Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Metabolic response of adult quail to fasting or refeeding was studied by measuring the main blood and hepatic metabolites. Moreover, the fine structure of hepatocytes in these physiological conditions was described. 2. Starvation or refeeding did not affect glycemia in male as in female quails. 3. Fasting had no effect on plasma free fatty acids in female quails, whereas plasma triglycerides were markedly decreased. 4. In fasted quails, there was an active ketogenesis with a high 3-hydroxybutyrate/acetoacetate ratio. 5. Ultrastructural aspect of liver parenchymal cells from fasted quails revealed alterations in the quantity of glycogen, smooth endoplasmic reticulum, lysosomes and in the form of the rough endoplasmic reticulum. 6. The significance of these morphological changes was discussed in relation to an hormonal stimulation.
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PMID:Changes in glucose and lipid metabolism in starved or starved-refed Japanese quail (coturnix coturnix japonica) in relation to fine structure of liver cells. 613 30

Cytoplasmic protein in hepatocytes is sequestered and degraded by two general classes of lysosomes, overt autophagic vacuoles (macroautophagy) and dense bodies (microautophagy). Volumes of the apparent space in each class that contain the internalized protein, together with estimates of cytoplasmic protein concentration, were used as a basis for predicting rates of protein degradation by the lysosomal system in livers of fed, 48-hr starved, and starved-refed mice. Assuming that the turnover of all sequestered protein is equal to that previously determined in overt autophagic vacuoles (0.087 min-1), we obtained close agreement between predicted and observed rates in the three conditions studied. The two autophagic components, though, exhibited different patterns of regulation. Microautophagy followed a downward course through starvation and into refeeding, a trend that explained fully the fall in absolute rates of protein degradation during starvation. By contrast, macroautophagy remained constant throughout starvation but was virtually abolished with refeeding. Whereas regulation of the latter can be explained largely by immediate responses to the supply of amino acids, present evidence together with results of others indicate that microsequestration could be linked to functional and quantitative alterations in the smooth endoplasmic reticulum. Both types of regulation contributed equally to the marked suppression of proteolysis during cytoplasmic regrowth.
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PMID:Quantitative correlation between proteolysis and macro- and microautophagy in mouse hepatocytes during starvation and refeeding. 634 Jan 16

A colorimetric method for the determination of lipid phosphorus in the nanomolar range was used to determine the total phospholipid content of isolated pancreatic islets. Freshly isolated islets of lean C57BL/6J mice contained significantly more phospholipids expressed per micrograms DNA as compared to C57BL/6J (ob/ob) mouse or Wistar rat islets. Starvation for 48 h (Wistar rats) or 60 h (NMRI mice) did not affect the islet phospholipid content. Phosphatidylcholine was the most abundant phospholipid class of NMRI mouse islets, followed by phosphatidylethanolamine, sphingomyelin, phosphatidylinositol, phosphatidylserine and lysophosphatidylcholine. When islets of NMRI mice were maintained for 5-7 days in tissue culture, the phospholipid content remained unchanged as compared to that of freshly isolated islets despite a considerable loss of the insulin stores. The islet phospholipid content was significantly increased when the glucose concentration of the culture medium was elevated from 3 to 28 mM. Leucine (10 mM) added to a low-glucose medium failed to increase the islet phospholipid content. Addition of glipizide (2 microM) to the culture medium decreased the islet insulin content significantly but failed to affect the total islet phospholipid content. Culture in a Ca2+-free medium containing 28 mM glucose increased the islet insulin content but, again, the phospholipid content remained unaffected. These data show that changes of the total phospholipid content of pancreatic islets are unrelated to the islet insulin content and presumably also to the content of secretory granules. Alterations of the islet content of phospholipids may rather reflect changes of the amount of endoplasmic reticulum of the islet cells.
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PMID:Effects of starvation and different culture conditions on the phospholipid content of isolated pancreatic islets. 639 54

Ineffective alfalfa nodules formed by Rhizobium meliloti nif::Tn5 mutants were examined by light and electron microscopy. R. meliloti nifH::Tn5 mutants formed nodules that were similar in structure to wild-type nodules except that nifH- bacteroids accumulated a compact, electron-dense body. In contrast to nodules induced by wild type and nifH mutants, nifDK- R. meliloti mutants induced nodules which contained numerous starch grains and prematurely senescent bacteroids. In addition, meristematic activity in nifDK- nodules ceased significantly earlier than in nifH- nodules. All mutant nodules exhibited elevated levels of rough endoplasmic reticulum and Golgi membranes compared to wild-type nodule cells. These elevated levels may reflect either a response to nitrogen starvation in the ineffective nodules or an abnormal synthesis and export of nodule-specific proteins during later developmental stages.
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PMID:Ultrastructural analysis of ineffective alfalfa nodules formed by nif::Tn5 mutants of Rhizobium meliloti. 657 11

The ultrastructure of the absorptive cells in the duodenum, jejunum and ileum after 7, 14 and 21 days of starvation was investigated using rats aged from 12 to 18 months weighing about 500 g. In the basal cytoplasm of the absorptive cells (in the duodenum and ileum of 21-day-starved rats and the jejunum of 14- and 21-day-starved rats), the following changes were found: atrophied mitochondrion-like bodies, small vesicles, a short and sparse rough-surfaced endoplasmic reticulum and a lack of density in a portion of the cytoplasm. Moreover, many autolysosomes of various sizes and shapes were encountered in the basal cytoplasm; occasionally these elements accumulated and appeared to fuse to one another. In contrast, in the apical cytoplasm of absorptive cells in the intestine of starved rats, the ultrastructure was similar to that of control rats. It was considered that the apical cytoplasm of the absorptive cells in the starved rat intestine might be preserved as long as possible during starvation in order to absorb nutrients when they become available again.
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PMID:Ultrastructure of the absorptive cells in the small intestine of the rat during starvation. 667 8

The cytological development of the silk gland has been studied by light and electron microscopy in silkworms experimentally starved at different periods of the natural feeding stage during the fifth instar. When newly molted animals are not provided with food, no sign of growth is observed. Starvation initiated early during the obligatory feeding period, stops cell growth and development of the organelles involved in protein synthesis and secretion, whereas it induces the appearance of organelles concerned with autolysis. These effects are reversible if starvation is not prolonged beyond two days. Starvation during the facultative feeding period, at the time of massive fibroin production, results in quantitative and qualitative modifications of organelles related to the decrease of fibroin production and the onset of autolysis. Rough endoplasmic reticulum, responsible for fibroin synthesis, forms transitory whorls. Fibroin transport via the Gjolgi apparatus and secretion of the protein into the gland lumen decrease parallel to fibroin synthesis, so that no fibroin storage can be detected in any organelle. After food deprivation, autophagosomes and secondary lysosomes rapidly develop in the cytopolasm, and if starvation continues portions opf the cytoplasm are sequestered and completely destroyed. If animals are refed, fibroin production is resumed and autolysis declines. These ultrastructural alterations of the silk gland during experimental starvation are very similar to those observed during the periods of physiological starvation (molt and cocoon spinning) and generally considered to be under hormonal control. Our results raise the question of the nature of interactions between alimentary and hormonal factors which control silk-gland development.
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PMID:The programming of silk-gland development in Bombyx mori. I. Effects of experimental starvation on growth, silk production, and autolysis during the fifth larval instar studied by electron microscopy. 746 3

The results of an electron microscopic study of the changes in hepatocytes induced by chronic intoxication with thioacetamide are reported. During the poisoning aspecific toxic changes are intermingled with progressive, preneoplastic ones. The main cell subpopulations identified are: 1) large hepatocytes with smooth endoplasmic reticulum (SER) hypertrophy, with or without rough endoplasmic reticulum (RER) neoformation and glycogen storage, which is starvation resistant; 2) smaller hepatocytes, where RER hypertrophy and ribosome accumulation are the prominent features. Such a pattern persists for months. After the withdrawal of the drug most of the cell changes disappear. However, during this time a simplification of the liver structure and cell composition takes place, allowing a sequence of cell events which seem relevant for establishment of neoplastic progression. The SER-hypertrophied cell appears first and gives rise, via several intermediate stages, to the RER-hypertrophied one, which is believed to play a key role as the ultimate precursor of cancer cells.
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PMID:Long-term evolution of the main changes induced by thioacetamide on hepatocytes. 746 22

The composition of phospholipids, sphingolipids, and sterols in the plasma membrane has a strong influence on the activity of the proteins associated or embedded in the lipid bilayer. Since most lipid-synthesizing enzymes in Saccharomyces cerevisiae are located in intracellular organelles, an extensive flux of lipids from these organelles to the plasma membrane is required. Although the pathway of protein traffic to the plasma membrane is similar to that of most of the lipids, the bulk flow of lipids is separate from vesicle-mediated protein transport. Recent advances in the analysis of membrane budding and membrane fusion indicate that the mechanisms of protein transport from the endoplasmic reticulum to the Golgi and from the Golgi to plasma membrane are similar. The majority of plasma membrane proteins transport solutes across the membrane. A number of ATP-dependent export systems have been detected that couple the hydrolysis of ATP to transport of molecules out of the cell. The hydrolysis of ATP by the plasma membrane H(+)-ATPase generates a proton motive force which is used to drive secondary transport processes. In S. cerevisiae, many substrates are transported by more than one system. Transport of monosaccharide is catalyzed by uniport systems, while transport of disaccharides, amino acids, and nucleosides is mediated by proton symport systems. Transport activity can be regulated at the level of transcription, e.g., induction and (catabolite) repression, but transport proteins can also be affected posttranslationally by a process termed catabolite inactivation. Catabolite inactivation is triggered by the addition of fermentable sugars, intracellular acidification, stress conditions, and/or nitrogen starvation. Phosphorylation and/or ubiquitination of the transport proteins has been proposed as an initial step in the controlled inactivation and degradation of the target enzyme. The use of artificial membranes, like secretory vesicles and plasma membranes fused with proteoliposomes, as model systems for studies on the mechanism and regulation of transport is evaluated.
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PMID:The plasma membrane of Saccharomyces cerevisiae: structure, function, and biogenesis. 760 12

Legionella pneumophila replicates within a membrane-bounded compartment that is studded with ribosomes. In this study we investigated whether these ribosomes originate from the cytoplasmic pool or are associated with host endoplasmic reticulum (ER). Immunofluorescence and electron microscopic localization studies of ER proteins in macrophages infected with L. pneumophila indicated that the bacteria reside in a compartment surrounded by ER. An L. pneumophila mutant that grows slowly in macrophages was slow to associate with host ER, providing genetic evidence in support of the hypothesis that this specialized vacuole is required for intracellular bacterial growth. Ultrastructural studies, in which the ER luminal protein BiP was labeled by immunoperoxidase cytochemistry, revealed that L. pneumophila replication vacuoles resemble nascent autophagosomes. Furthermore, short-term amino acid starvation of macrophages, which stimulated host autophagosomes. Furthermore, short-term amino acid starvation of macrophages, which stimulated host autophagy, increased association of the bacteria with the ER and enhanced bacterial growth. These results are compatible with the hypothesis that L. pneumophila exploits the autophagy machinery of macrophages to establish an intracellular niche favorable for replication.
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PMID:Association of Legionella pneumophila with the macrophage endoplasmic reticulum. 764 98

Morphologic changes in the hepatocytes of tumour-bearing rats at the pre-cachectic and cachectic stages were studied by electron microscopy and were quantitatively analysed by a morphometric method. Ten male F-344 rats, subcutaneously inoculated with methylcholanthrene-induced sarcoma cells (TBR) were compared with ten pair-fed controls (CTR). There was no significant difference in the size of the cells or their nuclei, the number of mitochondria, or the number of lysosomes, between TBR and CTR at either the pre-cachectic or cachectic stage. Although the size of mitochondria of TBR was already significantly enlarged at the pre-cachectic stage, before the food intake of the TBR had decreased, the micro-structure within the mitochondria was unaltered. Marked differences were observed in the number, arrangement and distribution of the rough endoplasmic reticulum, all of which decreased significantly in TBR compared with CTR at both the pericentral and periportal zones. Changes at the periportal region were further pronounced at the cachectic stage. These results, distinct from the changes seen in simple starvation, may confirm a part of the biochemical evidence specific to tumour induced metabolic alterations.
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PMID:Ultrastructural alterations of hepatocytes in the tumour-bearing, cachectic rat. 773 32


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