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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Membrane vesicles derived principally from the plasma membrane and endoplasmic reticulum of mouse 3T3 cells transformed by Simian virus 40 take up alpha-aminoisobutyric acid (AIB) and phosphate (Pi). When NaCl is added simultaneously with AIB or Pi, uptake rises two- to three-times above the equilibrium to accumulate AIB or Pi over the control value, in the presence of a Na+ gradient, is almost lost in membrane vesicles derived from benzpyrene-transformed 3T3 cells (BP3T3) arrested in the G1 phase of the cell cycle by serum starvation. When added to the membranes with NaCl and the uptake substrate, a combination of fibroblast growth factor (FGF) and epidermal growth factor EGF restores the ability of the membranes to accumulate AIB and Pi over the control value.
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PMID:Uptake of alpha-aminoisobutyric acid and phosphate by membrane vesicles derived from growing and quiescent fibroblasts. 18 50

The objective of this study was to compare the fine structure of presumptive preneoplastic hepatocytes at various times during liver carcinogenesis with that of normal, developing, and regenerating liver and of hepatocellular carcinomas, using transmission and scanning electron microscopy. A new model of liver carcinogenesis was used in which several of the early steps are quite well synchronized. A single initiating dose of diethylnitrosamine induced isolated islands of altered hepatocytes. The cells were characterized by persistence of glycogen despite starvation, increase in smooth endoplasmic reticulum, and hypertrophic nucleoli. Following intense selection of the altered hepatocytes by dietary 2-acetylaminofluorene plus partial hepatectomy, the affected hepatocytes proliferated rapidly to produce basophilic foci. These early hyperplastic lesions revealed stellate-shaped dilated bile canaliculi lined by blebs and abnormally thick elongated microvilli, a decreased number of microvilli on the sinusoidal surface, a marked increase in smooth endoplasmic reticulum, large nucleoli, and bundles of pericanalicular microfilaments. A majority of the proliferating lesions reacquired a normal organizational pattern within several weeks after partial hepatectomy and could not be distinguished from normal liver. A small number continued to grow and become typical persistent hyperplastic nodules. These showed significant widening of intercellular spaces between hepatocytes, elongated microvilli over large regions of the cell surface, many invaginations of the cell membrane, and irregularly shaped bile canaliculi. Sequential changes in focal hyperplastic hepatocytes during carcinogenesis could be distinguished from normal, developing, and regenerating liver. The major differences involved the cell surfaces and cytoplasmic organelles. The findings are compatible with the hypothesis that a carcinogen may act by inducing alterations in a small number of hepatocytes and that hepatocellular carcinomas arise through stepwise evolutional changes in these cells.
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PMID:Sequential analysis of hepatic carcinogenesis: a comparative study of the ultrastructure of preneoplastic, malignant, prenatal, postnatal, and regenerating liver. 22 39

During diethylnitrosamine (DEN) administration, a distinctive difference was observed between rats and guinea-pigs in the sequence of ultrastructural changes in the hepatic endoplasmic reticulum (ER). In DEN-induced hepatic tumour cells in the guinea-pig there was extensive proliferation of the rough ER, while the smooth ER was quite sparse; in the premalignant liver the opposite was noted. This is in contrast to the rat, in which administration of either DEN or 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) brings about, in both premalignant and malignant hepatic tissue, proliferation of the smooth ER and sparsity of the rough ER. Yet, as in the rat, the number of ribosomes on the outer surface of the guinea-pig liver rough ER is greatly reduced and this is paralleled by a 49% decrease of the RNA/protein ratio as early as 4 weeks of nitrosamine administration. The decrease of RNA/protein ratio and ultrastructurally observed loss of ribosomes from the ER, following nitrosamine administration, correlate with a decrease of photometric response of microsomal suspensions to the sulphydryl probe, p-chloromercuribenzoate. While azo-dye-reductase activity is higher in untreated rats than in untreated guinea-pigs, feeding 3'-Me-DAB for 6 weeks brings about a 76% decrease in the rat, but no significant decrease in the guinea-pig, which is refractory to azo-dye carcinogenesis. Thus, the ability of the liver to inactivate the dye is greatly decreased in the rat, but not in the guinea-pig, as administration progresses toward the threshold dose for tumorigenesis. On the other hand, constitutive levels of nitrosamine dealkylase are identical in the 2 species and remain essentially unchanged following administration of DEN for 10 weeks. Inasmuch as nitrosamine dealkylation represents activating metabolism, this provides a rationale for the comparable susceptibility of the rat and guinea-pig to DEN carcinogenesis. Of the 2 enzymes in the 2 species, it is only azo-dye reductase in the guinea-pig which appears to be unregulated by glucose repression, since starvation brings about no change in this activity. Starvation-induced increase of azo-dye reductase in the rat is not influenced by administration of 3'-Me-DAB and only slightly by DEN. The starvation-induced increase of nitrosamine dealkylation is abolished, however, in both species by administration of DEN but only slightly decreased by 3'-Me-DAB.
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PMID:Ultrastructural and metabolic determinants of resistance to azo-dye susceptibility to nitrosamine carcinogenesis of the guinea-pig. 41 61

Changes in the parameters of the volumetric fractions of the main cytoplasmic organellae were studied in the subcutaneous connective of albino rats subjected to experimental dehydration and starvation. There were some common features in the histiocytes reaction under these conditions, i. e. hypertrophy of the lysosomal apparatus and cell "infiltration" with lipids. At the same time the following differences are emphasized: dehydration caused an increase of the volumetric mitochondrial fractions and of the rough endoplasmic reticulum, and starvation of the phagosomal fraction.
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PMID:[Ultrastructural changes in loose connective tissue histiocytes in dehydration and starvation]. 43 32

The histology and ultrastructure of the rat gastric mucosa were investigated during 168 hours of starvation. An increased desquamation of individual foveolar cells was found. In the preserved cells of the foveolae, the content of the PAS positive mucosubstances did not change during starvation, and no changes took place in the appearance and in the amount of the mucous granules at the electron microscopic investigation. The number of lipid droplets increased in the mucous foveolar cells within 24 and 48 hours. During starvation the mitochondria (mainly in the parietal cells) were enlarged and contained rare mitochondrial cristae. Some mitochondria were distintegrated and removed by lysosomes. The number of lysosomes (mainly cytosergresomes) was markedly increased n parietal cells. A collapse of the intracellular canaliculi occurred as well as a narrowing in the tubulovesicular profiles. In chief cells the profiles of the granular endoplasmic reticulum and Golgi apparatus were reduced. It was shown that the ultrastructural changes induced by starvation can be interpreted functionally in changed histochemical parameters of the gastric mucosa.
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PMID:Influence of starving on the rat gastric mucosa -- light and electron microscopical findings. 59 Apr 16

An analysis of starvation and starvation followed by refeeding was undertaken to characterize some organismic, organ, and mitochondrial responses to these two circumstances. Body weight, organismic respiration as well as weight protein and succinic dehydrogenase activity for liver, kidney, and heart were determined over the course of 6 days of starvation and 5 days refeeding for adult male rats. Assays of marker enzyme activities for mitochondria (cytochrome oxidase), lysosomes (acid phosphatase), endoplasmic reticulum (glucose-6-phosphatase), and plasma membranes (5'-nucleotidase) were conducted for liver in addition to quantitations of mitochondrial protein. All enzyme determinations were done on whole tissue homogenates and reported as total organ activity. Liver mitochondria were harvested quantitatively directly from whole liver homogenates by zonal centrifugation for determination of mitochondrial protein. Starvation resulted in a major loss of body weight, organ weight, and organ protein; liver greater than kidney greater than heart. These changes were accompanied by a major reduction in organ succinic dehydrogenase activity; liver greater than kidney. In heart, succinic dehydrogenase was doubled in activity at day 2 of starvation and subsequently diminished to values not significantly lower than controls. In liver, mitochondrial mass (protein) was severely diminished. From analysis of marker enzyme activities, it appeared that lysosomes, endoplasmic reticulum, and plasma membrane were also decreased. Refeeding restored the greatest part of these losses within 5 days.
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PMID:Starvation and refeeding in rats: effect on organismic respiration, cytoplasmic constituents of liver, and succinic dehydrogenase activity in liver, kidney, and heart. 70 2

The effect of distension of the stomach by air (in vitro) upon the ultrastructural picture of gastric endocrine cells in rats starved for 72 hours was investigated. Distension of the stomach by air in vitro, lasting for 5, 10, 15 and 20 minutes, resulted in massive dissolution of gastrin granules that had accumulated in the course of starvation. In AL, D1, EC and ECL cells distension of the stomach by air failed to induce dissolution of granular content or release of granules by any other mechanism. In AL and D1 cells accumulation of secretory granules caused by starvation was observed, the ultrastructure of EC and ECL cells remained unchanged both under the effect of starvation and distension. Dilatation of endoplasmic reticulum profiles as well as other changes on some cell organelles observed on endocrine cells after distension of the stomach by air in vitro are due to the effect of autolysis.
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PMID:Experimental ultrastructural study on stimulation of the rat gastric endocrine cells. In vitro distension of the stomach by air inflation. 74 12

The pyloric gland of Styela clava contains large glycogen deposits that are digested by treatment with alpha amylase and depleted by 15 days starvation. The deposits are surrounded by cytoplasmic regions containing smooth endoplasmic reticulum and mitochondria. The cells also have rough endoplasmic reticulum, Golgi cisterns, lysosomes, microvilli, cilia, and lateral infoldings of the plasma membrane. The fine structure of the pyloric cells and the position of tubules between the absorptive epithelium and general circulation suggest that the gland functions as the vertebrate liver in carbohydrate metabolism. The pyloric cells of Styela do not appear to be excretory in a "renal" sense, since there is no infolding of the basal plasmalemma and mitochondria are usually associated only with the glycogen deposits. However, a hepatic-like excretory role is consistent with current findings. In light of the phylogenic affinities of vertebrates and ascidians, it is possible that the pyloric gland is homologous to the liver.
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PMID:Glycogen deposits in the pyloric gland of the ascidian Styela clava (Urochordata). 83 94

The ultrastructure of the epithelial cells in the posterior part of the midgut in female Aedes aegypti was partly changed after starvation periods of 5 or 8 days. Most obvious is a drastic reduction of the amount of rough endoplasmic reticulum (rer), which is responsible for the synthesis of enzymes for blood digestion. A similar influence on rer membranes is to be observed in mosquitoes fed on sucrose solution only, without additional blood meals.
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PMID:Ultrastructural changes in midgut cells of female Aedes aegypti L. (Insecta, Diptera) after starvation or sugar diet. 83 8

Search for the elucidation of the mode of action of amphetamines has revealed that this drug brought about changes in the activity of some enzymes bound to the hepatic endoplasmic reticulum of the pregnant and non-pregnant rat. Amphetamine administration caused loss of appetite and changes in enzyme activity due to starvation, however, its effects were assessed applying pair-feeding conditions. Drug-metabolizing activity was increased by amphetamine as measured by coumarin 3-hydroxylase and aminopyrine N-demethylase in both pregnant and non-pregnant animals; aniline hydroxylase was elevated only in pregnant rats. These changes were associated with the enhanced synthesis of microsomal phospholipids as indicated by the increased activity of [14C-Me]S-adenosyl-L-methionine : microsomal phospholipid methyl transferase, de novo synthesis and levels of microsomal phospholipids. These effects were mainly manifest in phosphatidylethanolamine and phosphatidylcholine fractions. Glucose-6-phosphatase activity remained unaltered by amphetamine. Pregnancy alone brought about a reduction of all these microsomal parameters. The rise of hepatic drug metabolism following the administration of amphetamine indicated a compensatory mechanism by means of stimulating enzyme induction processes.
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PMID:Effect of amphetamine on the hepatic endoplasmic reticulum of the pregnant rat. 84 87


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