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)

Experiments were performed to determine the effect of starvation on T-cell mediated host defences. In mice starved for 72 hr, the number of thymocytes fell by 98%, spleen cells by 82% and peripheral blood cells by 44%. By 7 days after the end of starvation, values had returned to within 50% of baseline. The percentage of L3T4 and Lyt-2 antigen-bearing cells fell in the thymus, but the percentage of Thy-1.2-positive cells did not change. Starvation decreased the percentage of lymphocytes in peripheral blood but increased the percentage of granulocytes. During starvation, the cellularity in thymuses, spleens and peripheral blood was preserved in adrenalectomized mice compared to normal or sham-adrenalectomized mice. Confirming previous results of ours, starved mice were resistant to i.v. challenge with Listeria monocytogenes immediately after starvation. However, when starved mice were immunized with a sublethal dose of Listeria immediately after starvation and challenged 3-4 weeks later, they were less resistant to Listeria than fed, immunized mice. Similarly, spleen cells of starved, immunized mice had a reduced capacity to transfer immunity passively to non-immune mice. Increasing the immunizing dose of Listeria in starved mice increased the level of immunity that developed. These data indicate that starved mice have a marked reduction in T-cell cellularity, possibly related to corticosteroid production during the stress of starvation. Although starved mice were relatively resistant to Listeria immediately after starvation, they had a reduced capacity to develop T-cell mediated immunity to Listeria. This deficiency could be partly overcome by increasing the immunizing dose of Listeria.
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PMID:Acute starvation in mice reduces the number of T cells and suppresses the development of T-cell-mediated immunity. 325 7

A delayed wasting syndrome similar to that induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was observed in male Sprague-Dawley rats exposed to 3,3', 4,4'-tetrachloroazoxybenzene (TCAOB) and 3,3',4,4'-tetrachloroazobenzene (TCAB). After a slow growth period, all treatment animals (25 mg/kg, i.p., 2 doses per week) exhibited a starvation-like syndrome characterized by reduced food intake, dramatic loss of body weight and subsequent death. Although the growth of all major organs in the treatment animals was affected, the thymus appeared severely atrophied. The growth kinetics during the earlier phase were further analyzed using serially-killed rats receiving TCAOB. In addition, TCAOB was found to markedly depress the specific activity (mumol/min/g wet liver) of glucose-6-phosphatase, fructose-1,6-bisphosphatase, phosphoenolpyruvate carboxykinase, and pyruvate kinase in the liver. Significant changes in the levels of cytochrome P-450, glutamic-pyruvic transaminase and malic enzyme in the liver were also observed.
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PMID:Delayed wasting syndrome and alterations of liver gluconeogenic enzymes in rats exposed to the TCDD congener 3,3', 4,4'-tetrachloroazoxybenzene. 401 2

The uptake of nucleosides and the synthesis of RNA in Tetrahymena thermophila were examined following amino acid starvation. Omission of leucine, phenylalanine, or arginine from the medium resulted in a rapid decrease in the incorporation of [3H]uridine into the acid-soluble pool and acid-insoluble material (RNA). Amino acid starvation inhibited the uptake of all ribo- and deoxyribonucleosides tested but did not affect the uptake of amino acids or glucose. In addition, under the conditions used, the omission of an amino acid did not result in a large decrease in amino acid incorporation into total protein. Treatment of cells with cycloheximide or emetine gave results similar to the effects of amino acid starvation, but in these experiments the inhibition of protein synthesis was essentially complete. Nucleotide pool sizes were also measured following amino acid starvation. ATP and UTP levels were essentially unchanged, but the dTTP pool size was decreased by 40%. The decrease in RNA synthesis in vivo in the absence of an essential amino acid was reflected in the endogenous RNA synthetic activity of isolated nuclei. However, when solubilized RNA polymerase activity was measured with calf thymus DNA as template, no significant difference was observed between control and amino acid-starved cells.
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PMID:The effect of amino acid starvation on nucleoside uptake and RNA synthesis in Tetrahymena. 615 97

The activity of ornithine decarboxylase, the rate-controlling enzyme in polyamine biosynthesis, was determined in tissues of normal control rats and rats made diabetic with streptozotocin. In untreated diabetic rats fed ad libitum, ornithine decarboxylase activity was markedly diminished in liver, skeletal muscle, heart and thymus. Ornithine decarboxylase was not diminished in a comparable group of diabetic rats maintained on insulin. Starvation for 48h decreased ornithine decarboxylase activity to very low values in tissues of both normal and diabetic rats. In the normal group, refeeding caused a biphasic increase in liver ornithine decarboxylase; there was a 20-fold increase in activity at 3h followed by a decrease in activity, and a second peak between 9 and 24h. Increases in ornithine decarboxylase in skeletal muscle, heart and thymus were not evident until after 24-48h of refeeding, and only a single increase occurred. The increase in liver ornithine decarboxylase in diabetic rats was greater than in normal rats after 3h of refeeding, but there was no second peak. In peripheral tissues, the increase in ornithine decarboxylase with refeeding was diminished. Skeletal-muscle ornithine decarboxylase is induced more rapidly when meal-fed rats are refed after a period without food. Refeeding these rats after a 48h period without food caused a 5-fold increase in ornithine decarboxylase in skeletal muscle at 3h in control rats but failed to increase activity in diabetic rats. When insulin was administered alone or together with food to the diabetic rats, muscle ornithine decarboxylase increased to activities even higher than in the refed controls. In conclusion, these findings indicate that the regulation of ornithine decarboxylase in many tissues is grossly impaired in diabetes and starvation. They also suggest that polyamine formation in vivo is an integral component of the growth-promoting effect of insulin or some factor dependent on insulin.
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PMID:Ornithine decarboxylase activity in insulin-deficient states. 701 16

Morphologic examinations of liver, spleen, mesenteric lymph nodes and groups of lymphatic follicles of small intestine (Peyer's patchs) of rats in condition of starvation were shown. Starvation of animals for 48 hours and most for 96 hours was caused statistic reliable decrease of body mass, concerning mass of thymus and liver. Centrolobular fatty infiltration and decrease of RNA and glycogen contents in hepatocytes of liver were shown. Decrease of content of small lymphocytes of T-dependent zones and alteration of cell's representation in B-dependent zones were discovered.
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PMID:[Morphologic changes of peripheral lymphoid tissue and liver in experimental animals under food deprivation]. 753 86

1. A systematic study is reported on the control of 1-phosphatidylinositol 4-kinase (PI kinase) and PI 4-phosphate 5-kinase (PIP kinase), enzymes of the phosphatidylinositol phosphorylation pathway which leads to the production of second messengers. IP3 and DAG. In liver of normal male, adult, fed Wistar rats the steady state activity of PI kinase was 0.5 +/- 0.01 and that of PIP kinase was 0.046 +/- 0.003 nmol/hr/mg protein. The concentration of IP3 was 1.8 +/- 0.1 pmol/mg protein. 2. That the two kinases have short half-lives was observed in starvation. where in the rat liver or bone marrow activities rapidly decreased and on refeeding were restored in a day. Injection to rats of the protein synthetic inhibitor, cycloheximide, yielded t1/2 = 80 min for the two enzymes in bone marrow and t1/2 = 80 min in liver. 3. Linkage of the signal transduction enzymes with proliferation was shown by the high activities as compared to liver of these enzymes in rat organs of high cell renewal capacity, e.g., thymus, bone marrow, spleen and testes. 4. Linkage with malignant proliferation was indicated by the observation that in rat hepatomas the enzyme activities increased 5- to 9-fold and were highest in rapidly growing hepatoma 3924A (29- and 45-fold). 5. In human primary ovarian carcinoma PI and PIP kinase activities were elevated 4.4 and 2.9-fold, respectively, and in OVCAR-5 cells, 32- and 11-fold, respectively. Similar increases were observed in MDA-MB-435 human breast carcinoma cells in comparison with normal breast parenchymal cells. 6. The linkage of signal transduction enzyme activities with malignant proliferation was also observed in experiments when human breast carcinoma cells were plated in flasks and expressed their proliferative capacity in the log phase. PI and PIP kinase activities steadily and coordinately increased to a peak 11-fold rise in mid-log phase. In late log and plateau phases the kinase activities gradually declined to the starting level. Similar observations were made for the two enzymes in human ovarian carcinoma OVCAR-5 cells and in rat hepatoma 3924A cells in tissue culture. 7. In animals injected with cycloheximide the bone marrow PI and PIP kinase activities exhibited t1/2 = 0.12 hr, the shortest decay rate in comparison with 8 enzymes of purine and pyrimidine biosynthesis with t1/2 = 0.6 to 4.3 hr. 8. Injection of tiazofurin decreased PI and PIP kinase activities in the bone marrow with t1/2 = 82 and 78 min, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Regulation of signal transduction. 757 37

Although various types of stress induce thymus atrophy and suppress immune functions, the mechanisms involved are unknown. To test the hypothesis that thymocyte apoptosis plays a role in stress-induced atrophy of the thymus, we studied the effects of starvation and hypoglycemia on the thymus in the rat. Administration of insulin caused marked hypoglycemia, increased the plasma corticosterone level, and induced fragmentation of thymocyte DNA in fasted but not in fed rats. Administration of either glucose or RU486, a glucocorticoid receptor antagonist, inhibited the apoptosis of thymocytes elicited by insulin. Available evidence suggest that insulin-induced hypoglycemia causes thymocyte apoptosis by promoting glucocorticoid secretion from the adrenal gland.
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PMID:Insulin-induced hypoglycemia elicits thymocyte apoptosis in the rat. 969 84

Thymic atrophy is a prominent feature of malnutrition. Forty-eight hours' starvation of normal mice reduced the total thymocyte count to 13% of that observed in freely fed controls, predominantly because of a diminution in the cortical CD4(+)CD8(+) thymocyte subpopulation. Prevention of the fasting-induced fall in the level of the adipocyte-derived hormone leptin by administering exogenous recombinant leptin protected mice from these starvation-induced thymic changes. The ob/ob mouse, which is unable to produce functional leptin because of a mutation in the obese gene, has impaired cellular immunity together with a marked reduction in the size and cellularity of the thymus. We found that ob/ob mice had a high level of thymocyte apoptosis resulting in a ratio of CD4(+)CD8(+) (cortical) to CD4(-)CD8(-) (precursor) thymocytes that was 4-fold lower than that observed in wild-type mice. Peripheral administration of recombinant leptin to ob/ob mice reduced thymocyte apoptosis and substantially increased both thymic cellularity and the CD4(+)CD8(+)/CD4(-)CD8(-) ratio. In contrast, a comparable weight loss in pair-fed PBS-treated ob/ob mice had no impact on thymocyte number. In vitro, leptin protected thymocytes from dexamethasone-induced apoptosis. These data indicate that reduced circulating leptin concentrations are pivotal in the pathogenesis of starvation-induced lymphoid atrophy.
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PMID:Leptin protects mice from starvation-induced lymphoid atrophy and increases thymic cellularity in ob/ob mice. 1052 43

With the decline of the former main causes of death in early childhood--infections and starvation--sudden infant death syndrome (SIDS) has emerged as the most important single cause of postneonatal infant mortality. It has adopted the role of a major indicator for the standard of public health care. Despite extensive input into research, its pathophysiology has remained rather obscure. The resulting helplessness of scientists and health care professionals have lead to adherence to unconfirmed pathophysiological hypotheses and to pursuit of preventive strategies of doubtful efficacy. In this overview, the medical and technical background of five major hypotheses is being presented. A lot can be learnt from the history of their development, efforts to refute them, and the reasons for unreflected adherence to them. (1) Due to its illustrative nature, the so-called 'status thymico-lymphaticus', the theory of asphixation by an enlarged thymus, could not be eradicated although well-reknowned physicians--including the Austrian pathologist Paltauf--have repeatedly attempted to do so. (2) Assumed familiarity, an aspect which attracted the attention of pediatricians to SIDS initially has been excluded, but an increased risk of SIDS for the siblings of affected babies is still common belief. (3) The sleep-apnea-hypothesis has turned out a complete error with serious consequences, but home apnea monitors are still being widely recommended. (4) The rise of SIDS in the 80ies and its subsequent decline in the 90ies has been interpreted as the advent and successful control of an epidemic although significant numbers of cot death have been reported long before the turn of the century, and the apparent increase which paralleled the introduction of the 9th edition of the ICD code is most likely due to improved registration. (5) Finally, SIDS is still being considered a random event--ignoring all evidence of an obvious role of socioeconomical factors.
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PMID:[Child's sudden death in 20th century--hypothesis, dogmas, dead wood]. 1076 30

A thymus-derived myoid precursor cell line (ST1), which differentiates to myoid cells in the growth arrest condition, was established by the cocultivation of F344 rat thymic cells with human T-lymphotropic virus type-I (HTLV-I)-producing human lymphoid cells. No integration of HTLV-I was detected in ST1 cells by Southern blot hybridization. In a differentiation culture condition such as confluent culture or serum starvation, ST1 cells began to fuse, creating multinuclear giant cells, with the induced expression of MyoD1 and various muscle-specific antigens, including alpha-sarcomeric actin, skeletal muscle myosin, myoglobin, desmin, and acetylcholine receptor. Ultrastructural investigation revealed that differentiated ST1B cells created aggregates of thick and thin filaments with Z-band-like composition, then formed sarcomeric structures and tubular honeycomb arrays. Finally, these cells spontaneously contracted with a frequency of 0.5-2.0 Hz and synchronized with adjoining cells. Transplantation of ST1B cells into nude mice produced a small tumor nodule, showing clear differentiation to skeletal muscle cells. ST1B cells did not indicate any colony-forming activities in soft agar, demonstrating that ST1B cells retain some of the physiologically normal phenotypes. This rare cell line is promising for use in various physiological and pathological investigations including functional research of thymic myoid cells and the pathological role in autoimmune diseases, as well as animal model experiments of cell therapy related to muscular degenerative disorders or regeneration of injured muscles.
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PMID:Differentiation of rat thymic myoid progenitor cell line established by coculture with human T-lymphotropic virus type-I producing human T cells. 1080 81


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