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PubMed1984

Stimulation of lactase synthesis induced by starvation in the jejunum of adult rat.

The effects of actinomycin D and of cycloheximide administration have been investigated on the enzyme activities of the jejunal brush border membrane in adult rats after a 48-hour period of starvation. The modifications in the protein and enzyme patterns of the brush border membrane and the incorporation of radiolabelled amino acid in the protein band corresponding to lactase have been studied in the nourished and in the starved animal. The results show that actinomycin D administration did not modify the stimulation of lactase activity caused by starvation whereas cycloheximide completely inhibited this process. The stimulation of lactase activity, in the starved animal, is related to a quantitative increase of the corresponding protein band and with enhanced incorporation of L-[3H]valine in this protein band after separation of brush border proteins by gel electrophoresis. It is concluded that the stimulation of lactase activity observed during starvation is the consequence of de novo synthesis of lactase molecules and that this process is regulated at a translational level. A general hypothesis is proposed in order to clear up partly the mechanism involved in the stimulation of lactase activity by food deprivation in the adult rat.

Animals↗
PubMed1978

Starvation---an interesting model for the study of the renin-angiotensin-aldosterone system.

Five obese subjects were studied during prolonged starvation. Then renin aldosterone system and urinary aldosterone excretion were studied during prolonged starvation and refeeding in five obese subjects. An uniform increase in aldosterone urinary excretion was observed in all subjects studied. A progressive increase in renin plasma activity was found in all patients along the starvation period with a striking additional increase after refeeding. The possible factors involved are discussed.

Adolescent↗
PubMed1984

Effect of acute maternal starvation on tyrosine metabolism and protein synthesis in fetal sheep.

To determine the effects of acute maternal starvation on intrauterine growth, tyrosine concentration and specific activity values in plasma, intracellular free and protein bound pools were determined in catheterized ovine fetuses following an 8 h continuous infusion of L-[2,3,5,6 3H] or L-[U-14C] tyrosine into the ewe and fetus respectively at 115-125 days of gestation. From the kinetic data the rates of whole body and tissue fractional protein synthesis were calculated. Although placental protein synthesis was not significantly changed as a result of acute maternal starvation, fetal whole body protein synthesis was reduced from 63 g/d/kg in the fed to 25 g/d/kg in the starved condition. There was also a 10 fold reduction in the net placental transfer of tyrosine to the fetus in the starved ewes. In addition, a three fold increase was observed in the quantity of tyrosine used for oxidation by the fetuses of starved ewes, changing from 5.2% of tyrosine net utilization in the fed to 13.7% in the starved condition. Significant reductions in tissue fractional protein synthesis rates were also seen in the liver, brain, lung kidney and GIT tissues from 78, 37, 65, 45 and 71%/d respectively in the fed to 12, 10, 23, 22 and 35%/d in the fetuses of starved ewes. The data indicate that during acute maternal starvation the sheep fetus utilizes more tyrosine for oxidation and less for anabolic purposes which is reflected in a decrease both in whole body and tissue fractional rates of protein synthesis.

Animals↗
PubMed1981

Glycogen metabolizing enzymes during starvation and feeding of Ascaris suum maintained in a perfusion chamber.

The glycogen content of muscle was correlated with the activity of glycogen synthase and glycogen phosphorylase from the parasitic roundworm Ascaris suum maintained in vitro. Adult female worms were maintained in the laboratory in a perfusion system during periods of starvation and feeding. During starvation, the levels of glucogen decreased at a rate of 0.1 to 0.2 mumoles/min/g wet weight of muscle-cuticle. During this time, 95% of the glycogen synthase (E.C. 2.4.1.11) was in the active D-form, and 48% of the phosphorylase (E.C. 2.4.1.1) was in the active a-form. Upon feeding, the rate of incorporation of glycosyl residues into glycogen proceeded at a rate of 0.75 to 1.0 mumoles/min/g muscle-cuticle. Glycogen synthase was 22% in the active I-form and phosphorylase a-levels remained virtually unchanged at 41% as compared with the starved worm. Total levels of both enzymes remained constant over the starvation-feeding period with 3.9 units/g phosphorylase and 0.4 units/g glycogen synthase. The apparent Km value for the substrate UDPG for glycogen synthase was 0.22 +/- 0.02 mM. For glycogen phosphorylase the Km value for G-1-P was 1.76 +/- 0.38 mM.

Animals↗
PubMedDate not supplied

[Metabolic and hematologic changes in the northern red-backed vole Clethrionomys rutilus and the large-toothed red-backed vole Clethrionomys rufocanus during short-term starvation and refeeding].

The effect of starvation has been investigated on the content of glucose and lipids in the blood plasma, on the level of leucocytes in the peripheral blood and on the concentration of total lipids and glycogen in the liver. It was found that in both species of the voles, starvation within 20-22 hours sharply decreases glucose content and increases lipid content of the blood plasma. The liver glycogen becomes almost completely exhausted. These changes are more significant than those observed under similar conditions in laboratory rodents (albino mice and rats). During starvation of the voles, the level of leucocytes drastically decreases, whereas lipid content of the liver significantly increased. These changes are absent in laboratory rodents. The decrease in the content of glucose and in the level of leucocytes in the blood is more significant in C. rufocanus than in C, rutilis. On the contrary, accumulation of the lipids in the liver is more intense in the latter. The recovery of the investigated indices after refeeding is very slow. Possible significance of these re-arrangements for temperature and immune homeostases, as well as for regulation of other functions in the organism, is discussed.

Animals↗
PubMed1981

[Adaptation of lipogenic enzymes of liver and adipose tissue to starvation and refeeding (author's transl)].

The lipogenic enzymes-6-phosphate dehydrogenase, citrate cleavage enzyme and malic enzyme of both liver and adipose tissue of rate of the wistar strain show a diminished activity in dependence on age. In the liver exists no age difference of the characteristic adaptation under the conditions of starvation and refeeding, but in adipose tissue of 18 months old rats the lipogenic enzymes show a poorer elevation of activity during refeeding after a 48 h period of starvation than in 3 months old animals. The serum inulin level and his variation in starvation and refeeding are independent of age.

Adipose Tissue↗
PubMedDate not supplied

[The effect of starvation of lipid peroxidation in synaptosomal and mitochondrial factions of various brain structures].

Content of lipid hydroperoxides (LHP) and malonic dialdehyde (MDA) was measured in homogenates of rat brain cortex (limbic, sensomotor and orbital cortex) and subcortex brain structures (hypothalamus, medulla oblongata, and midbrain) and in their synaptosomal and mitochondrial fractions within various periods of starvation 1, 2, 3, 5 and 7 days. Lipid peroxidation was shown to intensify distinctly in the brain regions studied especially in the sensomotor cortex only after relatively long-term starvation during 5-7 days. The rate of lipid peroxidation was considerably higher in mitochondrial fractions of these brain structures studied than in the synaptosomes; high contents of LHP and MDA was found in mitochondria. Activation of lipid peroxidation appears to be distinctly responsible for impairment of the structure and functional components of nervous cells occurring during long-term starvation.

Animals↗
PubMed1993

Ultrastructural alterations of the rat intestinal epithelium fed with polymeric, oligopeptidic or elementary full diet, following starvation.

In this study the ultrastructure of rat jejunal epithelial cells was examined, following a starvation period of 72 hours and an enteral refeeding period of 12 days, with either Nutrison, Pepti 2000, or Nutri 2000. Most changes occurred in the animals examined immediately after the 72-hour starvation period; these mainly included a significant decrease in microvilli population, occasional cell membrane disintegration, and a usual microvesicular appearance and degranulation of the rough endoplasmic reticulum. No alterations were found in the normally-fed animals (control group). This was also practically the same for the Pepti 2000 group. In the Nutrison group, a small amount of changes were found, while in the Nutri 2000 group many alterations were detected, which nevertheless were fewer than in the starved animals. The results demonstrate that the micromorphological alterations of the intestinal epithelium caused by starvation improve faster when an oligopeptidic formula is provided, which consequently results in faster and better absorption of the nutrients.

Amino Acids↗
PubMed1993

Opposite response to starvation of Trp/LNAA ratio in lean and obese Zucker rats.

Total blood and plasma free amino acids and plasma urea levels were studied in fed and 24 h fasted Zucker rats. In fed animals there were no differences between obese and lean rats in the overall essential and non essential blood free amino acids. However, starvation reduced blood amino acid levels in the obese animals compared to the lean group, mainly due to changes in the plasma compartment. The reduction of available amino acids from plasma in the obese rats during starvation affected most of the amino acids, including the branched chain amino acids, which showed higher levels in the fed situation than in lean rats. Of particular interest is the opposite response to starvation in lean and obese Zucker rats concerning the plasma ratio of tryptophan (Trp) to the large neutral amino acids (LNAA) which could be implicated in the alteration of food intake and energy expenditure characteristic of obesity.

Amino Acids↗
PubMed1977

Uncomplicated starvation versus cancer cachexia.

Host starvation is a common accompaniment to the presence of cancer. Diminished intake is a major contributor to this starvation and does not require that the oropharynx or gastrointestinal tract be the primary site. There is suggestive evidence that the normal adaptive mechanisms of the nontumor-bearing host to starvation that result in body protein conservation are not functioning in the tumor-bearing host. Cancer cachexia has some similarity to the metabolic disturbances of host metabolism that are seen in major injury or sepsis. The growing tumor shows little respect for normal constraints of host tissue growth. With the widespread availability of methods of total parenteral nutrition, the interrelationship of nutrition and host-tumor growth assumes greater importance.

Animals↗
PubMed1996

Differential catch-up in body weight and bone growth after short-term starvation in rats.

Catch-up or compensatory growth is known as a physiological phenomenon. However, most studies of catch-up growth were based on measurements of body weight, whereas changes in longitudinal bone growth remained largely undescribed. The present study describes the dynamics of both weight and longitudinal bone growth using mikro-knemometry, during normal feeding, severe food restriction (starvation), and refeeding of 14 intact and 28 GH-deficient male rats. Starvation induced rapid weight loss (P < 0.001), and stunted leg growth (P < 0.001). Refeeding led to rapid catch-up in weight of up to 4 times above normal daily weight gain, both in intact and GH-deficient animals, whereas an equivalent compensation of lower leg growth remained undetectable. Intact and GH-deficient animals show a circaseptan spontaneous variation of growth velocity (mini growth spurts). During starvation, mini growth spurts disappear, and return to normal after refeeding with no evidence of catch-up. In GH-deficient animals, GH (1 IU/rat, administered twice daily s.c. at 10:00 hand 16:00 h) was capable of augmenting catch-up in weight and, to a lesser extent, in leg length increment.

Animal Nutritional Physiological Phenomena↗
PubMed1998

Fetal hemoglobin in starvation ketosis of young women.

Ketones can reactivate the production of fetal hemoglobin (HbF) in vitro and in vivo. A reactivation of HbF by ketones, which are generated during starvation, remains largely speculative. Therefore, we investigated HbF in 31 women with anorexia nervosa or bulimia, using both of these as models of intermittent starvation ketosis. For comparison, we also studied 42 female control subjects matched for age. beta-Hydroxybutyrate levels were higher in patients than in controls (460 +/- 90 v 110 +/- 20 mumol/L; P < .0001). We correlated beta-hydroxybutyrate, metabolic, and hematologic parameters with HbF. HbF was measured with high pressure liquid chromatography. The data were analyzed with logistic regression analysis. An elevated HbF fraction (> 0.87%) was observed four times as often in patients than in controls (29% v 7%, P = .01). After adjustment for age, we found HbF elevations associated with beta-hydroxybutyrate levels (P = .005). No other correlations between the various metabolic/ hematologic parameters and HbF were significant. In conclusion, beta-hydroxybutyrate generated in starvation is associated with increased levels of HbF. Thus, unrestrained lipolysis can produce beta-hydroxybutyrate in sufficient quantities to induce a clinically measurable amount of HbF. These findings suggest that intermittent ketosis might also explain some increases of HbF in type 1 diabetes and pregnancy.

Adolescent↗
PubMedDate not supplied

[Effect of starvation on the metabolism of the xenobiotic p-nitroanisole in isolated hepatocytes of rats of both sexes].

Hepatocytes isolated from fed female rats are characterized by the lower contents of cytochrome P-450 and more slowly metabolize the xenobiotic p-nitroanisole (p-NA) than hepatocytes from males. The starvation does not change the cytochrome P-450 contents, but depresses the p-NA biotransformation. The inhibition of p-NA O-demethylation capacity is a result of insufficiently reduced equivalent supply, because the addition of exogenous NADPH to the cells with digitonin-permeabilized plasma membrane increases p-nitrophenol (p-NPh) formation. In the presence of exogenous NADPH hepatocytes from fasting male and female rats produce more p-NPh, than those from fed ones. That suggests the induction of xenobiotic biotransformation system during starvation. Sex differences in response of xenobiotic biotransformation system to starvation manifest themselves in different ratio in contents of free and conjugated p-NPh.

Animals↗
PubMed1996

The S. cerevisiae nitrogen starvation-induced Yvh1p and Ptp2p phosphatases play a role in control of sporulation.

Starvation for nitrogen in the absence of a fermentable carbon source causes diploid Saccharomyces cerevisiae cells to leave vegetative growth, enter meiosis, and sporulare; the former nutritional condition also induces expression of the YVH1 gene that encodes a protein phosphatase. This correlation prompted us to determine whether the Yvh1p phosphatase was a participant in the network that controls the onset of meiosis and sporulation. We found that expression of the IME2 gene, encoding a protein kinase homologue required for meiosis- and sporulation-specific gene expression, is decreased in a yvh1 disrupted strain. We also observed a decrease, albeit a smaller one, in the expression of IME1 which encodes an activator protein required for IME2 expression. Under identical experimental conditions, expression of the MCKI and IME4 genes (which promote sporulation but do not require Ime1p for expression) was not affected. These results demonstrate the specificity of the yvh1 disruption phenotype. They suggest that decreased steady-state levels of IME1 and IME2 mRNA were not merely the result of non-specific adverse affects on nucleic acid metabolism caused by the yvh1 disruption. Sporulation of a homozygous yvh1 disruption mutant was delayed and less efficient overall compared to an isogenic wild-type strain, a result which correlates with decreased IME1 and IME2 gene expression. We also observed that expression of the PTP2 tyrosine phosphatase gene (a negative regulator of the osmosensing MAP kinase cascade), but not the PTP1 gene (also encoding a tyrosine phosphatase) was induced by nitrogen-starvation. Although disruption of PTP2 alone did not demonstrably affect sporulation or IME2 gene expression, sporulation was decreased more in a yvh1, ptp2 double mutant than in a yvh1 single mutant; it was nearly abolished in the double mutant. These data suggest that the YVH1 and PTP2 encoded phosphatases likely participate in the control network regulating meiosis and sporulation. Expression of YVH1 and PTP2 was not affected by nitrogen source quality (asparagine compared to proline) suggesting that nitrogen starvation-induced YVH1 and PTP2 expression and sensitivity to nitrogen catabolite repression are on two different branches of the nitrogen regulatory network.

Cell Cycle Proteins↗
PubMed2000

Cell death induced by TNF or serum starvation is independent of ErbB receptor signaling in MCF-7 breast carcinoma cells.

The ErbB receptor tyrosine kinase family consists of the epidermal growth factor (EGF) receptor (ErbB1) and three related receptors (ErbB2, ErbB3, ErbB4). Their intrinsic tyrosine kinases can be activated by receptor-dimerization induced by numerous ligands or overexpression. ErbB receptors are frequently overexpressed in breast cancer, and their overexpression is associated with protection from apoptosis. To directly assess their role in apoptosis sensitivity of breast cancer cells, we established MCF-7 breast carcinoma cell lines overexpressing each ErbB receptor alone or in all possible pairs. Overexpression of ErbB1, ErbB2 and ErbB4 receptors was enough to activate them as judged by their phosphorylation, whereas co-expression of other ErbB receptors was necessary for the phosphorylation of the ErbB3. Surprisingly, overexpression of the ErbB receptors even when combined with treatment with their ligands (EGF, transforming growth factor alpha, betacellulin, neuregulins) failed to protect the MCF-7 cells from cell death induced by either tumor necrosis factor (TNF) or serum starvation. During starvation TGF-alpha, however, increased the cell size of the ErbB1 overexpressing cell line, and neuregulin1-beta1 increased that of all cell lines. In conclusion, our data does not support the role of ErbB receptors in the regulation of cell death induced by TNF or serum starvation, and the observed association in breast cancer may be due to other concomitant changes.

Breast Neoplasms↗
PubMed2000

Biomass evolution in porous media and its effects on permeability under starvation conditions.

The purpose of this study was to understand bacteria profile modification and its applications in subsurface biological operations such as biobarrier formation, in situ bioremediation, and microbial-enhanced oil recovery. Biomass accumulation and evolution in porous media were investigated both experimentally and theoretically. To study both nutrient-rich and carbon-source-depleted conditions, Leuconostoc mesenteroides was chosen because of its rapid growth rate and exopolymer production rate. Porous micromodels were used to study the effects of biomass evolution on the permeability of a porous medium. Bacterial starvation was initiated by switching the feed from a nutrient solution to a buffer solution in order to examine biofilm stability under nutrient-poor conditions. Four different evolution patterns were identified during the nutrient-rich and nutrient-depleted conditions used in the micromodel experiments. In phase I, the permeability of the porous micromodel decreased as a result of biomass accumulation in pore bodies and pore throats. In phase II, starvation conditions were initiated. The depletion of nutrient in the phase II resulted in slower growth of the biofilm causing the permeability to reach a minimum as all the remaining nutrients were consumed. In phase III, permeability began to increase due to biofilm sloughing caused by shear stress. In phase IV, shear stress remained below the critical shear stress for sloughing and the biofilm remained stable for long periods of time during starvation. The critical shear stress for biofilm sloughing provided an indication of biofilm strength. Shear removal of biofilms occurred when shear stress exceeded critical shear stress. A network model was used to describe the biofilm formation phenomenon and the existence of a critical shear stress. Simulations were in qualitative agreement with the experimental results, and demonstrate the existence of a critical shear stress.

Biomass↗
PubMed1991

Tumor cytokinetic effects of acute starvation versus polyamine depletion in tumor-bearing mice.

Previous investigations in our laboratory have demonstrated that both acute host starvation and polyamine depletion by means of the irreversible ODC-inhibitor (ODC = ornithine-decarboxylase) fluoro-methylornithine (DFMO) lead to pronounced growth retardation of rapidly proliferating tumors. The aim of this investigation was to elucidate how these different interventions affect cell kinetics and cell cycle phases in vivo. Adult nongrowing mice (C57Bl/J) bearing a poorly differentiated rapidly growing methylcholanthrene induced sarcoma were used. Combined measurements of bromodeoxyuridine incorporation into DNA and flow cytometric techniques were used. Starvation and DFMO treatment resulted in a prolonged cell cycle transit compared to freely fed animals. Tumor cells from DFMO-treated mice demonstrated an increased time for DNA synthesis and a relatively larger accumulation of cells in the G2M phase, whereas tumor cells from starved animals were accumulated in the G0G1 phase. The fractional cell loss of tumor cell during proliferation was calculated to be around 18% higher in DFMO-treated animals compared to starved and freely fed tumor-bearing mice. This study demonstrates that different mechanisms are involved in tumor growth suppression from substrate deficiency (starvation) and from inhibition of polyamine synthesis.

Animals↗
PubMed2004

Stem cell dynamics during growth, feeding, and starvation in the basal flatworm Macrostomum sp. (Platyhelminthes).

Development, growth, and regeneration in Macrostomum are based--as in all Platyhelminthes--on likely totipotent stem cells (neoblasts), basic for all Bilaterians. We demonstrate dynamics and migration of neoblasts during postembryonic development, starvation, and feeding of Macrostomum sp. Double labeling of S-phase and mitotic cells revealed a fast cell turnover. Conflicting with recent results from planarians, we have some indication of slow cycling neoblasts. As in planarians, starvation dramatically reduced mitotic activity and a very basic level was maintained after 30 days of starvation. Afterward, feeding induced a dramatic immediate proliferative response probably caused by G2-arrested neoblasts. The following 12 hr showed a significant mitotic decline, caused by the depletion of the G2 neoblast pool. Neoblasts that pass through S-phase led to a maximum of mitoses after 48 hr. Our results allow deeper insight into cellular dynamics of an ancestral bilaterian stem cell system of a basal Platyhelminth.

Animals↗