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PubMed1979

Influence of progressive starvation upon brain and adrenal monoaminergic activity in developing rats of two different ages.

Experiments show the influence of progressive starvation upon the synthetic and metabolic activity of monoaminergic function in the brain and the adrenal gland of young rats of two different ages. Brain and adrenal monoamine oxidase (MAO) showed a tendency to decline with the prolongation of the starvation interval. After 60 h of starvation, MAO activity was irreversibly decreased, even with 24 h of feeding, in the two age groups. Cerebral catechol-O-methyltransferase (COMT) activity was very slightly affected in response to the starvation in the older group, but the younger group showed an increased level of enzyme activity, and refeeding after 60 h of starvation of the young rats produced further increases. 60 h of starvation produced an increase in COMT activity of the adrenal gland of the older rats whereas the younger group did not show any marked change. Adrenal phenylethanolamine-N-methyltransferase (PNMT) declined after 24 and 48 h of starvation in the older rats, but the younger rats showed progressive increases after similar intervals of starvation. After 60 h of starvation, PNMT in the adrenal gland of the old rats increased significantly when compared to the control value, but the younger rats did not show any important change. Adrenal stores of adrenaline rose progressively up to 60 h of starvation in the old rats whereas the younger group responded in a contrary manner. Adrenal noradrenaline followed a similar pattern of evolution in both groups up to 60 h of starvation (when the results are expressed per milligram of adrenal protein), and refeeding had very little influence on the effects of starvation. The effects of starvation upon adrenal and cerebral MAO activity were verified with two different substrates. The results provide evidence that the metabolism of monoamines by oxidative deamination can be markedly affected by starvation, and this can be irreversible even after 24 h of feeding of starved rats. COMT activity augments when MAO activity declines.

Adrenal Glands↗

PubMed1996

Analysis of starvation conditions that allow for prolonged culturability of Vibrio vulnificus at low temperature.

The response of the estuarine human pathogen Vibrio vulnificus to starvation for carbon, nitrogen or phosphorus, or all three nutrients simultaneously (multiple-nutrient), was examined with respect to the maintenance of culturability during incubation at low temperature. V. vulnificus showed similar survival patterns during starvation for the individual nutrients when kept at 24 degrees C. On the other hand, cultures prestarved at 24 degrees C and then shifted to 5 degrees C maintained culturability at low temperature in a starvation-condition-dependent manner. Carbon and multiple-nutrient starvation were indistinguishable in their ability to mediate maintenance of culturability in the cold. Prolonged starvation for phosphorus had a similar effect, but nitrogen starvation did not allow for maintenance of culturability. Extracellular factors produced during starvation were not observed to have an effect on the culturability of cells incubated at low temperature. Protein synthesis during starvation for individual nutrients was analysed by two-dimensional PAGE of pulse-labelled proteins. Carbon and multiple-nutrient starvation gave nearly identical protein induction patterns involving at least 34 proteins, indicating that carbon starvation determines both responses. Nitrogen starvation for 1 h induced 24 proteins, while phosphorus starvation induced a set of 10 proteins after 1 h and about 40 proteins after 18 h. It is suggested that starvation for carbon or phosphorus induces maintenance of culturability of V. vulnificus incubated at low temperature via the synthesis of distinct sets of starvation-specific proteins.

Bacterial Proteins↗

PubMed2002

The starvation-stress response of Salmonella enterica serovar Typhimurium requires sigma(E)-, but not CpxR-regulated extracytoplasmic functions.

Starvation of Salmonella enterica serovar Typhimurium (S. Typhimurium) for an exogenous source of carbon and energy (C-starvation) induces the starvation-stress response (SSR). The SSR functions to (i) maintain viability during long-term C-starvation and (ii) generate cross-resistance to other environmental stresses. The SSR is, at least partially, under the control of the alternative sigma factor, sigma(S). It is hypothesized that C-starvation causes cell envelope stresses that could induce the sigma(E) and/or Cpx regulons, both of which control extracytoplasmic functions and, thus, may play a role in the regulation of the SSR. In support of this hypothesis, Western blot analysis showed that the relative levels of sigma(E) increased during C-starvation, peaking after approximately 72 h of C-starvation; in contrast, CpxR levels remained relatively constant from exponential phase up to 72 h of C-starvation. To determine if sigma(E), and thus the regulon it controls, is an essential component of the SSR, several mutant strains were compared for their abilities to survive long-term C-starvation and to develop C-starvation-induced (CSI) cross-resistances. An rpoE mutant strain was significantly impaired in both long-term C-starvation survival (LT-CSS) and in CSI cross-resistance to challenges with 20 mM H(2)O(2) for 40 min, 55 degrees C for 16 min, pH 3.1 for 60 min and 870.2 USP U polymyxin B ml(-1) (PmB) for 60 min, to varying degrees. These results suggest that C-starvation can generate signals that induce the rpoE regulon and that one or more members of the sigma(E) regulon are required for maximal SSR function. Furthermore, evidence suggests that the sigma(E) and sigma(S) regulons function through separate mechanisms in the SSR. In contrast, C-starvation does not appear to generate signals required for Cpx regulon induction which support the findings that it is not required for LT-CSS or cross-resistance to H(2)O(2), pH 3.1 or PmB challenges. However, it was required to achieve maximal cross-resistance to 55 degrees C. Therefore, sigma(E) is a key regulatory component of the SSR and represents an additional sigma factor required for the SSR of Salmonella.

Bacterial Proteins↗

PubMed2006

Membrane lipid alteration during phosphate starvation is regulated by phosphate signaling and auxin/cytokinin cross-talk.

During phosphate (Pi) starvation in plants, membrane phospholipid content decreases concomitantly with an increase in non-phosphorus glycolipids. Although several studies have indicated the involvement of phytohormones in various physiological changes upon Pi starvation, the regulation of Pi-starvation induced membrane lipid alteration remains unknown. Previously, we reported the response of type B monogalactosyl diacylglycerol synthase genes (atMGD2 and atMGD3) to Pi starvation, and suggested a role for these genes in galactolipid accumulation during Pi starvation. We now report our investigation of the regulatory mechanism for the response of atMGD2/3 and changes in membrane lipid composition to Pi starvation. Exogenous auxin activated atMGD2/3 expression during Pi starvation, whereas their expression was repressed by cytokinin treatment in the root. Moreover, auxin inhibitors and the axr4 aux1 double mutation in auxin signaling impaired the increase of atMGD2/3 expression during Pi starvation, showing that auxin is required for atMGD2/3 activation. The fact that hormonal effects during Pi starvation were also observed with regard to changes in membrane lipid composition demonstrates that both auxin and cytokinin are indeed involved in the dynamic changes in membrane lipids during Pi starvation. Phosphite is not metabolically available in plants; however, when we supplied phosphite to Pi-starved plants, the Pi-starvation response disappeared with respect to both atMGD2/3 expression and changes in membrane lipids. These results indicate that the observed global change in plant membranes during Pi starvation is not caused by Pi-starvation induced damage in plant cells but rather is strictly regulated by Pi signaling and auxin/cytokinin cross-talk.

Arabidopsis↗

PubMed1988

Differential regulation by cyclic AMP of starvation protein synthesis in Escherichia coli.

Of the 30 carbon starvation proteins whose induction has been previously shown to be important for starvation survival of Escherichia coli, two-thirds were not induced in cya or crp deletion mutants of E. coli at the onset of carbon starvation. The rest were induced, although not necessarily with the same temporal pattern as exhibited in the wild type. The starvation proteins that were homologous to previously identified heat shock proteins belonged to the latter class and were hyperinduced in delta cya or delta crp mutants during starvation. Most of the cyclic AMP-dependent proteins were synthesized in the delta cya mutant if exogenous cyclic AMP was added at the onset of starvation. Furthermore, beta-galactosidase induction of several carbon starvation response gene fusions occurred only in a cya+ genetic background. Thus, two-thirds of the carbon starvation proteins of E. coli require cyclic AMP and its receptor protein for induction; the rest do not. The former class evidently has no role in starvation survival, since delta cya or delta crp mutants of either E. coli or Salmonella typhimurium survived starvation as well as their wild-type parents did. The latter class, therefore, is likely to have a direct role in starvation survival. This possibility is strengthened by the finding that nearly all of the cya- and crp-independent proteins were also induced during nitrogen starvation and, as shown previously, during phosphate starvation. Proteins whose synthesis is independent of cya- and crp control are referred to as Pex (postexponential).

Bacterial Proteins↗

PubMed1990

Changes in the amount of cytochrome P450s in rat hepatic microsomes with starvation.

The effects of starvation on the composition of 12 different cytochrome P450s in rat hepatic microsomes were studied with a specific antibody. Changes in the metabolic activity of the microsomes were studied at the same time. P450 DM (P450j) was induced 2.5-fold by a 48-h starvation and its increase reflected the increase of metabolic activity of hepatic microsomes toward aniline, 7-ethoxycoumarin, and N-nitrosodimethylamine. P450 K-5, the major renal cytochrome P450 in untreated male rat, was also induced 2.5-fold by a 48-h starvation. P450 UT-2 (P450h) and P450 UT-5 (P450g), typical male-specific forms, decreased with starvation. P450 UT-2 had high testosterone 2 alpha- and 16 alpha-hydroxylation activities. These activities of hepatic microsomes were reduced with the decrease in P450 UT-2. P450 PB-1, testosterone 6 beta-hydroxylase, was increased time-dependently by starvation. P450 UT-4 (RLM2), a minor male-specific form, was not changed by starvation. P450 PB-2 (P450k), present in both sexes, was changed little by starvation. P450 PB-4 (P450b) and P450 PB-5 (P450e) are strongly induced in rat liver by phenobarbital in coordinate fashion. Starvation increased P450 PB-4 12-fold but reduced P450 PB-5 to 22% of the control level. P450 MC-1 (P450d) was decreased by starvation. P450 MC-5 (P450c) was barely detected in control rats and was not changed by starvation. P450 IF-3 (P450a), rich in immature rats, was increased by starvation, accompanied by an increase in testosterone 7 alpha-hydroxylation activity in the hepatic microsomes. We further investigated whether new cytochrome P450s appeared upon starvation by comparison of chromatographic profiles of cytochrome P450 from starved rats with those of cytochrome P450 from control rats using HPLC. Three new cytochrome P450s were detected in the starved rats. These cytochrome P450s were purified to homogeneity. One of them was P450 DM, judging from spectral properties, catalytic activity, and the NH2-terminal sequence. The two other forms were designated P450 3b and 4b. The minimum molecular weights of P450 3b and 4b were 53,000 and 52,000, respectively, and their CO-reduced absorption maxima were at 449 and 452 nm, respectively. P450 3b metabolized aminopyrine, N-nitrosodimethylamine, 7-ethoxycoumarin, and lauric acid, but with low activity. P450 4b was efficient in lauric acid omega- and (omega-1)-hydroxylation only. The spectral properties, catalytic activity, peptide map, and NH2-terminal sequence of P450 4b agreed with those of P450 K-5. P450 3b was a new cytochrome P450, judged by these criteria.

Amino Acid Sequence↗

PubMed1991

Preferential loss of body fat during starvation in dietary obese rats.

This study was undertaken to examine whether diet-induced obesity alters the amount and/or composition of weight lost during starvation. The amount and composition of weight lost during a 4-day period of starvation was determined before and at 17, 30 and 42 weeks after rats (350 g of body weight) were given a high fat diet (HFD). To control for effects of aging, a second group of rats, fed standard laboratory chow, was also subjected to similar periods of starvation. Although total weight loss during starvation was never greater for HFD rats than for chow-fed rats, the former group showed a clear patter of increasing loss of body fat and total energy and conservation of fat-free tissues with periods of starvation later in life. In addition, chow-fed rats showed substantial energy conservation during each period of starvation (i.e. they lost less energy each day than their pre-starvation energy requirements). In contrast, HFD rats demonstrated substantial energy conservation only at 17 weeks and not at 30 or 42 weeks; during the last period of starvation, their average daily loss of carcass energy exceeded their pre-starvation energy requirements. This suggests the increased fat mass of these rats may have led to increased fuel availability and to an increased metabolic rate during starvation. If these results are applicable to humans, the more obese subjects are likely to show greater total loss of energy than lean subjects, but show a lesser loss of lean body mass, at least initially. If protein requirements are reflected by the ability to mobilize protein during food restriction, protein requirements would be substantially lower in the dietary obese rats than in controls. In summary, diet-induced obesity leads to preferential loss of body fat and conservation of lean mass during starvation.

Adipose Tissue↗

PubMed1984

Energy metabolism during exercise in normal subjects undergoing total starvation.

Energy expenditure and the circulating concentration of various intermediary metabolites, insulin and glucagon, were measured in five lean subjects at rest and during a 20-min period of a standardized exercise (50-75 watts). Measurements were made before starvation, at the end of a 4-d period of total starvation and 24-32 h after refeeding. The respiratory quotient decreased in all subjects during starvation from 0.85 +/- 0.03 (s.e.m.) to 0.70 +/- 0.01 (P less than 0.01), and rose again on refeeding to 0.85 +/- 0.04. Resting metabolic rate (RMR) was not significantly affected by starvation. 'Work efficiency' (mechanical work done X 100 divided by metabolic rate during work - RMR) decreased in all subjects from a mean value of 23.9 per cent before starvation to 22.2 per cent during starvation and rose again on refeeding to 23.9 per cent, but with small numbers these differences did not reach statistical significance. All subjects felt that the work load (assessed on the Borg scale for perceived exertion) was greater during starvation than either before or after starvation (P less than 0.01). During exercise the circulating concentrations of glucose and glucagon remained virtually unchanged whereas insulin tended to decrease. In contrast, concentrations of lactate, pyruvate and alanine increased. The changes in the concentration of lactate, pyruvate and alanine were greater during starvation than before starvation, and are consistent with inhibition of the pyruvate dehydrogenase complex by ketone bodies, the circulating concentrations of which were elevated 20-fold during starvation. It is suggested that this inhibition may increase glucose recycling between muscle and liver and cause a small increase in energy expenditure.

Adult↗

PubMed1998

The starvation-stress response (SSR) of Salmonella.

Salmonella serovars are common etiologic agents of intestinal-based disease of animals and humans. As a result of their lifestyle, salmonellae occupy and survive in a wide range of niches where they can encounter an even broader range of environmental stresses. One of the most common stresses is starvation for an essential nutrient such as a carbon/energy (C)-source. The genetic and physiologic changes that the bacterium undergoes in response to starvation-stress are referred to as the starvation-stress response or SSR. The genetic loci whose expression increases in response to the starvation-stress compose the SSR stimulon. Several loci of the SSR stimulon have been identified in Salmonella typhimurium and grouped, based on putative or known functions or products, into transport systems, C-compound catabolic enzymes, known protective enzymes, respiratory enzyme systems, regulatory proteins, virulence loci and unclassified products. The majority of loci identified are under positive control by the rpoS-encoded sigma factor, sigma S. However, a few are under (indirect) negative control by sigma S, but only during starvation-induced stationary phase. Most of the loci identified are also under either positive or negative control by the cAMP:CRP complex. For many, additional regulatory proteins (e.g. FadR, OxyR, and RelA and others) play a role in their regulation as well. Furthermore, most of the SSR loci identified are induced during other stresses or environmental conditions. For example, some are induced during P- or N-starvation, in addition to C-starvation; some are induced by extremes in pH or osmolarity; and some are induced in the intracellular environment of epithelial cells, and/or macrophages, and/or medium designed to mimic the intracellular milieu of mammalian cells (ISM). Several SSR loci are required for long-term starvation-survival (core SSR loci), e.g. narZ, dadA, stiC and rpoS. In addition, a few of the core SSR loci are also required for stress-specific-inducible and/or C-starvation-inducible resistance to H2O2 (e.g. stiC), thermal (e.g. stiC), and/or acid pH (e.g. narZ), challenge. Interestingly, C-starved cells are resistant to challenge with the antimicrobial peptide, polymyxin B. However, this resistance mechanism(s) is different from the resistance mechanisms for H2O2 and other environmental stresses. Furthermore, a link between the SSR and Salmonella virulence can be hypothesized since the two major regulators of the SSR, sigma s and cAMP:CRP, are required for full virulence of Salmonella. Moreover, the spv (Salmonella plasmid-associated virulence) genes, required for Salmonella to cause systemic disease, are C (and P- and N-)-starvation-inducible. However, a direct link between starvation-stress and virulence has not been established conclusively.

Anti-Bacterial Agents↗

PubMed1994

Culturability and Expression of Outer Membrane Proteins during Carbon, Nitrogen, or Phosphorus Starvation of Pseudomonas fluorescens DF57 and Pseudomonas putida DF14.

Changes in culturability and outer membrane protein profiles were investigated in Pseudomonas fluorescens DF57 and Pseudomonas putida DF14 during starvation for carbon, nitrogen, and phosphorus. P. fluorescens DF57 remained fully culturable for 4 days in all starvation regimes. The cell mass increased during starvation for nitrogen and phosphorus, indicating the accumulation of storage compounds, whereas it decreased slightly in carbon-starved cells. P. putida DF14 lost culturability during phosphorus starvation, and the mass of phosphate-starved cells did not increase. Analysis of additional P. fluorescens and P. putida strains, however, showed that the ability to preserve culturability during phosphorus starvation was not species but strain dependent. In DF57, an outer membrane protein of 55 kDa appeared during starvation for phosphorus, while another protein of 63 kDa was seen during all starvation conditions. DF14 induced two outer membrane proteins of 28 and 29 kDa during starvation for carbon and nitrogen, but no phosphorus-specific starvation protein could be detected. Therefore, starvation-induced outer membrane proteins do not seem to be conserved among the fluorescent pseudomonads and a unique starvation response might be found in individual strains.

Journal Article↗

PubMed2003

Carbon starvation can induce energy deprivation and loss of fermentative capacity in Saccharomyces cerevisiae.

Seven different strains of Saccharomyces cerevisiae were tested for the ability to maintain their fermentative capacity during 24 h of carbon or nitrogen starvation. Starvation was imposed by transferring cells, exponentially growing in anaerobic batch cultures, to a defined growth medium lacking either a carbon or a nitrogen source. After 24 h of starvation, fermentative capacity was determined by addition of glucose and measurement of the resulting ethanol production rate. The results showed that 24 h of nitrogen starvation reduced the fermentative capacity by 70 to 95%, depending on the strain. Carbon starvation, on the other hand, provoked an almost complete loss of fermentative capacity in all of the strains tested. The absence of ethanol production following carbon starvation occurred even though the cells possessed a substantial glucose transport capacity. In fact, similar uptake capacities were recorded irrespective of whether the cells had been subjected to carbon or nitrogen starvation. Instead, the loss of fermentative capacity observed in carbon-starved cells was almost surely a result of energy deprivation. Carbon starvation drastically reduced the ATP content of the cells to values well below 0.1 micro mol/g, while nitrogen-starved cells still contained approximately 6 micro mol/g after 24 h of treatment. Addition of a small amount of glucose (0.1 g/liter at a cell density of 1.0 g/liter) at the initiation of starvation or use of stationary-phase instead of log-phase cells enabled the cells to preserve their fermentative capacity also during carbon starvation. The prerequisites for successful adaptation to starvation conditions are probably gradual nutrient depletion and access to energy during the adaptation period.

Adenosine Triphosphate↗

PubMed1994

Isolation and characterization of Bacillus subtilis genomic lacZ fusions induced during partial purine starvation.

Random genomic Bacillus subtilis lacZ fusions were screened in order to identify the possible existence of regulons responding to the stimuli generated by partial purine starvation. A leaky pur mutation (purL8) was isolated and used to generate the partial purine starvation conditions in the host strain used for screening. On the basis of their induction during partial purine starvation, seven genomic lacZ fusions were isolated. None of the fusions map in loci previously reported to contain purine-regulated genes. One fusion maps very close to the citB locus and may very well be a citB fusion. The fusions were divided into two types on the basis of their response to complete starvation for either ATP or GTP or both components at the same time. Except for one, type 2 fusions were induced by specific starvation for ATP and by simultaneous starvation for ATP and GTP, but not by specific GTP starvation in a gua strain or by GTP starvation induced by the addition of decoyinine. Type 1 fusions were equally well induced by all three kinds of purine starvation including GTP starvation induced by decoyinine. Further subdivisions of the fusions were obtained on the basis of their responses to the spo0A gene product. A total of five fusions showed that spo0A affected expression. One class was unable to induce lacZ expression in the absence of the spo0A gene product, whereas the other class had increased lacZ expression during partial purine starvation in a spo0A background.

Adenosine↗

PubMed2006

Environmental stress and reproduction in Drosophila melanogaster: starvation resistance, ovariole numbers and early age egg production.

BACKGROUND: The Y model of resource allocation predicts a tradeoff between reproduction and survival. Environmental stress could affect a tradeoff between reproduction and survival, but the physiological mechanisms underlying environmental mediation of the tradeoff are largely unknown. One example is the tradeoff between starvation resistance and early fecundity. One goal of the present study was to determine if reduced early age fecundity was indeed a robust indirect response to selection for starvation resistance, by investigation of a set of D. melanogaster starvation selected lines which had not previously been characterized for age specific egg production. Another goal of the present study was to investigate a possible relationship between ovariole number and starvation resistance. Ovariole number is correlated with maximum daily fecundity in outbred D. melanogaster. Thus, one might expect that a negative genetic correlation between starvation resistance and early fecundity would be accompanied by a decrease in ovariole number. RESULTS: Selection for early age female starvation resistance favored survival under food deprivation conditions apparently at the expense of early age egg production. The total number of eggs produced by females from selected and control lines was approximately the same for the first 26 days of life, but the timing of egg production differed such that selected females produced fewer eggs early in adult life. Females from lines selected for female starvation resistance exhibited a greater number of ovarioles than did unselected lines. Moreover, maternal starvation resulted in progeny with a greater number of ovarioles in both selected and unselected lines. CONCLUSION: Reduced early age egg production is a robust response to laboratory selection for starvation survival. Ovariole numbers increased in response to selection for female starvation resistance indicating that ovariole number does not account for reduced early age egg production. Further, ovariole number increased in a parallel response to maternal starvation, suggesting an evolutionary association between maternal environment and the reproductive system of female progeny.

Animals↗

PubMed1980

Protective effect of small amounts of glucose on abnormal liver function tests during starvation.

The effect of small amounts of oral glucose on hepatic function during starvation was studied. A group of 20, nondiabetic, obese, male patients were entered into the protocol. Ten were placed on absolute caloric starvation and the other ten were placed on a starvation diet modified by the daily addition of 8 or 16 g of oral glucose. Five patients in the starved group crossed over to the modified starvation protocol and 3 of the modified starvation group were switched to the starvation group at the end of the initial dietary period. Total serum bilirubin, serum glutamic pyruvic transaminase (SGOT) and lactic dehydrogenase (LDH) were significantly lower in the modified starvation group compared to the totally starved group. When the groups crossed over the values were similarly altered; the bilirubin and SGOT reduced with the addition of small amounts of glucose and were elevated with starvation. Fasting immunoreactive insulin (IRI), glucagon, and glucose were similar in both groups; but the 90-min postprandial IRI was doubled while only a 15 mg/dl change in blood sugar was seen. The results show that small amounts of oral glucose reduces the total serum bilirubin, SGOT, and LDH elevation of starvation. It is suggested that the postprandial increase in peripheral IRI seen in modified starvation may expose the liver to pulses of portal vein insulin that may exert a protective effect thru the known hepatotrophic effects of insulin.

Alkaline Phosphatase↗

PubMedDate not supplied

Proteolytic and lipolytic responses to starvation.

Mammals survive starvation by activating proteolysis and lipolysis in many different tissues. These responses are triggered, at least in part, by changing hormonal and neural statuses during starvation. Pathways of proteolysis that are activated during starvation are surprisingly diverse, depending on tissue type and duration of starvation. The ubiquitin-proteasome system is primarily responsible for increased skeletal muscle protein breakdown during starvation. However, in most other tissues, lysosomal pathways of proteolysis are stimulated during fasting. Short-term starvation activates macroautophagy, whereas long-term starvation activates chaperone-mediated autophagy. Lipolysis also increases in response to starvation, and the breakdown of triacylglycerols provides free fatty acids to be used as an energy source by skeletal muscle and other tissues. In addition, glycerol released from triacylglycerols can be converted to glucose by hepatic gluconeogenesis. During long-term starvation, oxidation of free fatty acids by the liver leads to the production of ketone bodies that can be used for energy by skeletal muscle and brain. Tissues that cannot use ketone bodies for energy respond to these small molecules by activating chaperone-mediated autophagy. This is one form of interaction between proteolytic and lipolytic responses to starvation.

Acyl Coenzyme A↗

PubMed1996

Muscle protein and amino acid turnover in rats in vivo: effects of short-term and prolonged starvation.

1. Protein loss in muscle can be caused by decreased protein synthesis, increased breakdown or both. In small animals the tracer incorporation technique is mostly used to measure protein synthesis, but for degradation measurements in vitro or ex vivo settings are required. In human and large animal studies the arteriovenous dilution technique is used because it enables the measurement of synthesis and breakdown rates simultaneously. The applicability in small animals has not yet been proven. We used a starvation model to compare both techniques. 2. A primed constant infusion of L-[2,6-(3H)]phenylalanine was given to male Lewis rats after 16, 40, 64 and 112 h starvation. Protein synthesis rates of the gastrocnemius muscle were measured by the incorporation technique and compared with hindquarter protein turnover calculated in a two- and three-compartment arteriovenous dilution model. 3. Whole-body phenylalanine rate of appearance decreased from 456 +/- 32 after 16 h to 334 +/- 34 (nmol min-1 100 g-1 body weight) after 112 h starvation. Protein synthesis rates of the gastrocnemius muscle measured by the tracer incorporation technique decreased from 3.6 +/- 0.4 after 16 h starvation to 2.2 +/- 0.3 after 64 h starvation and 1.8 +/- 0.4 (%/day) after 112 h starvation. Hindquarter protein breakdown, calculated with the tracer dilution model, increased after 112 h starvation from 28 +/- 12 to 77 +/- 15 nmol min-1 100 g-1 body weight. Using the tracer dilution model, however, the calculated protein synthesis rate across the hindquarter also increased after prolonged starvation (29 +/- 7 and 68 +/- 16 nmol min-1 100 g-1 body weight after 16 and 112 h respectively). In conjunction with this, calculated bidirectional membrane transport rates were also enhanced. Using valine and glutamine as tracers, the enhanced amino acid turnover rates were confirmed. 4. In conclusion, our results show that during short periods of starvation both methods give similar results. After prolonged starvation, however, an opposite change in disappearance rate and protein synthesis rate was observed. Assumptions made to calculate protein turnover using the arteriovenous dilution model may account for the discrepancy and care must be taken with the interpretation when using only one model in anaesthetized small animals.

Amino Acids↗

PubMed2001

The decrease of rat postprandial plasma triacylglycerol concentration after multiple cycles of starvation-refeeding.

The effect of multiple cycles of starvation-refeeding on rat body weight and on plasma lipid concentration was studied. After 1 cycle of starvation-refeeding, the rat body weight did not change significantly; however the postprandial plasma triacylglycerol concentration decreased approximately 2-fold as compared to rats fed ad libitum. After 8 cycles of starvation-refeeding, both rat body weight and plasma triacylglycerols concentration decreased. In contrast, the plasma cholesterol (both total and HDL cholesterol) concentration did not change appreciably either after 1 or 8 cycles of starvation-refeeding as compared to control. Although the postprandial plasma triacylglycerol concentration decreased in both groups (i.e. after 1 and 8 cycles of starvation-refeeding), this phenomenon appears to last longer after 8 cycles of starvation-refeeding. The epididymal white adipose tissue weight decreased after both 1 and 8 cycles of starvation-refeeding. After 1 cycle of starvation-refeeding followed by 3, 6 and 9 days of ad libitum feeding, the epididymal white adipose tissue weight increased progressively, reaching the control value at day 9. In contrast, after 8 cycles of starvation-refeeding followed by 9 days of ad libitum feeding, the epididymal white adipose tissue weight did not reach the control value. These results suggest that dieting is associated with body and adipose tissue weight loss as well as with the decrease of plasma triacylglycerol concentration. Furthermore, our results suggest that better maintenance of low adipose tissue weight and low plasma triacylglycerol concentration may be achieved after multiple cycles of starvation-refeeding.

Adipose Tissue↗

PubMed1986

Carnitine metabolism in lean and obese Zucker rats during starvation.

Carnitine metabolism during starvation was studied in adult lean and obese female Zucker rats. Comparisons were made between rats starved for 0, 3, 6 or 9 d. Total plasma carnitine was not affected by obesity or starvation, but free plasma carnitine decreased with starvation. Plasma acid-soluble acylcarnitine was lower in obese than in lean rats, and increased with starvation in both lean and obese rats. Plasma acid-insoluble acylcarnitine was not affected by obesity but increased with starvation. Liver free and acid-soluble acylcarnitine were lower in obese rats than lean rats, and starvation increased liver free carnitine and acid-insoluble acylcarnitine. Free carnitine was lower in muscle from obese rats than from lean rats. In kidney, free carnitine decreased during starvation. Heart carnitine was not affected by obesity or starvation. Urinary free carnitine and acid-soluble acylcarnitine clearance decreased during starvation. These studies indicate that: 1) lean and obese Zucker rats conserve carnitine during starvation; and 2) the decreases in liver carnitine concentration reflect the loss of cellular constituents rather than increases in total hepatic carnitine.

Animals↗