percentage fat as a determinant of biological variation in energy-partitioning between protein and fat (and hence in determining the partitioning characteristic of the individual) is relatively recent. The present paper addresses these issues by revisiting the classic Minnesota experiment of semi-starvation and refeeding from a standpoint of system physiology. In a quantitative analysis of the relationship between the initial body composition (ration FAT0: fat-free mass (FFM)0) and the composition of weight loss (ratio delta FAT: delta FFM) in the thirty-two men in the Minnesota study, the arguments are put forward that the fraction of FFM lost when the fat stores reach total depletion is independent of the initial percentage fat, and that this fraction represents the 'dispensable' component of the protein compartment that is compatible with life (i.e. the protein energy-reserve, rp). The concepts are developed that (1) the initial percentage body fat (which reflects the initial ratio FAT0:FFM0) provides a 'memory of partitioning' which dictates the control of partitioning between protein and fat in such a way that both the protein energy-reserve (rp) and the fat energy-reserve (rf) each complete depletion simultaneously, a strategy that would ensure maximum length of survival during long-term food scarcity, and that (2) variability in the relative sizes of these two energy reserves (i.e. in rf:rp) could, in addition to the initial percentage fat, also contribute to human variability in energy-partitioning. The basic assumptions underlying this re-analysis of the Minnesota data, and the concepts that are derived from it, have been integrated in the simple mathematical model for predicting the partitioning characteristic of the individual. This model is used to explain how variability in the fraction of the protein compartment that could function as an energy reserve (rp) can be as important as the initial percentage fat in determining inter-individual variability in protein-sparing during the early phase of starvation, in fuel partitioning during prolonged starvation, or in the maximum percentage weight loss during starvation. The elucidation of factors underlying variability in the size of the protein energy-reserve may have important implications for our understanding of the pathophysiology of starvation and age-associated susceptibility to muscle wasting, and in the clinical management of cachexia and obesity.

Body Composition↗

Effects of acute and chronic starvation on central and peripheral noradrenaline turnover, blood pressure and heart rate in the rat.

When faced with stress, an organism calls upon several mechanisms to maintain biological homeostasis. The cardiovascular system is the first to respond usually with an increase in arterial pressure and tachycardia. Therefore we investigated the central and peripheral sympathetic responses to acute and chronic starvation in Wistar rats. The noradrenaline (NA) turnover rate was determined in different catecholaminergic nuclei (A1, A2, A5, A6) as well as the arterial blood pressure and heart rate modifications. During acute starvation (3 days of starvation), the NA turnover was increased in the A1 and rostral A2 nuclei as well as in ventricles and kidneys and decreased in the A6 nucleus. During chronic starvation (4 consecutive cycles of 3 days of starvation plus 1 day of feeding), the NA turnover was increased in the A5 and caudal A2 nuclei as well as in ventricles and atria and decreased in the A1 nucleus and kidneys. The arterial blood pressure revealed a gradual decrease during the first 3 days of fasting but the heart rate was not modified. We conclude that starvation should be considered as an unusual state of stress because of the absence of locus coeruleus response (A6 nucleus) despite its well-defined role in stress reactions. One of the manifestations of these central and peripheral noradrenergic changes is the change in blood pressure during the starvation-feeding cycles.

Animals↗

Starvation survival, growth and recovery of Enterococcus faecalis in human serum.

The ability of Enterococcus faecalis to survive starvation for long periods in the obturated root canal is likely to be an important factor in the pathogenesis and maintenance of a persistent infection after endodontic treatment. The response of E. faecalis to starvation survival in water and glucose-, phosphate- or amino acid-limited chemically defined medium was studied, along with the capacity for growth and recovery of starved cells of E. faecalis in pooled human serum. After an initial rapid fall in cell numbers, a small remaining population of E. faecalis was able to survive in water for over 4 months and in nutrient-limited media for extended periods. A high cell density at the onset of starvation was critical for the ability of E. faecalis to endure prolonged nutrient limitation. Upon starvation, a static population of starved cells developed and were apparently in a minimal metabolic state, since blocking cell wall synthesis with penicillin G or inhibiting DNA synthesis with norfloxacin during starvation resulted in limited change in the rate of loss of viable cells. In 50% serum, E. faecalis grew, then stabilized at a relatively constant population of 106 colony-forming units/ml for 4 months, irrespective of the initial cell density. In summary, E. faecalis is capable of withstanding prolonged periods of starvation in a minimal metabolic state provided that there is a high cell density at the onset of starvation. Starved cells were capable of recovery upon addition of human serum.

Adaptation, Physiological↗

Effects of starvation on intermediary metabolism in the lactating cow. A comparison with metabolic changes occurring during bovine ketosis.

1. The purpose of this study was to determine the nature of the metabolic changes associated with carbohydrate and fat metabolism that occurred in the blood and liver of lactating dairy cows during starvation for 6 days. 2. During starvation, the blood concentrations of the free fatty acids and ketone bodies increased, whereas that of citrate decreased. After an initial increase, the blood concentration of glucose subsequently declined as starvation progressed. Starvation caused a significant decrease in the plasma concentration of serine and a significant increase in that of leucine. 3. After 6 days of starvation the hepatic concentrations of oxaloacetate, citrate, phosphoenolpyruvate, 2-phosphoglycerate, 3-phosphoglycerate, glucose, glycogen, ATP and NAD(+) had all decreased, as had the hepatic activities of phosphopyruvate carboxylase (EC 4.1.1.32) and pyruvate kinase (EC 2.7.1.40). 4. The above metabolic changes are similar to those previously found to occur in cows suffering from spontaneous ketosis (Baird et al., 1968; Baird & Heitzman, 1971). 5. Milk yield decreased progressively during starvation. 6. There were marked differences in the ability of individual animals to resist the onset of severe starvation ketosis.

Acidosis↗

The effect of starvation on insulin secretion and glucose metabolism in mouse pancreatic islets.

1. Rates of insulin secretion, glucose utilization, lactate output, incorporation of glucose into glycogen, contents of glucose 6-phosphate, fructose 1,6-diphosphate and ATP, and maximally extractable enzyme activities of hexokinase, high-K(m) glucose-phosphorylating activity (;glucokinase'), glucose 6-phosphatase and unspecific acid phosphatase were measured in isolated pancreatic islets from fed and 48-h-starved mice. 2. In the fed state insulin secretion from isolated islets was increased five- to six-fold when the extracellular glucose concentration was raised from 2.5mm to 16.7mm; 5mm-caffeine potentiated this effect. The secretory response to glucose of islets from mice starved for 48h was diminished at all glucose concentrations from 2.5mm up to approx. 40mm. Very high glucose concentrations (60mm and above) restored the secretory response to that found in the fed state, suggesting that the K(m) value for the overall secretory process had been increased (approx. fourfold) by starvation. Addition of 5mm-caffeine to islets from starved mice also restored the insulin secretory response to 2.5-16.7mm-glucose to normal values. 3. Extractable hexokinase, ;glucokinase', glucose 6-phosphatase and unspecific phosphatase activities were not changed by starvation. 4. Glucose utilization and glycolysis (measured as the rate of formation of (3)H(2)O from [5-(3)H]glucose over a 2h period) was decreased in islets from starved mice at all glucose concentrations up to approx. 55mm. At still higher glucose concentrations up to approx. 100mm, there was no difference between the fed and starved state, suggesting that the K(m) value for the rate-limiting glucose phosphorylation had been increased (approx. twofold) by starvation. Preparation of islets omitting substrates (glucose, pyruvate, fumarate and glutamate) from the medium during collagenase treatment lowered the glucose utilization measured subsequently at 16.7mm-glucose by 38 and 30% in islets from fed and starved mice respectively. Also the 2h lactate output by the islets at 16.7mm extracellular glucose was diminished by starvation. Incorporation of glucose into glycogen was extremely low, but the rate of incorporation was more than doubled by starvation. 5. After incubation for 30min at 16.7mm-glucose the content of glucose 6-phosphate was unchanged by starvation, that of ATP was increased and the concentration of (fructose 1,6-diphosphate plus triose phosphates) was decreased. 6. Possible mechanisms behind the correlated impairment in insulin secretion and islet glucose metabolism during starvation are discussed.

Acid Phosphatase↗

Effects of semi-starvation and potassium deficiency on the concentration of [3H]ouabain-binding sites and sodium and potassium contents in rat skeletal muscle.

1. Using vanadate-facilitated [3H]ouabain binding, the effect of semi-starvation on the total concentration of [3H]ouabain-binding sites was determined in samples of rat skeletal muscle. When 12-week-old rats were semi-starved for 1, 2 or 3 weeks on one-third to half the normal daily energy intake, the [3H]ouabain-binding site concentration in soleus muscle was reduced by 19, 24 and 25% respectively. In extensor digitorum longus, diaphragm and gastrocnemius muscles the decrease after 2 weeks of semi-starvation was 15, 18 and 17% respectively. The decrease was fully reversible within 3 d of free access to the diet. Complete deprivation of food for 5 d caused a reduction of 25% in soleus muscle [3H]ouabain-binding-site concentration. It was excluded that the reduction in [3H]ouabain binding was due to a reduced affinity of the binding site for [3H]ouabain. 2. Semi-starvation of 12-week-old rats for 3 weeks caused a reduction of 45 and 53% in 3,5,3'-triiodothyronine (T3) and thyroxine (T4) levels respectively. As reduced thyroid hormone levels have previously been found to decrease [3H]ouabain-binding-site concentration in skeletal muscle, this points to the importance of T3 and T4 in the down-regulation of the [3H]ouabain-binding-site concentration in skeletal muscle with semi-starvation. Whereas potassium depletion caused a decrease in K content as well as in [3H]ouabain-binding-site concentration in skeletal muscles, semi-starvation caused only a tendency to a decrease in K content. Thus, K depletion is not a major cause of the reduction in [3H]ouabain-binding-site concentration with semi-starvation. 3. Due to its high concentration of Na,K pumps, skeletal muscle has a considerable capacity for clearing K from the plasma as well as for the binding of digitalis glycosides. Semi-starvation causes a severe reduction in the total skeletal muscle pool of Na,K pumps and may therefore be associated with impairment of K tolerance and increased digitalis toxicity.

Animals↗

Effects of starvation and bowel resection on paracellular permeability in rat small-bowel mucosa in vitro.

BACKGROUND: Maintenance of intestinal integrity is essential after major abdominal surgery in malnourished subjects. The purpose of this experimental study was to investigate factors affecting small-bowel mucosa permeability in vitro in the immediate postoperative period in starved rats. METHODS: Male Wistar rats were randomly placed in five groups: Controls, Anesthesia, Resection, Starvation, and Starvation + resection. Controls consisted of fed rats. Anesthesia was induced intraperitoneally with xylazine and ketamine. Resection was 5 cm of the mid-jejunum, and the starvation period was 48 h. Two hours after surgery stripped mucosal segments from the jejunum and the ileum were mounted in Ussing chambers, and the transmucosal permeation of 51Cr-labeled ethylenediaminetetraacetic acid (EDTA) and dextran (40,000 Da) was studied for 120 min while electrophysiology was monitored. RESULTS: Starvation increased permeability to 51Cr-EDTA in both the jejunum and ileum. In the jejunum permeability was further increased by starvation + resection. Resection or anesthesia alone did not increase permeability. The villous height in the jejunum was reduced by starvation. Mucosal permeability was correlated to the change in transepithelial resistance during experiments. CONCLUSIONS: Starvation was the main cause of increased mucosal permeability in both intestinal segments of the rat, but surgical trauma had an additive effect, which was most pronounced in the jejunum.

Animals↗

Western diamondback rattlesnakes demonstrate physiological and biochemical strategies for tolerating prolonged starvation.

Because of the uncertainty in food resources in nature, all animals face the possibility of imposed periods of fasting (i.e., starvation) at some point in their lives. I investigated physiological and biochemical responses to starvation that occur in a species of rattlesnake known to tolerate successfully prolonged periods of starvation in the wild. Sixteen subadult Crotalus atrox were fasted for up to 24 wk under controlled conditions simulating their active season. Snakes exhibited significant reductions in plasma glucose but increased circulating ketone bodies. Fasting snakes lost mass at a linear rate and increased their relative moisture content during the experiment. The bodies of fasting snakes demonstrated an increase in their fatty acid (FA) unsaturation index and were apparently able to "spare" essential FAs effectively from beta -oxidation. Endogenous essential and nonessential amino acids were used indiscriminately to fuel energetic requirements, suggesting that essential amino acids are not preferentially spared during starvation. The (15)N signature of excreted nitrogenous waste increased significantly, presumably as a result of shifting amino acid source pools during starvation. Because our comparative knowledge of starvation physiology contains large taxonomic gaps, particularly with respect to amphibians and reptiles, an understanding of the biological responses exhibited by these animals may offer insight into the evolution of physiological strategies animals employ to cope with the pressures of starvation.

Amino Acids↗